cyclin d1 e3p5s xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyclin d1 e3p5s xp rabbit mab
    Cyclin D1 E3p5s Xp Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit monoclonal anti cyclin d1  (Danaher Inc)


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    Danaher Inc rabbit monoclonal anti cyclin d1
    A , B Expression of activated Caspase-3 in tumors of mice exposed to BBN for 5 months then treated with vehicle for 7 days, image shown with A and without B Ecad. C , D Expression of activated Caspase-3 in 5 M BBN tumors treated with Rosi+Tram for 7 days, image shown with C and without D Ecad. E Bar graph showing the percentage of cells expressing activated caspase-3 in BBN-induced tumors treated for 7 days with vehicle ( n = 3) or Rosi+Tram ( n = 3). Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ***p = 0.0001. F Bar graph showing the percentage of cells expressing Ki67 in BBN-treated mice after vehicle ( n = 3) or Rosi+Tram ( n = 3) for 7 days. Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ****p < 0.0001. G Apoptosis assayed by AnnexinV-eFluor450/7-AAD double staining in BBN963 cells treated with DMSO, Rosi, Tram, or combined Rosi+Tram for 72 h. Cells undergoing early apoptosis were AnnexinV+/7-AAD: late apoptosis: AnnexinV+/7-AAD+. H Heatmap showing normalized expression of proapoptotic genes, caspases, and pro-survival genes in Rosi+Tram treated BBN963 cells compared to controls based on RNAseq analysis. I – L Decreased proliferation determined by Ki67 staining in BBN963 cells after Rosi ( n = 4) J , Tram ( n = 4) K , or combined Rosi+Tram ( n = 4) L compared to controls ( n = 4) I . M – P Down-regulation of <t>Ccnd1</t> in BBN963 cells after treatment with Rosi N , Tram O , or Rosi+Tram P compared to controls M . Scale bars: 50 µm. Q Heatmap of normalized gene expression showing down-regulation of Ccnd1 and genes that positively regulate cell cycle progression and up-regulation of genes that inhibit progression in BBN963 cells treated with Rosi+Tram for 72 h compared to DMSO treated controls. R Bar graph showing number of Ccnd1-positive BBN963 cells after 72-h treatment with DMSO ( n = 4), Rosi ( n = 4), Tram ( n = 4), and combined Rosi+Tram ( n = 4). Data given as means ± SD, significance calculated using two-tailed unpaired Welch’s t-test, *** p = 0.0006, ****p < 0.0001. Source data are provided as a Source Data file. Cartoons in Fig. 3 created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license ( https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en ).
    Rabbit Monoclonal Anti Cyclin D1, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Rosiglitazone and trametinib exhibit potent anti-tumor activity in a mouse model of muscle invasive bladder cancer"

    Article Title: Rosiglitazone and trametinib exhibit potent anti-tumor activity in a mouse model of muscle invasive bladder cancer

    Journal: Nature Communications

    doi: 10.1038/s41467-024-50678-2

    A , B Expression of activated Caspase-3 in tumors of mice exposed to BBN for 5 months then treated with vehicle for 7 days, image shown with A and without B Ecad. C , D Expression of activated Caspase-3 in 5 M BBN tumors treated with Rosi+Tram for 7 days, image shown with C and without D Ecad. E Bar graph showing the percentage of cells expressing activated caspase-3 in BBN-induced tumors treated for 7 days with vehicle ( n = 3) or Rosi+Tram ( n = 3). Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ***p = 0.0001. F Bar graph showing the percentage of cells expressing Ki67 in BBN-treated mice after vehicle ( n = 3) or Rosi+Tram ( n = 3) for 7 days. Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ****p < 0.0001. G Apoptosis assayed by AnnexinV-eFluor450/7-AAD double staining in BBN963 cells treated with DMSO, Rosi, Tram, or combined Rosi+Tram for 72 h. Cells undergoing early apoptosis were AnnexinV+/7-AAD: late apoptosis: AnnexinV+/7-AAD+. H Heatmap showing normalized expression of proapoptotic genes, caspases, and pro-survival genes in Rosi+Tram treated BBN963 cells compared to controls based on RNAseq analysis. I – L Decreased proliferation determined by Ki67 staining in BBN963 cells after Rosi ( n = 4) J , Tram ( n = 4) K , or combined Rosi+Tram ( n = 4) L compared to controls ( n = 4) I . M – P Down-regulation of Ccnd1 in BBN963 cells after treatment with Rosi N , Tram O , or Rosi+Tram P compared to controls M . Scale bars: 50 µm. Q Heatmap of normalized gene expression showing down-regulation of Ccnd1 and genes that positively regulate cell cycle progression and up-regulation of genes that inhibit progression in BBN963 cells treated with Rosi+Tram for 72 h compared to DMSO treated controls. R Bar graph showing number of Ccnd1-positive BBN963 cells after 72-h treatment with DMSO ( n = 4), Rosi ( n = 4), Tram ( n = 4), and combined Rosi+Tram ( n = 4). Data given as means ± SD, significance calculated using two-tailed unpaired Welch’s t-test, *** p = 0.0006, ****p < 0.0001. Source data are provided as a Source Data file. Cartoons in Fig. 3 created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license ( https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en ).
    Figure Legend Snippet: A , B Expression of activated Caspase-3 in tumors of mice exposed to BBN for 5 months then treated with vehicle for 7 days, image shown with A and without B Ecad. C , D Expression of activated Caspase-3 in 5 M BBN tumors treated with Rosi+Tram for 7 days, image shown with C and without D Ecad. E Bar graph showing the percentage of cells expressing activated caspase-3 in BBN-induced tumors treated for 7 days with vehicle ( n = 3) or Rosi+Tram ( n = 3). Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ***p = 0.0001. F Bar graph showing the percentage of cells expressing Ki67 in BBN-treated mice after vehicle ( n = 3) or Rosi+Tram ( n = 3) for 7 days. Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ****p < 0.0001. G Apoptosis assayed by AnnexinV-eFluor450/7-AAD double staining in BBN963 cells treated with DMSO, Rosi, Tram, or combined Rosi+Tram for 72 h. Cells undergoing early apoptosis were AnnexinV+/7-AAD: late apoptosis: AnnexinV+/7-AAD+. H Heatmap showing normalized expression of proapoptotic genes, caspases, and pro-survival genes in Rosi+Tram treated BBN963 cells compared to controls based on RNAseq analysis. I – L Decreased proliferation determined by Ki67 staining in BBN963 cells after Rosi ( n = 4) J , Tram ( n = 4) K , or combined Rosi+Tram ( n = 4) L compared to controls ( n = 4) I . M – P Down-regulation of Ccnd1 in BBN963 cells after treatment with Rosi N , Tram O , or Rosi+Tram P compared to controls M . Scale bars: 50 µm. Q Heatmap of normalized gene expression showing down-regulation of Ccnd1 and genes that positively regulate cell cycle progression and up-regulation of genes that inhibit progression in BBN963 cells treated with Rosi+Tram for 72 h compared to DMSO treated controls. R Bar graph showing number of Ccnd1-positive BBN963 cells after 72-h treatment with DMSO ( n = 4), Rosi ( n = 4), Tram ( n = 4), and combined Rosi+Tram ( n = 4). Data given as means ± SD, significance calculated using two-tailed unpaired Welch’s t-test, *** p = 0.0006, ****p < 0.0001. Source data are provided as a Source Data file. Cartoons in Fig. 3 created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license ( https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en ).

    Techniques Used: Expressing, Two Tailed Test, MANN-WHITNEY, Double Staining, Staining


    Figure Legend Snippet:

    Techniques Used:

    cyclin d1 e3p5s xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyclin d1 e3p5s xp rabbit mab
    Cyclin D1 E3p5s Xp Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cyclin d1 e3p5s xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyclin d1 e3p5s xp rabbit mab
    (A) Scheme of sequence motif analysis of AS exons in epidermal differentiation. (B) Representative RBPs and their binding motifs enriched at each cassette exon splicing junction. A–D lettering corresponds to the exon-intron junctions shown in (A). The complete list of predicted RBPs and their binding motifs are in Table S2. (C) RNA immunoprecipitation of candidate RBPs and their predicted RNA targets. SRSF1 is a positive control. (D) Quantitative RT-PCR of RNA immunoprecipitation. HPRT is a negative/specificity control RNA. Data are means ± SEM (n = 3). (E) Quantitative RT-PCR and immunoblot of FUS after treatment of keratinocytes with control (siCTRL) or FUS-targeting siRNAs (siFUS). (F) RT-PCR of alternatively spliced SE events associated with FUS depletion. (G) Number and type of alternative mRNA splicing events associated with FUS depletion. (H) Immunofluorescence of control and FUS-depleted epidermal organotypic tissues. Ki-67 marks proliferating keratinocytes (pink, arrowheads); KRT10 is a differentiation-associated protein (orange/red). White asterisks indicate non-specific antibody staining of cornified layer. Scale bars (gray): 50 μm. (I) Quantitative RT-PCR of progenitor-associated (CCNB1, BNC1, <t>CCND1)</t> and differentiation-associated (KRT1, KRT10, FLG) transcripts in epidermal organotypic tissue. Data are means ± SEM (n = 2).
    Cyclin D1 E3p5s Xp Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Alternative mRNA splicing events and regulators in epidermal differentiation"

    Article Title: Alternative mRNA splicing events and regulators in epidermal differentiation

    Journal: Cell reports

    doi: 10.1016/j.celrep.2024.113814

    (A) Scheme of sequence motif analysis of AS exons in epidermal differentiation. (B) Representative RBPs and their binding motifs enriched at each cassette exon splicing junction. A–D lettering corresponds to the exon-intron junctions shown in (A). The complete list of predicted RBPs and their binding motifs are in Table S2. (C) RNA immunoprecipitation of candidate RBPs and their predicted RNA targets. SRSF1 is a positive control. (D) Quantitative RT-PCR of RNA immunoprecipitation. HPRT is a negative/specificity control RNA. Data are means ± SEM (n = 3). (E) Quantitative RT-PCR and immunoblot of FUS after treatment of keratinocytes with control (siCTRL) or FUS-targeting siRNAs (siFUS). (F) RT-PCR of alternatively spliced SE events associated with FUS depletion. (G) Number and type of alternative mRNA splicing events associated with FUS depletion. (H) Immunofluorescence of control and FUS-depleted epidermal organotypic tissues. Ki-67 marks proliferating keratinocytes (pink, arrowheads); KRT10 is a differentiation-associated protein (orange/red). White asterisks indicate non-specific antibody staining of cornified layer. Scale bars (gray): 50 μm. (I) Quantitative RT-PCR of progenitor-associated (CCNB1, BNC1, CCND1) and differentiation-associated (KRT1, KRT10, FLG) transcripts in epidermal organotypic tissue. Data are means ± SEM (n = 2).
    Figure Legend Snippet: (A) Scheme of sequence motif analysis of AS exons in epidermal differentiation. (B) Representative RBPs and their binding motifs enriched at each cassette exon splicing junction. A–D lettering corresponds to the exon-intron junctions shown in (A). The complete list of predicted RBPs and their binding motifs are in Table S2. (C) RNA immunoprecipitation of candidate RBPs and their predicted RNA targets. SRSF1 is a positive control. (D) Quantitative RT-PCR of RNA immunoprecipitation. HPRT is a negative/specificity control RNA. Data are means ± SEM (n = 3). (E) Quantitative RT-PCR and immunoblot of FUS after treatment of keratinocytes with control (siCTRL) or FUS-targeting siRNAs (siFUS). (F) RT-PCR of alternatively spliced SE events associated with FUS depletion. (G) Number and type of alternative mRNA splicing events associated with FUS depletion. (H) Immunofluorescence of control and FUS-depleted epidermal organotypic tissues. Ki-67 marks proliferating keratinocytes (pink, arrowheads); KRT10 is a differentiation-associated protein (orange/red). White asterisks indicate non-specific antibody staining of cornified layer. Scale bars (gray): 50 μm. (I) Quantitative RT-PCR of progenitor-associated (CCNB1, BNC1, CCND1) and differentiation-associated (KRT1, KRT10, FLG) transcripts in epidermal organotypic tissue. Data are means ± SEM (n = 2).

    Techniques Used: Sequencing, Binding Assay, RNA Immunoprecipitation, Positive Control, Quantitative RT-PCR, Control, Western Blot, Reverse Transcription Polymerase Chain Reaction, Immunofluorescence, Staining

    (A) Sashimi plot showing enriched relative expression of exon-12-containing isoforms of MAP3K7 upon epidermal differentiation. (B) Scheme of RT-PCR primers (red triangles) to discern MAP3K7 isoforms containing (MAP3K7-long) or excluding exon 12 (MAP3K7-short). Purple bars represent isoform-targeting siRNAs for short and long MAP3K7 transcripts. Bottom, RT-PCR of in vitro progenitor (P) and differentiated (D) keratinocytes and in vivo laser capture microdissected skin tissue of basal (Bs) progenitor and suprabasal (Sb) differentiated layers. CCND1 and LOR are control transcripts enriched in progenitor and differentiated states, respectively. (C) RT-PCR evaluating MAP3K7 isoform expression after transfection of isoform-targeting siRNAs against short and long isoforms. RPL32 is an invariant expression control. (D) Immunoblot for proteins in the NF-κB signaling pathway in progenitor keratinocytes after treatment with control or MAP3K7-isoform-targeted siRNAs, in the presence or absence of tumor necrosis factor α (TNF-α; 10 ng/mL), to stimulate NF-κB signaling. TNF-α was applied for 30 min, and protein lysates were harvested 48 h later. (E) Intensity quantitation of phospho-p65/RelA from immunoblot experiments. Phosphorylated p65 was normalized internally to total p65, and the unstimulated siCTRL signal was set to 1 for each biological replicate. Data are means ± SEM (n = 3) (one-way ANOVA with a Tukey’s honestly significant difference [HSD] post hoc test), *p < 0.05. (F) RT-PCR and immunoblot for TAK1, the protein product of MAP3K7, after overexpression (OE) of each isoform. (G) ELISA for phosphorylated p65 in keratinocytes after OE of empty vector or MAP3K7 short/long isoforms. Data are means ± SEM (n = 3) (one-way ANOVA with a Tukey’s HSD post hoc test), *p < 0.05.
    Figure Legend Snippet: (A) Sashimi plot showing enriched relative expression of exon-12-containing isoforms of MAP3K7 upon epidermal differentiation. (B) Scheme of RT-PCR primers (red triangles) to discern MAP3K7 isoforms containing (MAP3K7-long) or excluding exon 12 (MAP3K7-short). Purple bars represent isoform-targeting siRNAs for short and long MAP3K7 transcripts. Bottom, RT-PCR of in vitro progenitor (P) and differentiated (D) keratinocytes and in vivo laser capture microdissected skin tissue of basal (Bs) progenitor and suprabasal (Sb) differentiated layers. CCND1 and LOR are control transcripts enriched in progenitor and differentiated states, respectively. (C) RT-PCR evaluating MAP3K7 isoform expression after transfection of isoform-targeting siRNAs against short and long isoforms. RPL32 is an invariant expression control. (D) Immunoblot for proteins in the NF-κB signaling pathway in progenitor keratinocytes after treatment with control or MAP3K7-isoform-targeted siRNAs, in the presence or absence of tumor necrosis factor α (TNF-α; 10 ng/mL), to stimulate NF-κB signaling. TNF-α was applied for 30 min, and protein lysates were harvested 48 h later. (E) Intensity quantitation of phospho-p65/RelA from immunoblot experiments. Phosphorylated p65 was normalized internally to total p65, and the unstimulated siCTRL signal was set to 1 for each biological replicate. Data are means ± SEM (n = 3) (one-way ANOVA with a Tukey’s honestly significant difference [HSD] post hoc test), *p < 0.05. (F) RT-PCR and immunoblot for TAK1, the protein product of MAP3K7, after overexpression (OE) of each isoform. (G) ELISA for phosphorylated p65 in keratinocytes after OE of empty vector or MAP3K7 short/long isoforms. Data are means ± SEM (n = 3) (one-way ANOVA with a Tukey’s HSD post hoc test), *p < 0.05.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, In Vitro, In Vivo, Control, Transfection, Western Blot, Quantitation Assay, Over Expression, Enzyme-linked Immunosorbent Assay, Plasmid Preparation

    KEY RESOURCES TABLE
    Figure Legend Snippet: KEY RESOURCES TABLE

    Techniques Used: Recombinant, Blocking Assay, Staining, Lysis, Transfection, Reverse Transcription, SYBR Green Assay, Enzyme-linked Immunosorbent Assay, Negative Control, Software, Imaging, Real-time Polymerase Chain Reaction

    KEY RESOURCES TABLE
    Figure Legend Snippet: KEY RESOURCES TABLE

    Techniques Used: Recombinant, Blocking Assay, Staining, Lysis, Transfection, Reverse Transcription, SYBR Green Assay, Enzyme-linked Immunosorbent Assay, Negative Control, Software, Imaging, Real-time Polymerase Chain Reaction

    rabbit monoclonal anti cyclin d1  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc rabbit monoclonal anti cyclin d1
    Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and <t>cyclin</t> <t>D1,</t> with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.
    Rabbit Monoclonal Anti Cyclin D1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Proteomic insights into the regulatory function of ARID1A in colon cancer cells"

    Article Title: Proteomic insights into the regulatory function of ARID1A in colon cancer cells

    Journal: Oncology Letters

    doi: 10.3892/ol.2024.14525

    Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and cyclin D1, with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.
    Figure Legend Snippet: Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and cyclin D1, with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.

    Techniques Used: Generated, Western Blot, Control, Standard Deviation, Over Expression, Molecular Weight

    rabbit monoclonal anti cyclin d1  (Danaher Inc)


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    Danaher Inc rabbit monoclonal anti cyclin d1
    Rabbit Monoclonal Anti Cyclin D1, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cyclin d1 (e3p5s) xp® rabbit mab  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc cyclin d1 (e3p5s) xp® rabbit mab
    Cyclin D1 (E3p5s) Xp® Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cyclin d1 (e3p5s) xp® rabbit mab/product/Cell Signaling Technology Inc
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    rabbit monoclonal 92g2 anti cyclin d1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit monoclonal 92g2 anti cyclin d1
    Knockdown of TERC inhibits the nuclear functions of TERT (A) Relative telomere repeat number in NSCLC cells. Cellular DNA was extracted from A549, H322, H460, and H1299 cells without (ctrl) or with TERC knockdown (TERC-si1, TERC-si2), or treated with 10 μM BIBR1532, and qPCR was performed for each extract to obtain the relative telomere repeat number as described previously, using 36B4 as the single-copy gene control. (B) Binding of TERT at the indicated genomic regions. ChIP was performed with TERT antibody, or IgG as control, and qPCR was run with primers specific for the tested target regions in A549 cells without or with TERC knockdown, or treated with 10 μM BIBR1532. Reported values correspond to the signal for each site relative to that of the IgG control. (C) Gene expression analysis of pre-tRNA, pre-rRNA, rRNA, as well as c-Myc, <t>cyclin</t> <t>D1,</t> and VEGF mRNA transcripts in A549 cells. RT-qPCR was performed, and U6 served as the control for pre-tRNA, pre-rRNA, and rRNA transcripts, while β-actin served as the control for mRNA transcripts. Data in (A–C) were presented as mean ± SD ( n ≥ 2), and p values between the control and the TERC-si1/2 groups were calculated by Student’s t -test. (D) Gene expression analysis in xenograft tumors from A549 cells without (control) or with TERC stably knocked down (TERC-sh). Data were presented as individual dots and mean ± SD ( n = 4), and p values were determined by Student’s t -test. (E) Protein expression of cyclin D1. Western blotting was used to detect cyclin D1 levels in A549 cells. Histone H3 served as the loading control.
    Rabbit Monoclonal 92g2 Anti Cyclin D1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit monoclonal 92g2 anti cyclin d1/product/Cell Signaling Technology Inc
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    1) Product Images from "TERC promotes non-small cell lung cancer progression by facilitating the nuclear localization of TERT"

    Article Title: TERC promotes non-small cell lung cancer progression by facilitating the nuclear localization of TERT

    Journal: iScience

    doi: 10.1016/j.isci.2024.109869

    Knockdown of TERC inhibits the nuclear functions of TERT (A) Relative telomere repeat number in NSCLC cells. Cellular DNA was extracted from A549, H322, H460, and H1299 cells without (ctrl) or with TERC knockdown (TERC-si1, TERC-si2), or treated with 10 μM BIBR1532, and qPCR was performed for each extract to obtain the relative telomere repeat number as described previously, using 36B4 as the single-copy gene control. (B) Binding of TERT at the indicated genomic regions. ChIP was performed with TERT antibody, or IgG as control, and qPCR was run with primers specific for the tested target regions in A549 cells without or with TERC knockdown, or treated with 10 μM BIBR1532. Reported values correspond to the signal for each site relative to that of the IgG control. (C) Gene expression analysis of pre-tRNA, pre-rRNA, rRNA, as well as c-Myc, cyclin D1, and VEGF mRNA transcripts in A549 cells. RT-qPCR was performed, and U6 served as the control for pre-tRNA, pre-rRNA, and rRNA transcripts, while β-actin served as the control for mRNA transcripts. Data in (A–C) were presented as mean ± SD ( n ≥ 2), and p values between the control and the TERC-si1/2 groups were calculated by Student’s t -test. (D) Gene expression analysis in xenograft tumors from A549 cells without (control) or with TERC stably knocked down (TERC-sh). Data were presented as individual dots and mean ± SD ( n = 4), and p values were determined by Student’s t -test. (E) Protein expression of cyclin D1. Western blotting was used to detect cyclin D1 levels in A549 cells. Histone H3 served as the loading control.
    Figure Legend Snippet: Knockdown of TERC inhibits the nuclear functions of TERT (A) Relative telomere repeat number in NSCLC cells. Cellular DNA was extracted from A549, H322, H460, and H1299 cells without (ctrl) or with TERC knockdown (TERC-si1, TERC-si2), or treated with 10 μM BIBR1532, and qPCR was performed for each extract to obtain the relative telomere repeat number as described previously, using 36B4 as the single-copy gene control. (B) Binding of TERT at the indicated genomic regions. ChIP was performed with TERT antibody, or IgG as control, and qPCR was run with primers specific for the tested target regions in A549 cells without or with TERC knockdown, or treated with 10 μM BIBR1532. Reported values correspond to the signal for each site relative to that of the IgG control. (C) Gene expression analysis of pre-tRNA, pre-rRNA, rRNA, as well as c-Myc, cyclin D1, and VEGF mRNA transcripts in A549 cells. RT-qPCR was performed, and U6 served as the control for pre-tRNA, pre-rRNA, and rRNA transcripts, while β-actin served as the control for mRNA transcripts. Data in (A–C) were presented as mean ± SD ( n ≥ 2), and p values between the control and the TERC-si1/2 groups were calculated by Student’s t -test. (D) Gene expression analysis in xenograft tumors from A549 cells without (control) or with TERC stably knocked down (TERC-sh). Data were presented as individual dots and mean ± SD ( n = 4), and p values were determined by Student’s t -test. (E) Protein expression of cyclin D1. Western blotting was used to detect cyclin D1 levels in A549 cells. Histone H3 served as the loading control.

    Techniques Used: Binding Assay, Expressing, Quantitative RT-PCR, Stable Transfection, Western Blot


    Figure Legend Snippet:

    Techniques Used: Virus, Recombinant, Modification, Immunoprecipitation, Transfection, Membrane, DNA Purification, SYBR Green Assay, Isolation, Staining, Methylation, Software


    Structured Review

    Cell Marque rabbit monoclonal igg human cyclin d1

    Rabbit Monoclonal Igg Human Cyclin D1, supplied by Cell Marque, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Comprehensive proteogenomic characterization of rare kidney tumors"

    Article Title: Comprehensive proteogenomic characterization of rare kidney tumors

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2024.101547


    Figure Legend Snippet:

    Techniques Used: Software

    cyclin d1 rabbit mab  (Bioss)


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    Structured Review

    Bioss cyclin d1 rabbit mab
    Molecular docking between ginsenoside Rb1 and core targets protein. ( A ) The binding energy of molecular docking. ( B ) <t>CCND1</t> and ginsenoside Rb1 molecular docking visualization.
    Cyclin D1 Rabbit Mab, supplied by Bioss, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Exploring the anti-atherosclerosis mechanism of ginsenoside Rb1 by integrating network pharmacology and experimental verification"

    Article Title: Exploring the anti-atherosclerosis mechanism of ginsenoside Rb1 by integrating network pharmacology and experimental verification

    Journal: Aging (Albany NY)

    doi: 10.18632/aging.205680

    Molecular docking between ginsenoside Rb1 and core targets protein. ( A ) The binding energy of molecular docking. ( B ) CCND1 and ginsenoside Rb1 molecular docking visualization.
    Figure Legend Snippet: Molecular docking between ginsenoside Rb1 and core targets protein. ( A ) The binding energy of molecular docking. ( B ) CCND1 and ginsenoside Rb1 molecular docking visualization.

    Techniques Used: Binding Assay

    Ginsenoside Rb1 inhibited the interaction of CCND1 and CDK4 complex.
    Figure Legend Snippet: Ginsenoside Rb1 inhibited the interaction of CCND1 and CDK4 complex.

    Techniques Used:

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    Cell Signaling Technology Inc cyclin d1 e3p5s xp rabbit mab
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    A , B Expression of activated Caspase-3 in tumors of mice exposed to BBN for 5 months then treated with vehicle for 7 days, image shown with A and without B Ecad. C , D Expression of activated Caspase-3 in 5 M BBN tumors treated with Rosi+Tram for 7 days, image shown with C and without D Ecad. E Bar graph showing the percentage of cells expressing activated caspase-3 in BBN-induced tumors treated for 7 days with vehicle ( n = 3) or Rosi+Tram ( n = 3). Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ***p = 0.0001. F Bar graph showing the percentage of cells expressing Ki67 in BBN-treated mice after vehicle ( n = 3) or Rosi+Tram ( n = 3) for 7 days. Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ****p < 0.0001. G Apoptosis assayed by AnnexinV-eFluor450/7-AAD double staining in BBN963 cells treated with DMSO, Rosi, Tram, or combined Rosi+Tram for 72 h. Cells undergoing early apoptosis were AnnexinV+/7-AAD: late apoptosis: AnnexinV+/7-AAD+. H Heatmap showing normalized expression of proapoptotic genes, caspases, and pro-survival genes in Rosi+Tram treated BBN963 cells compared to controls based on RNAseq analysis. I – L Decreased proliferation determined by Ki67 staining in BBN963 cells after Rosi ( n = 4) J , Tram ( n = 4) K , or combined Rosi+Tram ( n = 4) L compared to controls ( n = 4) I . M – P Down-regulation of <t>Ccnd1</t> in BBN963 cells after treatment with Rosi N , Tram O , or Rosi+Tram P compared to controls M . Scale bars: 50 µm. Q Heatmap of normalized gene expression showing down-regulation of Ccnd1 and genes that positively regulate cell cycle progression and up-regulation of genes that inhibit progression in BBN963 cells treated with Rosi+Tram for 72 h compared to DMSO treated controls. R Bar graph showing number of Ccnd1-positive BBN963 cells after 72-h treatment with DMSO ( n = 4), Rosi ( n = 4), Tram ( n = 4), and combined Rosi+Tram ( n = 4). Data given as means ± SD, significance calculated using two-tailed unpaired Welch’s t-test, *** p = 0.0006, ****p < 0.0001. Source data are provided as a Source Data file. Cartoons in Fig. 3 created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license ( https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en ).
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    Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and <t>cyclin</t> <t>D1,</t> with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.
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    Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and <t>cyclin</t> <t>D1,</t> with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.
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    Knockdown of TERC inhibits the nuclear functions of TERT (A) Relative telomere repeat number in NSCLC cells. Cellular DNA was extracted from A549, H322, H460, and H1299 cells without (ctrl) or with TERC knockdown (TERC-si1, TERC-si2), or treated with 10 μM BIBR1532, and qPCR was performed for each extract to obtain the relative telomere repeat number as described previously, using 36B4 as the single-copy gene control. (B) Binding of TERT at the indicated genomic regions. ChIP was performed with TERT antibody, or IgG as control, and qPCR was run with primers specific for the tested target regions in A549 cells without or with TERC knockdown, or treated with 10 μM BIBR1532. Reported values correspond to the signal for each site relative to that of the IgG control. (C) Gene expression analysis of pre-tRNA, pre-rRNA, rRNA, as well as c-Myc, <t>cyclin</t> <t>D1,</t> and VEGF mRNA transcripts in A549 cells. RT-qPCR was performed, and U6 served as the control for pre-tRNA, pre-rRNA, and rRNA transcripts, while β-actin served as the control for mRNA transcripts. Data in (A–C) were presented as mean ± SD ( n ≥ 2), and p values between the control and the TERC-si1/2 groups were calculated by Student’s t -test. (D) Gene expression analysis in xenograft tumors from A549 cells without (control) or with TERC stably knocked down (TERC-sh). Data were presented as individual dots and mean ± SD ( n = 4), and p values were determined by Student’s t -test. (E) Protein expression of cyclin D1. Western blotting was used to detect cyclin D1 levels in A549 cells. Histone H3 served as the loading control.
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    Molecular docking between ginsenoside Rb1 and core targets protein. ( A ) The binding energy of molecular docking. ( B ) <t>CCND1</t> and ginsenoside Rb1 molecular docking visualization.
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    A , B Expression of activated Caspase-3 in tumors of mice exposed to BBN for 5 months then treated with vehicle for 7 days, image shown with A and without B Ecad. C , D Expression of activated Caspase-3 in 5 M BBN tumors treated with Rosi+Tram for 7 days, image shown with C and without D Ecad. E Bar graph showing the percentage of cells expressing activated caspase-3 in BBN-induced tumors treated for 7 days with vehicle ( n = 3) or Rosi+Tram ( n = 3). Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ***p = 0.0001. F Bar graph showing the percentage of cells expressing Ki67 in BBN-treated mice after vehicle ( n = 3) or Rosi+Tram ( n = 3) for 7 days. Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ****p < 0.0001. G Apoptosis assayed by AnnexinV-eFluor450/7-AAD double staining in BBN963 cells treated with DMSO, Rosi, Tram, or combined Rosi+Tram for 72 h. Cells undergoing early apoptosis were AnnexinV+/7-AAD: late apoptosis: AnnexinV+/7-AAD+. H Heatmap showing normalized expression of proapoptotic genes, caspases, and pro-survival genes in Rosi+Tram treated BBN963 cells compared to controls based on RNAseq analysis. I – L Decreased proliferation determined by Ki67 staining in BBN963 cells after Rosi ( n = 4) J , Tram ( n = 4) K , or combined Rosi+Tram ( n = 4) L compared to controls ( n = 4) I . M – P Down-regulation of Ccnd1 in BBN963 cells after treatment with Rosi N , Tram O , or Rosi+Tram P compared to controls M . Scale bars: 50 µm. Q Heatmap of normalized gene expression showing down-regulation of Ccnd1 and genes that positively regulate cell cycle progression and up-regulation of genes that inhibit progression in BBN963 cells treated with Rosi+Tram for 72 h compared to DMSO treated controls. R Bar graph showing number of Ccnd1-positive BBN963 cells after 72-h treatment with DMSO ( n = 4), Rosi ( n = 4), Tram ( n = 4), and combined Rosi+Tram ( n = 4). Data given as means ± SD, significance calculated using two-tailed unpaired Welch’s t-test, *** p = 0.0006, ****p < 0.0001. Source data are provided as a Source Data file. Cartoons in Fig. 3 created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license ( https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en ).

    Journal: Nature Communications

    Article Title: Rosiglitazone and trametinib exhibit potent anti-tumor activity in a mouse model of muscle invasive bladder cancer

    doi: 10.1038/s41467-024-50678-2

    Figure Lengend Snippet: A , B Expression of activated Caspase-3 in tumors of mice exposed to BBN for 5 months then treated with vehicle for 7 days, image shown with A and without B Ecad. C , D Expression of activated Caspase-3 in 5 M BBN tumors treated with Rosi+Tram for 7 days, image shown with C and without D Ecad. E Bar graph showing the percentage of cells expressing activated caspase-3 in BBN-induced tumors treated for 7 days with vehicle ( n = 3) or Rosi+Tram ( n = 3). Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ***p = 0.0001. F Bar graph showing the percentage of cells expressing Ki67 in BBN-treated mice after vehicle ( n = 3) or Rosi+Tram ( n = 3) for 7 days. Data given as means ± SD, significance calculated using two-tailed Mann-Whitney test, ****p < 0.0001. G Apoptosis assayed by AnnexinV-eFluor450/7-AAD double staining in BBN963 cells treated with DMSO, Rosi, Tram, or combined Rosi+Tram for 72 h. Cells undergoing early apoptosis were AnnexinV+/7-AAD: late apoptosis: AnnexinV+/7-AAD+. H Heatmap showing normalized expression of proapoptotic genes, caspases, and pro-survival genes in Rosi+Tram treated BBN963 cells compared to controls based on RNAseq analysis. I – L Decreased proliferation determined by Ki67 staining in BBN963 cells after Rosi ( n = 4) J , Tram ( n = 4) K , or combined Rosi+Tram ( n = 4) L compared to controls ( n = 4) I . M – P Down-regulation of Ccnd1 in BBN963 cells after treatment with Rosi N , Tram O , or Rosi+Tram P compared to controls M . Scale bars: 50 µm. Q Heatmap of normalized gene expression showing down-regulation of Ccnd1 and genes that positively regulate cell cycle progression and up-regulation of genes that inhibit progression in BBN963 cells treated with Rosi+Tram for 72 h compared to DMSO treated controls. R Bar graph showing number of Ccnd1-positive BBN963 cells after 72-h treatment with DMSO ( n = 4), Rosi ( n = 4), Tram ( n = 4), and combined Rosi+Tram ( n = 4). Data given as means ± SD, significance calculated using two-tailed unpaired Welch’s t-test, *** p = 0.0006, ****p < 0.0001. Source data are provided as a Source Data file. Cartoons in Fig. 3 created with BioRender.com released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license ( https://creativecommons.org/licenses/by-nc-nd/4.0/deed.en ).

    Article Snippet: Rabbit Monoclonal Anti- Cyclin D1 , Abcam , Cat#ab16663 , SP4 , 1:200.

    Techniques: Expressing, Two Tailed Test, MANN-WHITNEY, Double Staining, Staining

    Journal: Nature Communications

    Article Title: Rosiglitazone and trametinib exhibit potent anti-tumor activity in a mouse model of muscle invasive bladder cancer

    doi: 10.1038/s41467-024-50678-2

    Figure Lengend Snippet:

    Article Snippet: Rabbit Monoclonal Anti- Cyclin D1 , Abcam , Cat#ab16663 , SP4 , 1:200.

    Techniques:

    Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and cyclin D1, with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.

    Journal: Oncology Letters

    Article Title: Proteomic insights into the regulatory function of ARID1A in colon cancer cells

    doi: 10.3892/ol.2024.14525

    Figure Lengend Snippet: Involvement of ARID1A and altered proteins in the Wnt signaling pathway. (A) Wnt signaling pathway information generated using Kyoto Encyclopedia of Genes and Genomes (hsa04310). The pathway is illustrated using data from the KEGG database ( https://www.genome.jp/pathway/hsa04310 ) . Red boxes indicate differentially altered proteins. (B) Western blot images for c-Myc, TCF1/TCF7 and cyclin D1, with GAPDH as the loading control. (C) Band intensity of proteins relative to GAPDH. The bar graph represents the mean ± standard deviation (n=3 per group). *P<0.05. ARID1A, AT-rich interacting domain-containing protein 1A; TCF, T cell factor; O/E, overexpression; MW, molecular weight.

    Article Snippet: The membrane was incubated with 5% skimmed milk in PBS at 25°C for 1 h. Subsequently, it was incubated with rabbit polyclonal anti-ARID1A (1:1,000; cat. no. HPA005456; Sigma-Aldrich; Merck KGaA), rabbit monoclonal anti-c-Myc (1:1,000; cat. no. 5605; Cell Signaling Technology, Inc.), rabbit monoclonal anti-T cell factor (TCF)1/7 (1:1,000; cat. no. 2203; Cell Signaling Technology, Inc.), rabbit monoclonal anti-cyclin D1 (1:1,000; cat. no. 2978; Cell Signaling Technology, Inc.), rabbit polyclonal anti-zinc and ring finger 3 (ZNRF3; 1:1,000; cat. no. DF14289; Affinity Biosciences), or mouse monoclonal anti-GAPDH (1:5,000; cat. no. ab8245; Abcam) antibodies at 4°C overnight.

    Techniques: Generated, Western Blot, Control, Standard Deviation, Over Expression, Molecular Weight

    Knockdown of TERC inhibits the nuclear functions of TERT (A) Relative telomere repeat number in NSCLC cells. Cellular DNA was extracted from A549, H322, H460, and H1299 cells without (ctrl) or with TERC knockdown (TERC-si1, TERC-si2), or treated with 10 μM BIBR1532, and qPCR was performed for each extract to obtain the relative telomere repeat number as described previously, using 36B4 as the single-copy gene control. (B) Binding of TERT at the indicated genomic regions. ChIP was performed with TERT antibody, or IgG as control, and qPCR was run with primers specific for the tested target regions in A549 cells without or with TERC knockdown, or treated with 10 μM BIBR1532. Reported values correspond to the signal for each site relative to that of the IgG control. (C) Gene expression analysis of pre-tRNA, pre-rRNA, rRNA, as well as c-Myc, cyclin D1, and VEGF mRNA transcripts in A549 cells. RT-qPCR was performed, and U6 served as the control for pre-tRNA, pre-rRNA, and rRNA transcripts, while β-actin served as the control for mRNA transcripts. Data in (A–C) were presented as mean ± SD ( n ≥ 2), and p values between the control and the TERC-si1/2 groups were calculated by Student’s t -test. (D) Gene expression analysis in xenograft tumors from A549 cells without (control) or with TERC stably knocked down (TERC-sh). Data were presented as individual dots and mean ± SD ( n = 4), and p values were determined by Student’s t -test. (E) Protein expression of cyclin D1. Western blotting was used to detect cyclin D1 levels in A549 cells. Histone H3 served as the loading control.

    Journal: iScience

    Article Title: TERC promotes non-small cell lung cancer progression by facilitating the nuclear localization of TERT

    doi: 10.1016/j.isci.2024.109869

    Figure Lengend Snippet: Knockdown of TERC inhibits the nuclear functions of TERT (A) Relative telomere repeat number in NSCLC cells. Cellular DNA was extracted from A549, H322, H460, and H1299 cells without (ctrl) or with TERC knockdown (TERC-si1, TERC-si2), or treated with 10 μM BIBR1532, and qPCR was performed for each extract to obtain the relative telomere repeat number as described previously, using 36B4 as the single-copy gene control. (B) Binding of TERT at the indicated genomic regions. ChIP was performed with TERT antibody, or IgG as control, and qPCR was run with primers specific for the tested target regions in A549 cells without or with TERC knockdown, or treated with 10 μM BIBR1532. Reported values correspond to the signal for each site relative to that of the IgG control. (C) Gene expression analysis of pre-tRNA, pre-rRNA, rRNA, as well as c-Myc, cyclin D1, and VEGF mRNA transcripts in A549 cells. RT-qPCR was performed, and U6 served as the control for pre-tRNA, pre-rRNA, and rRNA transcripts, while β-actin served as the control for mRNA transcripts. Data in (A–C) were presented as mean ± SD ( n ≥ 2), and p values between the control and the TERC-si1/2 groups were calculated by Student’s t -test. (D) Gene expression analysis in xenograft tumors from A549 cells without (control) or with TERC stably knocked down (TERC-sh). Data were presented as individual dots and mean ± SD ( n = 4), and p values were determined by Student’s t -test. (E) Protein expression of cyclin D1. Western blotting was used to detect cyclin D1 levels in A549 cells. Histone H3 served as the loading control.

    Article Snippet: Rabbit monoclonal (92G2) anti-Cyclin D1 , Cell Signaling Technology , Cat#2978; RRID: AB_2259616.

    Techniques: Binding Assay, Expressing, Quantitative RT-PCR, Stable Transfection, Western Blot

    Journal: iScience

    Article Title: TERC promotes non-small cell lung cancer progression by facilitating the nuclear localization of TERT

    doi: 10.1016/j.isci.2024.109869

    Figure Lengend Snippet:

    Article Snippet: Rabbit monoclonal (92G2) anti-Cyclin D1 , Cell Signaling Technology , Cat#2978; RRID: AB_2259616.

    Techniques: Virus, Recombinant, Modification, Immunoprecipitation, Transfection, Membrane, DNA Purification, SYBR Green Assay, Isolation, Staining, Methylation, Software

    Journal: Cell Reports Medicine

    Article Title: Comprehensive proteogenomic characterization of rare kidney tumors

    doi: 10.1016/j.xcrm.2024.101547

    Figure Lengend Snippet:

    Article Snippet: Rabbit Monoclonal IgG Human Cyclin D1 , Cell Marque , Catalog: 241R-18 RRID: AB_1158233.

    Techniques: Software

    Molecular docking between ginsenoside Rb1 and core targets protein. ( A ) The binding energy of molecular docking. ( B ) CCND1 and ginsenoside Rb1 molecular docking visualization.

    Journal: Aging (Albany NY)

    Article Title: Exploring the anti-atherosclerosis mechanism of ginsenoside Rb1 by integrating network pharmacology and experimental verification

    doi: 10.18632/aging.205680

    Figure Lengend Snippet: Molecular docking between ginsenoside Rb1 and core targets protein. ( A ) The binding energy of molecular docking. ( B ) CCND1 and ginsenoside Rb1 molecular docking visualization.

    Article Snippet: According to the manufacturer’s instructions, prewash beads two times with 1X Modified Coupling Buffer and bind with 5 μg cyclin D1 rabbit mAb (bsm-52046R, dilution ratio 1:200, Bioss, USA) or CDK4 mouse mAb (bsm-52028M, dilution ratio 1:200, Bioss, USA) specific primary antibody for 15 min. Next, wash beads three times with 1X Modified Coupling Buffer and crosslink antibody to beads with DSS for 30 min. Then, wash beads three times with Elution Buffer followed by two washes with IP Lysis/Wash Buffer.

    Techniques: Binding Assay

    Ginsenoside Rb1 inhibited the interaction of CCND1 and CDK4 complex.

    Journal: Aging (Albany NY)

    Article Title: Exploring the anti-atherosclerosis mechanism of ginsenoside Rb1 by integrating network pharmacology and experimental verification

    doi: 10.18632/aging.205680

    Figure Lengend Snippet: Ginsenoside Rb1 inhibited the interaction of CCND1 and CDK4 complex.

    Article Snippet: According to the manufacturer’s instructions, prewash beads two times with 1X Modified Coupling Buffer and bind with 5 μg cyclin D1 rabbit mAb (bsm-52046R, dilution ratio 1:200, Bioss, USA) or CDK4 mouse mAb (bsm-52028M, dilution ratio 1:200, Bioss, USA) specific primary antibody for 15 min. Next, wash beads three times with 1X Modified Coupling Buffer and crosslink antibody to beads with DSS for 30 min. Then, wash beads three times with Elution Buffer followed by two washes with IP Lysis/Wash Buffer.

    Techniques: