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prb s795  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc prb s795
    Prb S795, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 421 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/prb+s795/pmc11599852-194-6-46?v=Cell+Signaling+Technology+Inc
    Average 94 stars, based on 421 article reviews
    prb s795 - by Bioz Stars, 2026-07
    94/100 stars

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    anti prb s795  (Cell Signaling Technology Inc)
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    A, IHC for pAKT S473 in mouse prostate tissues from 16–20 weeks of age. Wild-type n=8, Pb-ERG n=9, DMT n=10, TMT n=12, Ptenpc−/− n= 8. B, Protein levels of pAKT S473, total AKT, and AR in mouse prostate tissues at 16–20 weeks of age. Both blots for each protein of interest were exposed and developed on the same piece of film. ERK2 as a loading control. Band intensity was quantified and normalized to ERK2 for each lane. Asterisk = outlier samples with significantly low levels of total protein. C, IHC for pRB <t>S795</t> in mouse prostate tissues from 16–20 weeks of age as described in (A). D, Quantification of pRB S795 staining as shown in (C). E, IHC for Ki67 in mouse prostate tissues from 16–20 weeks of age as described in (A). F, Quantification of Ki67 IHC as shown in (E).
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    A, IHC for pAKT S473 in mouse prostate tissues from 16–20 weeks of age. Wild-type n=8, Pb-ERG n=9, DMT n=10, TMT n=12, Ptenpc−/− n= 8. B, Protein levels of pAKT S473, total AKT, and AR in mouse prostate tissues at 16–20 weeks of age. Both blots for each protein of interest were exposed and developed on the same piece of film. ERK2 as a loading control. Band intensity was quantified and normalized to ERK2 for each lane. Asterisk = outlier samples with significantly low levels of total protein. C, IHC for pRB S795 in mouse prostate tissues from 16–20 weeks of age as described in (A). D, Quantification of pRB S795 staining as shown in (C). E, IHC for Ki67 in mouse prostate tissues from 16–20 weeks of age as described in (A). F, Quantification of Ki67 IHC as shown in (E).

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: TMPRSS2-ERG controls luminal epithelial lineage and antiandrogen sensitivity in PTEN and TP53 -mutated prostate cancer

    doi: 10.1158/1078-0432.CCR-18-0653

    Figure Lengend Snippet: A, IHC for pAKT S473 in mouse prostate tissues from 16–20 weeks of age. Wild-type n=8, Pb-ERG n=9, DMT n=10, TMT n=12, Ptenpc−/− n= 8. B, Protein levels of pAKT S473, total AKT, and AR in mouse prostate tissues at 16–20 weeks of age. Both blots for each protein of interest were exposed and developed on the same piece of film. ERK2 as a loading control. Band intensity was quantified and normalized to ERK2 for each lane. Asterisk = outlier samples with significantly low levels of total protein. C, IHC for pRB S795 in mouse prostate tissues from 16–20 weeks of age as described in (A). D, Quantification of pRB S795 staining as shown in (C). E, IHC for Ki67 in mouse prostate tissues from 16–20 weeks of age as described in (A). F, Quantification of Ki67 IHC as shown in (E).

    Article Snippet: Antibodies include: anti-ERG (ab92513, Abcam; CM421C, Biocare Medical), anti-PTEN (CST9559L, Cell Signaling Technology), anti-p53 (sc126, Santa Cruz Biotechnology), anti-AR (sc816, Santa Cruz Biotechnology), anti-NKX3.1 (NB100-1828, Novus Biologicals), anti-RB (554136, BD Biosciences), anti-pRB S795 (CST9301S, Cell Signaling Technology), anti-SKP2 (32-3300, Life Technologies), anti-CCND1 (sc718, Santa Cruz Biotechnology), anti-CDK1 (sc54, Santa Cruz Biotechnology), anti-TWIST (sc6269, Santa Cruz Biotechnology), anti-CDH1 (610181, BD Biosciences), anti-VIM (sc73258, Santa Cruz Biotechnology), anti-ERK2 (sc1647, Santa Cruz Biotechnology), anti-CDK2 (sc6248, Santa Cruz Biotechnology), anti-E2F1 (sc193, Santa Cruz Biotechnology), anti-pAKT S473 (CST4060L, Cell Signaling Technology), anti-AKT (CST9272, Cell Signaling Technology). qRT-PCR qRT-PCR was performed as described previously ( 15 ).

    Techniques: Control, Staining

    A, Western blot analysis of expression of key AR pathway, cell cycle, and EMT-related proteins in LNCaP-RF cells with or without lentiviral-mediated ERG (T1-E4) expression after treatment with vehicle, enzalutamide (ENZ, 10 μM), palbociclib (PD, 1 μM), or combination (ENZ + PD). B, Cell proliferation as measured by SRB assay for LNCaP-RF cells with or without lentiviral-mediated ERG (T1-E4) expression after treatment with vehicle, ENZ (10 μM), PD (1 μM), or combination. C, LNCaP-RF xenograft tumor volume with or without lentiviral-mediated ERG (T1-E4) expression during three weeks treatment with vehicle, ENZ (30 mg/kg/day), PD (100 mg/kg/day), or combination. Six xenografts (n = 6) per cell line, per drug treatment. D, ERG−/ARlow/KRTlow DMT and ERG+/ARhigh/KRThigh TMT allograft tumor volume during three weeks of treatment with vehicle, ENZ (30 mg/kg/day), PD (100 mg/kg/day), or combination. Five allografts (n = 5) per genotype, per drug treatment. E, Characterization of allograft tumors from (D) after three weeks of treatment. Top, H&E. Subsequent rows, IHC for ERG, AR, pRB S795, and Ki67. F, A hypothetical model. In prostate cancer cells without the TMPRSS2-ERG fusion, PTEN deletion/mutation and TP53 deletion/mutation favor cell cycle gene expression, CDK activation, and RB inhibition (hyperphosphorylation), which in turn leads to E2F1 activation and luminal-epithelial-to-mesenchymal cell identity transition, antiandrogen resistance and increased CDK4/6 inhibitor sensitivity. In contrast, in prostate cancer cells harboring the TMPRSS2-ERG fusion, overexpression of ERG results in decreased expression of a subset of cell cycle-promoting genes and RB activation (hypophosphorylation), thereby leading to E2F1 inhibition and maintenance of luminal epithelial cell identity, increased antiandrogen sensitivity, but CDK4/6 inhibitor resistance.

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: TMPRSS2-ERG controls luminal epithelial lineage and antiandrogen sensitivity in PTEN and TP53 -mutated prostate cancer

    doi: 10.1158/1078-0432.CCR-18-0653

    Figure Lengend Snippet: A, Western blot analysis of expression of key AR pathway, cell cycle, and EMT-related proteins in LNCaP-RF cells with or without lentiviral-mediated ERG (T1-E4) expression after treatment with vehicle, enzalutamide (ENZ, 10 μM), palbociclib (PD, 1 μM), or combination (ENZ + PD). B, Cell proliferation as measured by SRB assay for LNCaP-RF cells with or without lentiviral-mediated ERG (T1-E4) expression after treatment with vehicle, ENZ (10 μM), PD (1 μM), or combination. C, LNCaP-RF xenograft tumor volume with or without lentiviral-mediated ERG (T1-E4) expression during three weeks treatment with vehicle, ENZ (30 mg/kg/day), PD (100 mg/kg/day), or combination. Six xenografts (n = 6) per cell line, per drug treatment. D, ERG−/ARlow/KRTlow DMT and ERG+/ARhigh/KRThigh TMT allograft tumor volume during three weeks of treatment with vehicle, ENZ (30 mg/kg/day), PD (100 mg/kg/day), or combination. Five allografts (n = 5) per genotype, per drug treatment. E, Characterization of allograft tumors from (D) after three weeks of treatment. Top, H&E. Subsequent rows, IHC for ERG, AR, pRB S795, and Ki67. F, A hypothetical model. In prostate cancer cells without the TMPRSS2-ERG fusion, PTEN deletion/mutation and TP53 deletion/mutation favor cell cycle gene expression, CDK activation, and RB inhibition (hyperphosphorylation), which in turn leads to E2F1 activation and luminal-epithelial-to-mesenchymal cell identity transition, antiandrogen resistance and increased CDK4/6 inhibitor sensitivity. In contrast, in prostate cancer cells harboring the TMPRSS2-ERG fusion, overexpression of ERG results in decreased expression of a subset of cell cycle-promoting genes and RB activation (hypophosphorylation), thereby leading to E2F1 inhibition and maintenance of luminal epithelial cell identity, increased antiandrogen sensitivity, but CDK4/6 inhibitor resistance.

    Article Snippet: Antibodies include: anti-ERG (ab92513, Abcam; CM421C, Biocare Medical), anti-PTEN (CST9559L, Cell Signaling Technology), anti-p53 (sc126, Santa Cruz Biotechnology), anti-AR (sc816, Santa Cruz Biotechnology), anti-NKX3.1 (NB100-1828, Novus Biologicals), anti-RB (554136, BD Biosciences), anti-pRB S795 (CST9301S, Cell Signaling Technology), anti-SKP2 (32-3300, Life Technologies), anti-CCND1 (sc718, Santa Cruz Biotechnology), anti-CDK1 (sc54, Santa Cruz Biotechnology), anti-TWIST (sc6269, Santa Cruz Biotechnology), anti-CDH1 (610181, BD Biosciences), anti-VIM (sc73258, Santa Cruz Biotechnology), anti-ERK2 (sc1647, Santa Cruz Biotechnology), anti-CDK2 (sc6248, Santa Cruz Biotechnology), anti-E2F1 (sc193, Santa Cruz Biotechnology), anti-pAKT S473 (CST4060L, Cell Signaling Technology), anti-AKT (CST9272, Cell Signaling Technology). qRT-PCR qRT-PCR was performed as described previously ( 15 ).

    Techniques: Western Blot, Expressing, Sulforhodamine B Assay, Mutagenesis, Gene Expression, Activation Assay, Inhibition, Over Expression