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    Cell Signaling Technology Inc rabbit anti pten
    Deletion of <t>Klf5</t> accelerates the development and severity of mPIN induced by hemizygous deletion of <t>Pten</t> . H E-stained tissue section images of DPs and LPs at 6, 12, and 18 months with Klf5 and Pten deletions indicated. + and − indicate wild-type and deleted Klf5 or Pten alleles, respectively.
    Rabbit Anti Pten, 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 pten/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti pten - by Bioz Stars, 2022-11
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    94
    Vector Laboratories vectastain abc kit
    Deletion of <t>Klf5</t> accelerates the development and severity of mPIN induced by hemizygous deletion of <t>Pten</t> . H E-stained tissue section images of DPs and LPs at 6, 12, and 18 months with Klf5 and Pten deletions indicated. + and − indicate wild-type and deleted Klf5 or Pten alleles, respectively.
    Vectastain Abc Kit, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/vectastain abc kit/product/Vector Laboratories
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    vectastain abc kit - by Bioz Stars, 2022-11
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    93
    Tocris alda 1
    ALDH 2 activation reduced TGF ‐β1‐induced HSC ‐T6 cell activation along with attenuation of ROS generation. A, Representative western blot pictures of rat hepatic stellate cells transfected with scramble, ALDH 2 knockdown and ALDH 2 overexpression lentiviral vectors. B, Western blot analyses of α‐ SMA indicated HSC ‐T6 activation induced by a variety concentration of TGF ‐β1. C, Representative western blot pictures of α‐ SMA with or without TGF ‐β1 administration. D, Quantification analyses of the expression of α‐ SMA . E, Representative DHE staining with or without TGF ‐β1 administration. F, Representative DHE staining with or without <t>Alda‐1</t> administration. G, H, Quantification of DHE staining. The values represent means ± SEM . * P
    Alda 1, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/alda 1/product/Tocris
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    Image Search Results


    Deletion of Klf5 accelerates the development and severity of mPIN induced by hemizygous deletion of Pten . H E-stained tissue section images of DPs and LPs at 6, 12, and 18 months with Klf5 and Pten deletions indicated. + and − indicate wild-type and deleted Klf5 or Pten alleles, respectively.

    Journal: Neoplasia (New York, N.Y.)

    Article Title: Klf5 Deletion Promotes Pten Deletion–Initiated Luminal-Type Mouse Prostate Tumors through Multiple Oncogenic Signaling Pathways

    doi: 10.1016/j.neo.2014.09.006

    Figure Lengend Snippet: Deletion of Klf5 accelerates the development and severity of mPIN induced by hemizygous deletion of Pten . H E-stained tissue section images of DPs and LPs at 6, 12, and 18 months with Klf5 and Pten deletions indicated. + and − indicate wild-type and deleted Klf5 or Pten alleles, respectively.

    Article Snippet: The primary antibodies used in this study (IHC or IF) and dilutions were given as follows: rabbit anti-KLF5 (IHC, 1:6000 dilution) , rabbit anti-PTEN (Cell Signaling Technology, Danvers, MA; IHC, 1:100), rabbit anti-Ki67 (Thermo Fisher Scientific, Waltham, MA; IHC, 1:200), rabbit anti–phospho-Akt (Cell Signaling Technology; IHC, 1:150), mouse anti–phospho-Erk1/2 (Cell Signaling Technology; IHC, 1:200), rabbit anti–phospho-mammalian target of rapamycin (mTOR) (Cell Signaling Technology; IHC, 1:100), rabbit anti–phospho-S6 (Cell Signaling Technology; IHC, 1:200), rabbit anti-p15/INK4B (Cell Signaling Technology; IHC, 1:1000), rabbit anti-CK5 (Covance, Princeton, NJ; IHC, 1:1000; IF, 1:200), mouse anti-Ck14 (Thermo Fisher Scientific; IF, 1:200), mouse anti-p63 (Santa Cruz Biotechnology, Santa Cruz, CA; IF, 1:100), rabbit anti-Ck18 (GeneTex, Irvine, CA; IHC, 1:1500; IF, 1:400), mouse anti–smooth muscle actin (Sma; Sigma-Aldrich, St Louis, MO; IHC, 1:5000), rabbit anti-EGF (Abcam, Cambridge, MA; IHC, 1:400), and rabbit anti–phospho–Egf receptor (Egfr) Y1068 (Cell Signaling Technology; IHC, 1:100).

    Techniques: Staining

    Knockout of Klf5 disrupts the architecture of prostate tumors induced by Pten deletion. Expression of basal cell markers Ck5, Ck14, and p63, luminal cell marker Ck18, and smooth muscle marker Sma was detected by IHC staining (A) or IF staining (B and C) in consecutive tissue sections (panel A only) of mouse prostates at 6 months of age. Pictures of basal and luminal markers were taken from the same area of tissue for better comparison (panel A only). DAPI staining was used to show nuclei (blue). Gene deletion status is indicated at the top and marker names at the left. The magnification for images of basal and luminal markers is × 200, and two magnifications are shown for Sma (× 10 in the upper and × 40 in the lower). + and − indicate the presence and absence of a Klf5 or a Pten allele.

    Journal: Neoplasia (New York, N.Y.)

    Article Title: Klf5 Deletion Promotes Pten Deletion–Initiated Luminal-Type Mouse Prostate Tumors through Multiple Oncogenic Signaling Pathways

    doi: 10.1016/j.neo.2014.09.006

    Figure Lengend Snippet: Knockout of Klf5 disrupts the architecture of prostate tumors induced by Pten deletion. Expression of basal cell markers Ck5, Ck14, and p63, luminal cell marker Ck18, and smooth muscle marker Sma was detected by IHC staining (A) or IF staining (B and C) in consecutive tissue sections (panel A only) of mouse prostates at 6 months of age. Pictures of basal and luminal markers were taken from the same area of tissue for better comparison (panel A only). DAPI staining was used to show nuclei (blue). Gene deletion status is indicated at the top and marker names at the left. The magnification for images of basal and luminal markers is × 200, and two magnifications are shown for Sma (× 10 in the upper and × 40 in the lower). + and − indicate the presence and absence of a Klf5 or a Pten allele.

    Article Snippet: The primary antibodies used in this study (IHC or IF) and dilutions were given as follows: rabbit anti-KLF5 (IHC, 1:6000 dilution) , rabbit anti-PTEN (Cell Signaling Technology, Danvers, MA; IHC, 1:100), rabbit anti-Ki67 (Thermo Fisher Scientific, Waltham, MA; IHC, 1:200), rabbit anti–phospho-Akt (Cell Signaling Technology; IHC, 1:150), mouse anti–phospho-Erk1/2 (Cell Signaling Technology; IHC, 1:200), rabbit anti–phospho-mammalian target of rapamycin (mTOR) (Cell Signaling Technology; IHC, 1:100), rabbit anti–phospho-S6 (Cell Signaling Technology; IHC, 1:200), rabbit anti-p15/INK4B (Cell Signaling Technology; IHC, 1:1000), rabbit anti-CK5 (Covance, Princeton, NJ; IHC, 1:1000; IF, 1:200), mouse anti-Ck14 (Thermo Fisher Scientific; IF, 1:200), mouse anti-p63 (Santa Cruz Biotechnology, Santa Cruz, CA; IF, 1:100), rabbit anti-Ck18 (GeneTex, Irvine, CA; IHC, 1:1500; IF, 1:400), mouse anti–smooth muscle actin (Sma; Sigma-Aldrich, St Louis, MO; IHC, 1:5000), rabbit anti-EGF (Abcam, Cambridge, MA; IHC, 1:400), and rabbit anti–phospho–Egf receptor (Egfr) Y1068 (Cell Signaling Technology; IHC, 1:100).

    Techniques: Knock-Out, Expressing, Marker, Immunohistochemistry, Staining

    Klf5 deletion upregulates EGF in Pten -null mouse prostate tumors and human prostate epithelial cell line. (A, B, and E) Detection of EGF mRNA expression by real-time RT-PCR (A) and Egf and p-Egfr proteins by IHC staining (B and E) in 6-month-old Pten -null mouse DPs with indicated Klf5 deletion status. Data for each genotype in A was from eight mice. (C and D) Detection of protein expression of KLF5 and PTEN by Western blot analysis (C) and mRNA expression of KLF5 , PTEN , and EGF by real-time RT-PCR (D) in the PNT2 immortalized human prostate luminal epithelial cell line with the knockdown of KLF5 , PTEN , or both by RNA interference.

    Journal: Neoplasia (New York, N.Y.)

    Article Title: Klf5 Deletion Promotes Pten Deletion–Initiated Luminal-Type Mouse Prostate Tumors through Multiple Oncogenic Signaling Pathways

    doi: 10.1016/j.neo.2014.09.006

    Figure Lengend Snippet: Klf5 deletion upregulates EGF in Pten -null mouse prostate tumors and human prostate epithelial cell line. (A, B, and E) Detection of EGF mRNA expression by real-time RT-PCR (A) and Egf and p-Egfr proteins by IHC staining (B and E) in 6-month-old Pten -null mouse DPs with indicated Klf5 deletion status. Data for each genotype in A was from eight mice. (C and D) Detection of protein expression of KLF5 and PTEN by Western blot analysis (C) and mRNA expression of KLF5 , PTEN , and EGF by real-time RT-PCR (D) in the PNT2 immortalized human prostate luminal epithelial cell line with the knockdown of KLF5 , PTEN , or both by RNA interference.

    Article Snippet: The primary antibodies used in this study (IHC or IF) and dilutions were given as follows: rabbit anti-KLF5 (IHC, 1:6000 dilution) , rabbit anti-PTEN (Cell Signaling Technology, Danvers, MA; IHC, 1:100), rabbit anti-Ki67 (Thermo Fisher Scientific, Waltham, MA; IHC, 1:200), rabbit anti–phospho-Akt (Cell Signaling Technology; IHC, 1:150), mouse anti–phospho-Erk1/2 (Cell Signaling Technology; IHC, 1:200), rabbit anti–phospho-mammalian target of rapamycin (mTOR) (Cell Signaling Technology; IHC, 1:100), rabbit anti–phospho-S6 (Cell Signaling Technology; IHC, 1:200), rabbit anti-p15/INK4B (Cell Signaling Technology; IHC, 1:1000), rabbit anti-CK5 (Covance, Princeton, NJ; IHC, 1:1000; IF, 1:200), mouse anti-Ck14 (Thermo Fisher Scientific; IF, 1:200), mouse anti-p63 (Santa Cruz Biotechnology, Santa Cruz, CA; IF, 1:100), rabbit anti-Ck18 (GeneTex, Irvine, CA; IHC, 1:1500; IF, 1:400), mouse anti–smooth muscle actin (Sma; Sigma-Aldrich, St Louis, MO; IHC, 1:5000), rabbit anti-EGF (Abcam, Cambridge, MA; IHC, 1:400), and rabbit anti–phospho–Egf receptor (Egfr) Y1068 (Cell Signaling Technology; IHC, 1:100).

    Techniques: Expressing, Quantitative RT-PCR, Immunohistochemistry, Staining, Mouse Assay, Western Blot

    Molecular characterization of prostate tumors induced by Klf5 and Pten deletion. (A) IHC staining of the Ki67 proliferation marker, oncogenic kinases p-Akt, p-Erk1/2, and p-S6, and the p15 cell cycle inhibitor in tissue sections of APs at 6 months of age with different deletion status of Klf5 and Pten . Marker names are indicated at the left, and the deletion status of genes is indicated at the top. The ratio (%) of Ki67-positive cells, as determined by cell counting, is shown at the lower right corner of each image of the Ki67 panels. (B) Detection of protein expression for Klf5, p-Akt, Akt, p-Erk1/2, Erk1/2, p-S6, p15, and β-actin by Western blot analysis in tissue lysates from anterior mouse prostates with the same genotype and age used in A. Relative protein level was determined by using the ImageJ software, and statistical significance was evaluated by using Student’s t test. Marker names are indicated at the left, and the deletion status of genes is indicated at the top. + and − indicate the presence and absence of an allele for Klf5 and Pten . * P

    Journal: Neoplasia (New York, N.Y.)

    Article Title: Klf5 Deletion Promotes Pten Deletion–Initiated Luminal-Type Mouse Prostate Tumors through Multiple Oncogenic Signaling Pathways

    doi: 10.1016/j.neo.2014.09.006

    Figure Lengend Snippet: Molecular characterization of prostate tumors induced by Klf5 and Pten deletion. (A) IHC staining of the Ki67 proliferation marker, oncogenic kinases p-Akt, p-Erk1/2, and p-S6, and the p15 cell cycle inhibitor in tissue sections of APs at 6 months of age with different deletion status of Klf5 and Pten . Marker names are indicated at the left, and the deletion status of genes is indicated at the top. The ratio (%) of Ki67-positive cells, as determined by cell counting, is shown at the lower right corner of each image of the Ki67 panels. (B) Detection of protein expression for Klf5, p-Akt, Akt, p-Erk1/2, Erk1/2, p-S6, p15, and β-actin by Western blot analysis in tissue lysates from anterior mouse prostates with the same genotype and age used in A. Relative protein level was determined by using the ImageJ software, and statistical significance was evaluated by using Student’s t test. Marker names are indicated at the left, and the deletion status of genes is indicated at the top. + and − indicate the presence and absence of an allele for Klf5 and Pten . * P

    Article Snippet: The primary antibodies used in this study (IHC or IF) and dilutions were given as follows: rabbit anti-KLF5 (IHC, 1:6000 dilution) , rabbit anti-PTEN (Cell Signaling Technology, Danvers, MA; IHC, 1:100), rabbit anti-Ki67 (Thermo Fisher Scientific, Waltham, MA; IHC, 1:200), rabbit anti–phospho-Akt (Cell Signaling Technology; IHC, 1:150), mouse anti–phospho-Erk1/2 (Cell Signaling Technology; IHC, 1:200), rabbit anti–phospho-mammalian target of rapamycin (mTOR) (Cell Signaling Technology; IHC, 1:100), rabbit anti–phospho-S6 (Cell Signaling Technology; IHC, 1:200), rabbit anti-p15/INK4B (Cell Signaling Technology; IHC, 1:1000), rabbit anti-CK5 (Covance, Princeton, NJ; IHC, 1:1000; IF, 1:200), mouse anti-Ck14 (Thermo Fisher Scientific; IF, 1:200), mouse anti-p63 (Santa Cruz Biotechnology, Santa Cruz, CA; IF, 1:100), rabbit anti-Ck18 (GeneTex, Irvine, CA; IHC, 1:1500; IF, 1:400), mouse anti–smooth muscle actin (Sma; Sigma-Aldrich, St Louis, MO; IHC, 1:5000), rabbit anti-EGF (Abcam, Cambridge, MA; IHC, 1:400), and rabbit anti–phospho–Egf receptor (Egfr) Y1068 (Cell Signaling Technology; IHC, 1:100).

    Techniques: Immunohistochemistry, Staining, Marker, Cell Counting, Expressing, Western Blot, Software

    Deletion of Klf5 promotes the development and severity of prostate tumor induced by homozygous deletion of Pten . Upper row panels are images of H E-stained tissue sections from the entire prostate gland at lower magnification, and lower row panels are magnified images of the boxed areas from the upper row panels. The prostates were from mice at 6 months of age. Note enlarged prostate glands and significant phenotypic alterations caused by Klf5 deletion. Prostates from two mice are shown for each genotype. + and − indicate wild-type and deleted Klf5 or Pten alleles, respectively.

    Journal: Neoplasia (New York, N.Y.)

    Article Title: Klf5 Deletion Promotes Pten Deletion–Initiated Luminal-Type Mouse Prostate Tumors through Multiple Oncogenic Signaling Pathways

    doi: 10.1016/j.neo.2014.09.006

    Figure Lengend Snippet: Deletion of Klf5 promotes the development and severity of prostate tumor induced by homozygous deletion of Pten . Upper row panels are images of H E-stained tissue sections from the entire prostate gland at lower magnification, and lower row panels are magnified images of the boxed areas from the upper row panels. The prostates were from mice at 6 months of age. Note enlarged prostate glands and significant phenotypic alterations caused by Klf5 deletion. Prostates from two mice are shown for each genotype. + and − indicate wild-type and deleted Klf5 or Pten alleles, respectively.

    Article Snippet: The primary antibodies used in this study (IHC or IF) and dilutions were given as follows: rabbit anti-KLF5 (IHC, 1:6000 dilution) , rabbit anti-PTEN (Cell Signaling Technology, Danvers, MA; IHC, 1:100), rabbit anti-Ki67 (Thermo Fisher Scientific, Waltham, MA; IHC, 1:200), rabbit anti–phospho-Akt (Cell Signaling Technology; IHC, 1:150), mouse anti–phospho-Erk1/2 (Cell Signaling Technology; IHC, 1:200), rabbit anti–phospho-mammalian target of rapamycin (mTOR) (Cell Signaling Technology; IHC, 1:100), rabbit anti–phospho-S6 (Cell Signaling Technology; IHC, 1:200), rabbit anti-p15/INK4B (Cell Signaling Technology; IHC, 1:1000), rabbit anti-CK5 (Covance, Princeton, NJ; IHC, 1:1000; IF, 1:200), mouse anti-Ck14 (Thermo Fisher Scientific; IF, 1:200), mouse anti-p63 (Santa Cruz Biotechnology, Santa Cruz, CA; IF, 1:100), rabbit anti-Ck18 (GeneTex, Irvine, CA; IHC, 1:1500; IF, 1:400), mouse anti–smooth muscle actin (Sma; Sigma-Aldrich, St Louis, MO; IHC, 1:5000), rabbit anti-EGF (Abcam, Cambridge, MA; IHC, 1:400), and rabbit anti–phospho–Egf receptor (Egfr) Y1068 (Cell Signaling Technology; IHC, 1:100).

    Techniques: Staining, Mouse Assay

    ALDH 2 activation reduced TGF ‐β1‐induced HSC ‐T6 cell activation along with attenuation of ROS generation. A, Representative western blot pictures of rat hepatic stellate cells transfected with scramble, ALDH 2 knockdown and ALDH 2 overexpression lentiviral vectors. B, Western blot analyses of α‐ SMA indicated HSC ‐T6 activation induced by a variety concentration of TGF ‐β1. C, Representative western blot pictures of α‐ SMA with or without TGF ‐β1 administration. D, Quantification analyses of the expression of α‐ SMA . E, Representative DHE staining with or without TGF ‐β1 administration. F, Representative DHE staining with or without Alda‐1 administration. G, H, Quantification of DHE staining. The values represent means ± SEM . * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Aldehyde dehydrogenase 2 activation ameliorates CCl4‐induced chronic liver fibrosis in mice by up‐regulating Nrf2/ HO‐1 antioxidant pathway, et al. Aldehyde dehydrogenase 2 activation ameliorates CCl4‐induced chronic liver fibrosis in mice by up‐regulating Nrf2/HO‐1 antioxidant pathway

    doi: 10.1111/jcmm.13677

    Figure Lengend Snippet: ALDH 2 activation reduced TGF ‐β1‐induced HSC ‐T6 cell activation along with attenuation of ROS generation. A, Representative western blot pictures of rat hepatic stellate cells transfected with scramble, ALDH 2 knockdown and ALDH 2 overexpression lentiviral vectors. B, Western blot analyses of α‐ SMA indicated HSC ‐T6 activation induced by a variety concentration of TGF ‐β1. C, Representative western blot pictures of α‐ SMA with or without TGF ‐β1 administration. D, Quantification analyses of the expression of α‐ SMA . E, Representative DHE staining with or without TGF ‐β1 administration. F, Representative DHE staining with or without Alda‐1 administration. G, H, Quantification of DHE staining. The values represent means ± SEM . * P

    Article Snippet: Notably, ALDH2 deficiency partly reversed the up‐regulation of HO‐1 after CCl4 challenge, whereas administration of Alda‐1 could up‐regulate Nrf2/HO‐1 pathway as well as significantly decreased α‐SMA protein expression, which shed light on the application of Alda‐1 in clinical liver diseases.

    Techniques: Activation Assay, Western Blot, Transfection, Over Expression, Concentration Assay, Expressing, Staining

    Alda‐1 activated the Nrf‐2/ HO ‐1 antioxidant pathway and Parkin‐mediated mitophagy. A, Representative western blot pictures of Nrf‐2 and HO ‐1. B, Quantification analyses of the expression of Nrf‐2 and HO ‐1. The values represent means ± SEM (n = 6‐9). * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Aldehyde dehydrogenase 2 activation ameliorates CCl4‐induced chronic liver fibrosis in mice by up‐regulating Nrf2/ HO‐1 antioxidant pathway, et al. Aldehyde dehydrogenase 2 activation ameliorates CCl4‐induced chronic liver fibrosis in mice by up‐regulating Nrf2/HO‐1 antioxidant pathway

    doi: 10.1111/jcmm.13677

    Figure Lengend Snippet: Alda‐1 activated the Nrf‐2/ HO ‐1 antioxidant pathway and Parkin‐mediated mitophagy. A, Representative western blot pictures of Nrf‐2 and HO ‐1. B, Quantification analyses of the expression of Nrf‐2 and HO ‐1. The values represent means ± SEM (n = 6‐9). * P

    Article Snippet: Notably, ALDH2 deficiency partly reversed the up‐regulation of HO‐1 after CCl4 challenge, whereas administration of Alda‐1 could up‐regulate Nrf2/HO‐1 pathway as well as significantly decreased α‐SMA protein expression, which shed light on the application of Alda‐1 in clinical liver diseases.

    Techniques: Western Blot, Expressing

    Alda‐1 alleviated chronic CC l 4 ‐induced liver fibrosis. A, Liver/bodyweight ratio. B, Representative histopathological pictures of the liver. Upper panel: Representative H E staining. Middle panel: Representative Masson's trichrome staining. Lower panel: Representative images of α‐ SMA staining. C, Quantification of Masson's trichrome and α‐ SMA ‐positive area. D, Representative western blot pictures of α‐ SMA . E, Quantification analyses of the expression of α‐ SMA . The values represent means ± SEM (n = 6‐9). * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Aldehyde dehydrogenase 2 activation ameliorates CCl4‐induced chronic liver fibrosis in mice by up‐regulating Nrf2/ HO‐1 antioxidant pathway, et al. Aldehyde dehydrogenase 2 activation ameliorates CCl4‐induced chronic liver fibrosis in mice by up‐regulating Nrf2/HO‐1 antioxidant pathway

    doi: 10.1111/jcmm.13677

    Figure Lengend Snippet: Alda‐1 alleviated chronic CC l 4 ‐induced liver fibrosis. A, Liver/bodyweight ratio. B, Representative histopathological pictures of the liver. Upper panel: Representative H E staining. Middle panel: Representative Masson's trichrome staining. Lower panel: Representative images of α‐ SMA staining. C, Quantification of Masson's trichrome and α‐ SMA ‐positive area. D, Representative western blot pictures of α‐ SMA . E, Quantification analyses of the expression of α‐ SMA . The values represent means ± SEM (n = 6‐9). * P

    Article Snippet: Notably, ALDH2 deficiency partly reversed the up‐regulation of HO‐1 after CCl4 challenge, whereas administration of Alda‐1 could up‐regulate Nrf2/HO‐1 pathway as well as significantly decreased α‐SMA protein expression, which shed light on the application of Alda‐1 in clinical liver diseases.

    Techniques: Staining, Western Blot, Expressing