mouse anti ph2ax  (Cell Signaling Technology Inc)


Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 95
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc mouse anti ph2ax
    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, <t>pH2AX</t> in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Mouse Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti ph2ax/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse anti ph2ax - by Bioz Stars, 2023-12
    95/100 stars

    Images

    1) Product Images from "Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors"

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    Journal: bioRxiv

    doi: 10.1101/2023.03.27.534412

    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Figure Legend Snippet: A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Techniques Used: Staining

    A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).
    Figure Legend Snippet: A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Techniques Used: Staining, Marker

    A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.
    Figure Legend Snippet: A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Techniques Used: Expressing, Immunofluorescence, Staining, Fluorescence

    rabbit anti ph2ax ser139  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc rabbit anti ph2ax ser139
    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, <t>pH2AX</t> in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Rabbit Anti Ph2ax Ser139, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti ph2ax ser139/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti ph2ax ser139 - by Bioz Stars, 2023-12
    98/100 stars

    Images

    1) Product Images from "Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors"

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    Journal: bioRxiv

    doi: 10.1101/2023.03.27.534412

    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Figure Legend Snippet: A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Techniques Used: Staining

    A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).
    Figure Legend Snippet: A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Techniques Used: Staining, Marker

    A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.
    Figure Legend Snippet: A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Techniques Used: Expressing, Immunofluorescence, Staining, Fluorescence

    mouse anti ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 95
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc mouse anti ph2ax
    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, <t>pH2AX</t> in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Mouse Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti ph2ax/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse anti ph2ax - by Bioz Stars, 2023-12
    95/100 stars

    Images

    1) Product Images from "Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors"

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    Journal: bioRxiv

    doi: 10.1101/2023.03.27.534412

    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Figure Legend Snippet: A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Techniques Used: Staining

    A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).
    Figure Legend Snippet: A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Techniques Used: Staining, Marker

    A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.
    Figure Legend Snippet: A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Techniques Used: Expressing, Immunofluorescence, Staining, Fluorescence

    anti ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc anti ph2ax
    KEY RESOURCES TABLE Primary and secondary antibodies
    Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ph2ax - by Bioz Stars, 2023-12
    98/100 stars

    Images

    1) Product Images from "Deletion of STAT3 from Foxd1 cell population protects mice from kidney fibrosis by inhibiting pericytes trans-differentiation and migration"

    Article Title: Deletion of STAT3 from Foxd1 cell population protects mice from kidney fibrosis by inhibiting pericytes trans-differentiation and migration

    Journal: Cell reports

    doi: 10.1016/j.celrep.2022.110473

    KEY RESOURCES TABLE Primary and secondary antibodies
    Figure Legend Snippet: KEY RESOURCES TABLE Primary and secondary antibodies

    Techniques Used:

    rabbit anti ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 95
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc rabbit anti ph2ax
    Rabbit Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti ph2ax/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti ph2ax - by Bioz Stars, 2023-12
    95/100 stars

    Images

    ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc ph2ax
    Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ph2ax - by Bioz Stars, 2023-12
    98/100 stars

    Images

    anti ph2ax ser139  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc anti ph2ax ser139
    Anti Ph2ax Ser139, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ph2ax ser139/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ph2ax ser139 - by Bioz Stars, 2023-12
    98/100 stars

    Images

    antibodies for ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc antibodies for ph2ax
    Antibodies For Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies for ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies for ph2ax - by Bioz Stars, 2023-12
    98/100 stars

    Images

    antibodies for ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc antibodies for ph2ax
    (A) Chemical structure of LJ4425, (B) Graphical presentation of Adenosine kinase analogue, LJ4425, interfering in DNA elongation due to the existence of 5’-hydroxyl group (C) Derivatives of LJ4425 by replacing 5’-hydroxyl group to amine (LJ4760, left), azide (LJ4827, middle) and urea (LJ4857, right) (E) Immunoblotting analysis for <t>pH2AX</t> on HeLa cells after each derivatives treatment (500nM), β-actin for equal protein loading control (F) Graphical presentation of EC 50 value of LJ4760 and LJ4827 on cell growth inhibition of six different cell lines
    Antibodies For Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies for ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies for ph2ax - by Bioz Stars, 2023-12
    98/100 stars

    Images

    1) Product Images from "Identification of a novel HASPIN inhibitor and its synergism with the PLK1 inhibitor"

    Article Title: Identification of a novel HASPIN inhibitor and its synergism with the PLK1 inhibitor

    Journal: bioRxiv

    doi: 10.1101/2022.09.01.506282

    (A) Chemical structure of LJ4425, (B) Graphical presentation of Adenosine kinase analogue, LJ4425, interfering in DNA elongation due to the existence of 5’-hydroxyl group (C) Derivatives of LJ4425 by replacing 5’-hydroxyl group to amine (LJ4760, left), azide (LJ4827, middle) and urea (LJ4857, right) (E) Immunoblotting analysis for pH2AX on HeLa cells after each derivatives treatment (500nM), β-actin for equal protein loading control (F) Graphical presentation of EC 50 value of LJ4760 and LJ4827 on cell growth inhibition of six different cell lines
    Figure Legend Snippet: (A) Chemical structure of LJ4425, (B) Graphical presentation of Adenosine kinase analogue, LJ4425, interfering in DNA elongation due to the existence of 5’-hydroxyl group (C) Derivatives of LJ4425 by replacing 5’-hydroxyl group to amine (LJ4760, left), azide (LJ4827, middle) and urea (LJ4857, right) (E) Immunoblotting analysis for pH2AX on HeLa cells after each derivatives treatment (500nM), β-actin for equal protein loading control (F) Graphical presentation of EC 50 value of LJ4760 and LJ4827 on cell growth inhibition of six different cell lines

    Techniques Used: Western Blot, Inhibition

    (A) Scheme of transcriptome-guided MoA inference using Connectivity Map database (B) Frequency of matched compound’s mode of action in query (total=18) (C) Tanimoto coefficients of compounds predicted in (B), (D) Chemical structures of 5-iodotubercidin (E) Adenosine kinase activity (arbitrary unit: A.U) after LJ4827 or 5ITU treatment, Neg: Negative control, Pos: Positive control, n.s: not significant, (F) Scheme of gene ontology (Biological process: BP) analysis of downregulated genes after LJ4827 or 5ITU treatment, (G) Gene ontology (BP) analysis of downregulated genes by both LJ4827 and 5ITU treatment, (H) GSEA plot of the enrichment of the “Cell_cycle_mitotic” signature (left) and “Mitotic_spindle_Checkpoint” signature (right) in control group in comparison with treatment group (I) GSEA plot of the enrichment of the “DNA_double_strand_breeak_repair” signature in 5ITU treated group in comparison with LJ4827 treated group, (J) Immunoblotting for pH2AX at 24 hours after treatment of LJ or 5ITU (500nM) in HeLa, β-actin for equal loading control
    Figure Legend Snippet: (A) Scheme of transcriptome-guided MoA inference using Connectivity Map database (B) Frequency of matched compound’s mode of action in query (total=18) (C) Tanimoto coefficients of compounds predicted in (B), (D) Chemical structures of 5-iodotubercidin (E) Adenosine kinase activity (arbitrary unit: A.U) after LJ4827 or 5ITU treatment, Neg: Negative control, Pos: Positive control, n.s: not significant, (F) Scheme of gene ontology (Biological process: BP) analysis of downregulated genes after LJ4827 or 5ITU treatment, (G) Gene ontology (BP) analysis of downregulated genes by both LJ4827 and 5ITU treatment, (H) GSEA plot of the enrichment of the “Cell_cycle_mitotic” signature (left) and “Mitotic_spindle_Checkpoint” signature (right) in control group in comparison with treatment group (I) GSEA plot of the enrichment of the “DNA_double_strand_breeak_repair” signature in 5ITU treated group in comparison with LJ4827 treated group, (J) Immunoblotting for pH2AX at 24 hours after treatment of LJ or 5ITU (500nM) in HeLa, β-actin for equal loading control

    Techniques Used: Activity Assay, Negative Control, Positive Control, Western Blot

    (A) Scheme of FUCCI system (left) and temporal intensity profiles of green (GF) or red fluorescence (RF) from FUCCI-HeLa at indicated time after release from double thymidine block (DTB) (B) temporal intensity profiles of green (GF) or red fluorescence (RF) from FUCCI-HeLa at indicated time after release from double thymidine block (DTB) with treatment of 500 nM of each compound, LJ4827: LJ, CHR6494:CHR, 5ITU respectively (top), Summary of time (minute: min) at peak of green or red fluorescence intensity after DTB, n.d: not determined (bottom) (C) Representative images of clonogenic assay after treatment of indicated dose of compounds (left), graphical quantification of relative area of survived colonies (right) (D) Immunoblotting analysis for pH2AX on A549 cells at 24 hours after 500nM treatment of each compound, β-actin for equal protein loading control (E) Immunoblotting analysis for Cyclin B1, phospho-Histone H3 [threonine 3, pH3(T3)] and phospho-Histone H3 [serine 10, pH3 (S10)] of A549 at indicative times (hr: hours) after release from G1/S (DTB Cont), synchronized by DTB in the absence (DMSO for vehicle) or presence of LJ4827 (500nM, LJ), β-actin for equal protein loading control, (F) Graphical presentation of % of cell population of G1 (green), S (red) and G2/M (blue) at indicated time after G1/S release in the absence (Mock) or presence of LJ4827 (500nM, LJ), Asyn: Asynchronized control (G) Immunofluorescent images of Aurora B (red) and CENP-F (green) in HeLa (I: interphase, PM: prometaphase, M: metaphase and A: Anaphase), (H and I) Immunofluorescent images of Aurora B (red) and CENP-F (I) in HeLa in the absence (Mock) or presence of LJ4827 (500nM, LJ) (J) Immunofluorescent images of phospho-Histone H3 (serine 10, pH3) Aurora B (red) and CENP-F (I) in hMSCs in the absence (Mock) or presence of LJ4827 (500nM, LJ)
    Figure Legend Snippet: (A) Scheme of FUCCI system (left) and temporal intensity profiles of green (GF) or red fluorescence (RF) from FUCCI-HeLa at indicated time after release from double thymidine block (DTB) (B) temporal intensity profiles of green (GF) or red fluorescence (RF) from FUCCI-HeLa at indicated time after release from double thymidine block (DTB) with treatment of 500 nM of each compound, LJ4827: LJ, CHR6494:CHR, 5ITU respectively (top), Summary of time (minute: min) at peak of green or red fluorescence intensity after DTB, n.d: not determined (bottom) (C) Representative images of clonogenic assay after treatment of indicated dose of compounds (left), graphical quantification of relative area of survived colonies (right) (D) Immunoblotting analysis for pH2AX on A549 cells at 24 hours after 500nM treatment of each compound, β-actin for equal protein loading control (E) Immunoblotting analysis for Cyclin B1, phospho-Histone H3 [threonine 3, pH3(T3)] and phospho-Histone H3 [serine 10, pH3 (S10)] of A549 at indicative times (hr: hours) after release from G1/S (DTB Cont), synchronized by DTB in the absence (DMSO for vehicle) or presence of LJ4827 (500nM, LJ), β-actin for equal protein loading control, (F) Graphical presentation of % of cell population of G1 (green), S (red) and G2/M (blue) at indicated time after G1/S release in the absence (Mock) or presence of LJ4827 (500nM, LJ), Asyn: Asynchronized control (G) Immunofluorescent images of Aurora B (red) and CENP-F (green) in HeLa (I: interphase, PM: prometaphase, M: metaphase and A: Anaphase), (H and I) Immunofluorescent images of Aurora B (red) and CENP-F (I) in HeLa in the absence (Mock) or presence of LJ4827 (500nM, LJ) (J) Immunofluorescent images of phospho-Histone H3 (serine 10, pH3) Aurora B (red) and CENP-F (I) in hMSCs in the absence (Mock) or presence of LJ4827 (500nM, LJ)

    Techniques Used: Fluorescence, Blocking Assay, Clonogenic Assay, Western Blot

    ph2ax  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 98
      Buy from Supplier

    Structured Review

    Cell Signaling Technology Inc ph2ax
    Loss of Trip13 triggers mitotic failure to induce cell death. A) BrdU incorporation at days 1, 2, or 3, post‐transfection in HLF cells transfected with control or Trip13‐targeting siRNA ( n = 3). B) Mitotic index in HLF cells at days 1, 2, or 3 after siControl or siTrip13 transfection. C) Number of mitotic poles per cell in control or Trip13 KD HLF cells. Cells were IF stained for tubulin and spindle poles were counted ( n = 3). D) Representative immunofluorescence (IF) images of HLF cells showing mitotic shapes at day 3 after Trip13 KD. Green (tubulin), blue (DAPI) ( n = 3). E) Quantification of pericentrin IF foci per mitotic cell in HLF control or Trip13 KD cells ( n = 3). F) Representative images showing pericentrin foci in Trip13 KD HLF cells. G) HLF cells expressing H2B‐Cherry and transfected with siControl or siTrip13 were followed during mitosis by live microscopy from the time of nuclear envelope breakdown (NEBD) to anaphase ( n = 2). H) Protein extracts from control or Trip13 KD HLF cells were used for <t>pH2Ax,</t> pH3, and Cyclin b1 western blot analysis ( n = 6). I) Growth curve of HLF cells transfected with siControl, siTrip13, siAurora kinase A, or combinations ( n = 3). J) Protein levels of cleaved caspase 3 and pH2Ax in HLF cells transfected as in (I) ( n = 3). K) Apoptosis measured by caspase 3/7 activity of HLF cells transfected with siControl, siTrip13, siAurora kinase A, or siTrip13 and siAurora kinase A ( n = 2). L) Western blot of siControl‐ or siTrip13‐transfected HLF cells after synchronization in G2 or mitosis, showing levels of Aurora kinase A ( n = 3). All data in the figure are shown as the mean ± SEM. n numbers refer to biological replicates. (A, B, E, K) 1‐way ANOVA with Tukey's Multiple Comparison test. (C, G) Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ph2ax - by Bioz Stars, 2023-12
    98/100 stars

    Images

    1) Product Images from "Trip13 Depletion in Liver Cancer Induces a Lipogenic Response Contributing to Plin2‐Dependent Mitotic Cell Death"

    Article Title: Trip13 Depletion in Liver Cancer Induces a Lipogenic Response Contributing to Plin2‐Dependent Mitotic Cell Death

    Journal: Advanced Science

    doi: 10.1002/advs.202104291

    Loss of Trip13 triggers mitotic failure to induce cell death. A) BrdU incorporation at days 1, 2, or 3, post‐transfection in HLF cells transfected with control or Trip13‐targeting siRNA ( n = 3). B) Mitotic index in HLF cells at days 1, 2, or 3 after siControl or siTrip13 transfection. C) Number of mitotic poles per cell in control or Trip13 KD HLF cells. Cells were IF stained for tubulin and spindle poles were counted ( n = 3). D) Representative immunofluorescence (IF) images of HLF cells showing mitotic shapes at day 3 after Trip13 KD. Green (tubulin), blue (DAPI) ( n = 3). E) Quantification of pericentrin IF foci per mitotic cell in HLF control or Trip13 KD cells ( n = 3). F) Representative images showing pericentrin foci in Trip13 KD HLF cells. G) HLF cells expressing H2B‐Cherry and transfected with siControl or siTrip13 were followed during mitosis by live microscopy from the time of nuclear envelope breakdown (NEBD) to anaphase ( n = 2). H) Protein extracts from control or Trip13 KD HLF cells were used for pH2Ax, pH3, and Cyclin b1 western blot analysis ( n = 6). I) Growth curve of HLF cells transfected with siControl, siTrip13, siAurora kinase A, or combinations ( n = 3). J) Protein levels of cleaved caspase 3 and pH2Ax in HLF cells transfected as in (I) ( n = 3). K) Apoptosis measured by caspase 3/7 activity of HLF cells transfected with siControl, siTrip13, siAurora kinase A, or siTrip13 and siAurora kinase A ( n = 2). L) Western blot of siControl‐ or siTrip13‐transfected HLF cells after synchronization in G2 or mitosis, showing levels of Aurora kinase A ( n = 3). All data in the figure are shown as the mean ± SEM. n numbers refer to biological replicates. (A, B, E, K) 1‐way ANOVA with Tukey's Multiple Comparison test. (C, G) Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: Loss of Trip13 triggers mitotic failure to induce cell death. A) BrdU incorporation at days 1, 2, or 3, post‐transfection in HLF cells transfected with control or Trip13‐targeting siRNA ( n = 3). B) Mitotic index in HLF cells at days 1, 2, or 3 after siControl or siTrip13 transfection. C) Number of mitotic poles per cell in control or Trip13 KD HLF cells. Cells were IF stained for tubulin and spindle poles were counted ( n = 3). D) Representative immunofluorescence (IF) images of HLF cells showing mitotic shapes at day 3 after Trip13 KD. Green (tubulin), blue (DAPI) ( n = 3). E) Quantification of pericentrin IF foci per mitotic cell in HLF control or Trip13 KD cells ( n = 3). F) Representative images showing pericentrin foci in Trip13 KD HLF cells. G) HLF cells expressing H2B‐Cherry and transfected with siControl or siTrip13 were followed during mitosis by live microscopy from the time of nuclear envelope breakdown (NEBD) to anaphase ( n = 2). H) Protein extracts from control or Trip13 KD HLF cells were used for pH2Ax, pH3, and Cyclin b1 western blot analysis ( n = 6). I) Growth curve of HLF cells transfected with siControl, siTrip13, siAurora kinase A, or combinations ( n = 3). J) Protein levels of cleaved caspase 3 and pH2Ax in HLF cells transfected as in (I) ( n = 3). K) Apoptosis measured by caspase 3/7 activity of HLF cells transfected with siControl, siTrip13, siAurora kinase A, or siTrip13 and siAurora kinase A ( n = 2). L) Western blot of siControl‐ or siTrip13‐transfected HLF cells after synchronization in G2 or mitosis, showing levels of Aurora kinase A ( n = 3). All data in the figure are shown as the mean ± SEM. n numbers refer to biological replicates. (A, B, E, K) 1‐way ANOVA with Tukey's Multiple Comparison test. (C, G) Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: BrdU Incorporation Assay, Transfection, Staining, Immunofluorescence, Expressing, Microscopy, Western Blot, Activity Assay

    Prevention of Trip13‐KD‐induced accumulation of lipid droplets rescues mitotic abnormalities and cell death. A) Representative images of HLF control cells and cells upon KD of Trip13 and/or insulin receptor showing lipid droplets and mitotic spindles. Red (Aurora kinase A), green (bodipy), blue (DAPI) ( n = 3). B) Quantification of the proportion of cells displaying lipid droplets transfected as in (A). C) Quantification of the number of centrosomes in mitotic HLF cells. D) Representative images of control and Trip13 KD HLF cells showing lipid droplets (Bodipy) and centrosomes (p350) ( n = 3). E) Number of MTOCs formed during mitosis in Trip13 KD cells. The green bar represents the time of metaphase initiation in control cells, the red bar represents the time of anaphase in control cells ( n = 5). F) Western blots showing FASN, ACC, and pACLY in Trip13 KD HLF cells ( n = 4). G) Levels of cleaved caspase 3, pH2Ax, and pH3 in HLF control cells or upon KD of Trip13 and/or ACLY ( n = 3). H) Representative images of HLF cells with KD of Trip13 alone or in combination with ACLY KD showing spindle abnormalities and lipid droplet accumulation ( n = 3). I) Growth curve of HLF control cells or upon KD of Trip13 and/or ACLY ( n = 3). J) Mitotic index of HLF cells upon Trip13 KD alone or in combination with KD of ACLY, ACC, or AGPAT2 ( n = 3). K) Percentage of HLF cells displaying lipid droplets transfected as in (J) ( n = 3). L) Lipidomic analysis showing log2 fold changes of TG concentrations between Trip13 KD (siTrip13) and control (siControl) HLF cells at 30 h post‐transfection ( n = 5). The x ‐axis represents triglycerides (TGs) with number of carbon atoms and number of double bonds. The y ‐axis indicates one fatty acid (out of three per TG) that can be specified using the multiple reaction monitoring (MRM)‐based Lipidyzer assay. (B, C, J, K) Data are shown as the mean ± SEM and analyzed by 1‐way ANOVA with Tukey's Multiple Comparison test. * p < 0.05, ** p < 0.01, *** p < 0.001. (L) Data were analyzed using unpaired Wilcoxon rank‐sum tests corrected for multiple comparisons using the Benjamini–Hochberg method. q values <0.05 (*) were considered as statistically significant. n numbers refer to biological replicates. See also Figure in the Supporting Information.
    Figure Legend Snippet: Prevention of Trip13‐KD‐induced accumulation of lipid droplets rescues mitotic abnormalities and cell death. A) Representative images of HLF control cells and cells upon KD of Trip13 and/or insulin receptor showing lipid droplets and mitotic spindles. Red (Aurora kinase A), green (bodipy), blue (DAPI) ( n = 3). B) Quantification of the proportion of cells displaying lipid droplets transfected as in (A). C) Quantification of the number of centrosomes in mitotic HLF cells. D) Representative images of control and Trip13 KD HLF cells showing lipid droplets (Bodipy) and centrosomes (p350) ( n = 3). E) Number of MTOCs formed during mitosis in Trip13 KD cells. The green bar represents the time of metaphase initiation in control cells, the red bar represents the time of anaphase in control cells ( n = 5). F) Western blots showing FASN, ACC, and pACLY in Trip13 KD HLF cells ( n = 4). G) Levels of cleaved caspase 3, pH2Ax, and pH3 in HLF control cells or upon KD of Trip13 and/or ACLY ( n = 3). H) Representative images of HLF cells with KD of Trip13 alone or in combination with ACLY KD showing spindle abnormalities and lipid droplet accumulation ( n = 3). I) Growth curve of HLF control cells or upon KD of Trip13 and/or ACLY ( n = 3). J) Mitotic index of HLF cells upon Trip13 KD alone or in combination with KD of ACLY, ACC, or AGPAT2 ( n = 3). K) Percentage of HLF cells displaying lipid droplets transfected as in (J) ( n = 3). L) Lipidomic analysis showing log2 fold changes of TG concentrations between Trip13 KD (siTrip13) and control (siControl) HLF cells at 30 h post‐transfection ( n = 5). The x ‐axis represents triglycerides (TGs) with number of carbon atoms and number of double bonds. The y ‐axis indicates one fatty acid (out of three per TG) that can be specified using the multiple reaction monitoring (MRM)‐based Lipidyzer assay. (B, C, J, K) Data are shown as the mean ± SEM and analyzed by 1‐way ANOVA with Tukey's Multiple Comparison test. * p < 0.05, ** p < 0.01, *** p < 0.001. (L) Data were analyzed using unpaired Wilcoxon rank‐sum tests corrected for multiple comparisons using the Benjamini–Hochberg method. q values <0.05 (*) were considered as statistically significant. n numbers refer to biological replicates. See also Figure in the Supporting Information.

    Techniques Used: Transfection, Western Blot

    Perilipin‐2 confers susceptibility to Trip13‐KD‐induced cell death. A) Western blots showing levels of cleaved caspase3 pH2Ax and pH3 in Trip13 KD U2OS cells ( n = 4). B) Growth curve of U2OS cells transfected as in (A). C) Western blot of HLF and SK‐BR3 cells transfected with siControl or siTrip13 showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). D) Growth curve of Trip13 KD SK‐BR3 cells. E) Lipid droplet accumulation and mitotic index of SK‐BR3 cells KD for Trip13. F) Western blot of HLF and U87MG cells transfected with siTrip13 showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). G) Western blot of HLF wt or Plin2 overexpressing cells transfected with siTrip13, showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). H) Growth curve of cells transfected as in (G). I) Representative images of HLF Trip13 KD cells with high or J) low levels of Plin2 overexpression showing Plin2 and Aurora kinase A localization ( n = 3). K) Mitotic index of cells transfected as in (G) ( n = 3). L) Western blot of HLF and HeLa cells transfected with siTrip13 showing levels of Plin2, cleaved caspase3, pH2Ax, and pH3 ( n = 2). M) Representative images of HeLa cells KD for Trip13 showing lipid droplets ( n = 3). N) Western blot of HeLa wt or Plin2‐overexpressing cells transfected with siTrip13, showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). All data are shown as the mean ± SEM. n numbers refer to biological replicates. (E, K) 1‐way ANOVA with Tukey's Multiple Comparison test. * p < 0.05, ** p < 0.01, *** p < 0.001. See also Figure in the Supporting Information.
    Figure Legend Snippet: Perilipin‐2 confers susceptibility to Trip13‐KD‐induced cell death. A) Western blots showing levels of cleaved caspase3 pH2Ax and pH3 in Trip13 KD U2OS cells ( n = 4). B) Growth curve of U2OS cells transfected as in (A). C) Western blot of HLF and SK‐BR3 cells transfected with siControl or siTrip13 showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). D) Growth curve of Trip13 KD SK‐BR3 cells. E) Lipid droplet accumulation and mitotic index of SK‐BR3 cells KD for Trip13. F) Western blot of HLF and U87MG cells transfected with siTrip13 showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). G) Western blot of HLF wt or Plin2 overexpressing cells transfected with siTrip13, showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). H) Growth curve of cells transfected as in (G). I) Representative images of HLF Trip13 KD cells with high or J) low levels of Plin2 overexpression showing Plin2 and Aurora kinase A localization ( n = 3). K) Mitotic index of cells transfected as in (G) ( n = 3). L) Western blot of HLF and HeLa cells transfected with siTrip13 showing levels of Plin2, cleaved caspase3, pH2Ax, and pH3 ( n = 2). M) Representative images of HeLa cells KD for Trip13 showing lipid droplets ( n = 3). N) Western blot of HeLa wt or Plin2‐overexpressing cells transfected with siTrip13, showing levels of cleaved caspase3 pH2Ax and pH3 ( n = 3). All data are shown as the mean ± SEM. n numbers refer to biological replicates. (E, K) 1‐way ANOVA with Tukey's Multiple Comparison test. * p < 0.05, ** p < 0.01, *** p < 0.001. See also Figure in the Supporting Information.

    Techniques Used: Western Blot, Transfection, Over Expression

    High perilipin‐2 levels sensitize tumor cells to mitosis‐targeting paclitaxel. A) Western blot of HLF cells transfected with siPlin2 and treated with 2 n m paclitaxel for 48 h, showing levels of pH2Ax and pH3 ( n = 3). B) Growth curve of HLF cells transfected as in (A) and treated with 0–5 n m paclitaxel ( n = 3). C) Western blot of U87MG control or Plin2 overexpressing cells treated with 2 n m paclitaxel for 48 h, showing levels of pH2Ax and pH3 ( n = 3). D) Growth curve of U87MG cells transfected as in (C) and treated with 0–5 n m paclitaxel ( n = 3). E) Western blot of HeLa wt or Plin2‐overexpressing cells treated with 2 n m paclitaxel for 48 h, showing levels of pH2Ax and pH3 ( n = 3). F) Growth curve of HeLa cells transfected as in (E) and treated with 0–5 n m paclitaxel ( n = 3). All data are shown as the mean ± SEM. n numbers refer to biological replicates.
    Figure Legend Snippet: High perilipin‐2 levels sensitize tumor cells to mitosis‐targeting paclitaxel. A) Western blot of HLF cells transfected with siPlin2 and treated with 2 n m paclitaxel for 48 h, showing levels of pH2Ax and pH3 ( n = 3). B) Growth curve of HLF cells transfected as in (A) and treated with 0–5 n m paclitaxel ( n = 3). C) Western blot of U87MG control or Plin2 overexpressing cells treated with 2 n m paclitaxel for 48 h, showing levels of pH2Ax and pH3 ( n = 3). D) Growth curve of U87MG cells transfected as in (C) and treated with 0–5 n m paclitaxel ( n = 3). E) Western blot of HeLa wt or Plin2‐overexpressing cells treated with 2 n m paclitaxel for 48 h, showing levels of pH2Ax and pH3 ( n = 3). F) Growth curve of HeLa cells transfected as in (E) and treated with 0–5 n m paclitaxel ( n = 3). All data are shown as the mean ± SEM. n numbers refer to biological replicates.

    Techniques Used: Western Blot, Transfection

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • mouse anti ph2ax  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc mouse anti ph2ax
    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, <t>pH2AX</t> in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Mouse Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti ph2ax/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse anti ph2ax - by Bioz Stars, 2023-12
    95/100 stars
    		  Buy from Supplier
    rabbit anti ph2ax ser139  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc rabbit anti ph2ax ser139
    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, <t>pH2AX</t> in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.
    Rabbit Anti Ph2ax Ser139, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti ph2ax ser139/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti ph2ax ser139 - by Bioz Stars, 2023-12
    98/100 stars
    		  Buy from Supplier
    anti ph2ax  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc anti ph2ax
    KEY RESOURCES TABLE Primary and secondary antibodies
    Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ph2ax - by Bioz Stars, 2023-12
    98/100 stars
    		  Buy from Supplier
    rabbit anti ph2ax  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc rabbit anti ph2ax
    KEY RESOURCES TABLE Primary and secondary antibodies
    Rabbit Anti Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti ph2ax/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti ph2ax - by Bioz Stars, 2023-12
    95/100 stars
    		  Buy from Supplier
    ph2ax  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc ph2ax
    KEY RESOURCES TABLE Primary and secondary antibodies
    Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ph2ax - by Bioz Stars, 2023-12
    98/100 stars
    		  Buy from Supplier
    anti ph2ax ser139  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc anti ph2ax ser139
    KEY RESOURCES TABLE Primary and secondary antibodies
    Anti Ph2ax Ser139, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti ph2ax ser139/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti ph2ax ser139 - by Bioz Stars, 2023-12
    98/100 stars
    		  Buy from Supplier
    antibodies for ph2ax  (Cell Signaling Technology Inc)
    98
    Cell Signaling Technology Inc antibodies for ph2ax
    KEY RESOURCES TABLE Primary and secondary antibodies
    Antibodies For Ph2ax, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies for ph2ax/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies for ph2ax - by Bioz Stars, 2023-12
    98/100 stars
    		  Buy from Supplier

    Image Search Results


    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Journal: bioRxiv

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    doi: 10.1101/2023.03.27.534412

    Figure Lengend Snippet: A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Article Snippet: Cells were then washed and fixed with 4% paraformaldehyde (PFA) for 15 minutes at room temperature, blocked and permeabilized PBS-BSA + 0.3% Triton X-100 for 15 minutes at room temperature, and incubated with primary antibodies (rabbit anti-pTIF1β/pKAP1 (Ser824) (1:500, CST # 4127S) and Mouse anti-pH2AX (1:600, CST #80312) in PBS-BSA overnight at +4°C.

    Techniques: Staining

    A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Journal: bioRxiv

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    doi: 10.1101/2023.03.27.534412

    Figure Lengend Snippet: A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Article Snippet: Cells were then washed and fixed with 4% paraformaldehyde (PFA) for 15 minutes at room temperature, blocked and permeabilized PBS-BSA + 0.3% Triton X-100 for 15 minutes at room temperature, and incubated with primary antibodies (rabbit anti-pTIF1β/pKAP1 (Ser824) (1:500, CST # 4127S) and Mouse anti-pH2AX (1:600, CST #80312) in PBS-BSA overnight at +4°C.

    Techniques: Staining, Marker

    A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Journal: bioRxiv

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    doi: 10.1101/2023.03.27.534412

    Figure Lengend Snippet: A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Article Snippet: Cells were then washed and fixed with 4% paraformaldehyde (PFA) for 15 minutes at room temperature, blocked and permeabilized PBS-BSA + 0.3% Triton X-100 for 15 minutes at room temperature, and incubated with primary antibodies (rabbit anti-pTIF1β/pKAP1 (Ser824) (1:500, CST # 4127S) and Mouse anti-pH2AX (1:600, CST #80312) in PBS-BSA overnight at +4°C.

    Techniques: Expressing, Immunofluorescence, Staining, Fluorescence

    A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Journal: bioRxiv

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    doi: 10.1101/2023.03.27.534412

    Figure Lengend Snippet: A. Tabulated summary of IHC stainings indicating the number of premalignant (green) and malignant (blue) gastric lesions scored for each staining criterion. DDR/replication stress markers-53BP1, H2AX, pH2AX in red; Cell cycle regulators-p53, p16, p21 in purple. B. Summary of the stainings (DDR markers and the cell cycle regulation markers) in paired premalignant and malignant gastric lesions from gastric cancer patient8. PM= Premalignant gastric lesion, M= Malignant gastric lesion. C. Representative IHC images of paired premalignant and malignant gastric lesions from a gastric cancer patient (patient8) stained for DDR markers and cell cycle regulation markers, including H&E staining. Insets represent the zoomed area for each image.

    Article Snippet: The primary antibodies used for immunohistochemistry were: Human tissue-rabbit anti-ki67 (1:1000, Biocare Medical, #CRM325-5b6), rabbit anti-H2AX (1:1000, CST, #7631), rabbit anti-pH2AX ser139 (1:1000, CST, #9718), mouse anti-53BP1 (1:1000, Millipore, #3802), mouse anti-p53 (1:1000, CST, #48818), mouse anti-P16INK4 (1:1000, Abcam, #54210), rabbit anti-p21 (1:1000, CST, #2947), Murine tissue-rabbit anti-ki67 (1:1000, Biocare Medical, #CRM325-5b6), rabbit anti-pH2AX ser139, (1:1000, CST, #9718), rabbit anti-p53 (1:1000, Abcam, #1431), rabbit anti-p21 (1:1000, Abcam, #188224).

    Techniques: Staining

    A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Journal: bioRxiv

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    doi: 10.1101/2023.03.27.534412

    Figure Lengend Snippet: A. Summary of dysplasia grade and staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal (grey), premalignant (green), and malignant (blue) gastric lesions of four MNU treated mice. B. Representative IHC images of the staining pattern of proliferation marker ki67, DDR marker pH2AX, and cell cycle regulation markers (p53 and p21) in paired normal, premalignant, and malignant gastric lesions of MNU treated mouse4 (dysplasia score 5).

    Article Snippet: The primary antibodies used for immunohistochemistry were: Human tissue-rabbit anti-ki67 (1:1000, Biocare Medical, #CRM325-5b6), rabbit anti-H2AX (1:1000, CST, #7631), rabbit anti-pH2AX ser139 (1:1000, CST, #9718), mouse anti-53BP1 (1:1000, Millipore, #3802), mouse anti-p53 (1:1000, CST, #48818), mouse anti-P16INK4 (1:1000, Abcam, #54210), rabbit anti-p21 (1:1000, CST, #2947), Murine tissue-rabbit anti-ki67 (1:1000, Biocare Medical, #CRM325-5b6), rabbit anti-pH2AX ser139, (1:1000, CST, #9718), rabbit anti-p53 (1:1000, Abcam, #1431), rabbit anti-p21 (1:1000, Abcam, #188224).

    Techniques: Staining, Marker

    A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Journal: bioRxiv

    Article Title: Replicative stress in gastroesophageal adenocarcinoma is associated with chromosomal instability and sensitivity to DNA damage response inhibitors

    doi: 10.1101/2023.03.27.534412

    Figure Lengend Snippet: A. Correlation plot between H2AX gene expression (log2(TPM+1)) and CIN25 score (DNA damage checkpoint expression) for the CCLE gastric cancer cell lines; R squared value and p-value calculated by simple linear correlation analysis. B. H2AX expression (log2(TPM+1)) between ‘No WGD (0)’ (grey) and ‘with WGD (1/2)’ (green) groups of gastric cancer cell lines available in the BROAD institute PRISM repurposing drug screen dataset; Difference between the H2AX expression is represented as the mean±S.D.; P-value calculated by unpaired t-test. C. Ploidy abnormalities scores for the five gastric cancer cell lines. D. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in untreated five gastric cancer cell lines and RPE1 cells (non-neoplastic cell line) representing intrinsic replication stress/double-stranded DNA breaks (DSBs); Nucleus stained with DAPI (blue). E. Quantification of data in D., expressed as mean fluorescence intensity per cell (MFI) ± S.D from the following number of cells-RPE1-718, AGS-2080, HGC27, 1031, NUGC3-2119, GSU-2092, KE39-577. F. Quantification of pH2AX staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (red). Data expressed as mean fluorescence intensity (MFI) of pH2AX signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. G. Quantification of pKAP1 staining in prexasertib (Chk1/2) dose-dependent induced replication stress in cell lines with ‘intrinsic low-replication stress’-RPE1, AGS (grey) and ‘intrinsic high-replication stress’-GSU, KE39 (green). Data expressed as mean fluorescence intensity of pKAP1 signal per cell ± S.D from the following number of cells-RPE1: Control-718, 0.2nM-888, 2.0nM-524, 20.0nM-570, 200.0nM-350; AGS: Control-2080, 0.2nM-1487, 2.0nM-1996, 20.0nM-1211, 200.0nM-1396; GSU: Control-2092, 0.2nM-3319, 2.0nM-4035, 20.0nM-2057, 200.0nM-2402; KE39: Control-577, 0.2nM-1004, 2.0nM-1022, 20.0nM-728, 200.0nM-958. H. Representative immunofluorescence images of pH2AX (red) and pKAP1 (green) stainings in prexasertib (20nM) treated cell lines with intrinsic ‘low-replication stress’-RPE1, AGS, and intrinsic ‘high-replication stress’-GSU, KE39.

    Article Snippet: The primary antibodies used for immunohistochemistry were: Human tissue-rabbit anti-ki67 (1:1000, Biocare Medical, #CRM325-5b6), rabbit anti-H2AX (1:1000, CST, #7631), rabbit anti-pH2AX ser139 (1:1000, CST, #9718), mouse anti-53BP1 (1:1000, Millipore, #3802), mouse anti-p53 (1:1000, CST, #48818), mouse anti-P16INK4 (1:1000, Abcam, #54210), rabbit anti-p21 (1:1000, CST, #2947), Murine tissue-rabbit anti-ki67 (1:1000, Biocare Medical, #CRM325-5b6), rabbit anti-pH2AX ser139, (1:1000, CST, #9718), rabbit anti-p53 (1:1000, Abcam, #1431), rabbit anti-p21 (1:1000, Abcam, #188224).

    Techniques: Expressing, Immunofluorescence, Staining, Fluorescence

    KEY RESOURCES TABLE Primary and secondary antibodies

    Journal: Cell reports

    Article Title: Deletion of STAT3 from Foxd1 cell population protects mice from kidney fibrosis by inhibiting pericytes trans-differentiation and migration

    doi: 10.1016/j.celrep.2022.110473

    Figure Lengend Snippet: KEY RESOURCES TABLE Primary and secondary antibodies

    Article Snippet: Anti-pH2AX , Cell Signaling , 20E3 , 9718.

    Techniques: