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candidate pklr inhibitors  (MedChemExpress)


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    MedChemExpress candidate pklr inhibitors
    A , B IHC staining of <t>PKLR</t> and ZBTB10 on consecutive sections of a PCa TMA (CA4) in two selected cases. Scale bars, 100 μm. C Correlation analysis of the intensities of PKLR and ZBTB10 of the PCa TMA ( n = 49). PKLR expression was negatively associated with ZBTB10-expressing PCa samples. R , correlation coefficient; p , two-tailed p value. Significance was determined by correlation XY analyses in GraphPad Prism. D , E Tumor grade association analysis using a Chi-squared test of the CA9 PCa TMA. Intensities of PKLR ( D ) and ZBTB10 ( E ) staining were semiquantitatively scored using the H-index as follows: negative, weakly positive, moderately positive, and strongly positive. p values were calculated by a Chi-squared test performed using SPSS statistical 18.0 software. p < 0.001. F Proposed model for ADT-induced PKLR drives hormone-refractory PCa. Hormone-sensitive PCa activates AR signaling by increasing ZBTB10 leading to increased binding to the PKLR regulatory sequence and mediation of its transcriptional suppression. ADT induced inactivation of the AR-ZBTB10 pathway, leading to an abundance of PKLR through ZBTB10 loss of function. Overexpression of PKLR may upregulate glucose metabolism and NED progression of PCa cells. Targeting PKLR by potential PKLR <t>inhibitors</t> may reduce the PKLR-driven glycolysis and NED of ADT-resistant PCa.
    Candidate Pklr Inhibitors, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/candidate+pklr+inhibitors/Fosinopril/pmc08934352-325-47-58
    Average 94 stars, based on 5 article reviews
    candidate pklr inhibitors - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Pyruvate kinase L/R links metabolism dysfunction to neuroendocrine differentiation of prostate cancer by ZBTB10 deficiency"

    Article Title: Pyruvate kinase L/R links metabolism dysfunction to neuroendocrine differentiation of prostate cancer by ZBTB10 deficiency

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-022-04694-z

    A , B IHC staining of PKLR and ZBTB10 on consecutive sections of a PCa TMA (CA4) in two selected cases. Scale bars, 100 μm. C Correlation analysis of the intensities of PKLR and ZBTB10 of the PCa TMA ( n = 49). PKLR expression was negatively associated with ZBTB10-expressing PCa samples. R , correlation coefficient; p , two-tailed p value. Significance was determined by correlation XY analyses in GraphPad Prism. D , E Tumor grade association analysis using a Chi-squared test of the CA9 PCa TMA. Intensities of PKLR ( D ) and ZBTB10 ( E ) staining were semiquantitatively scored using the H-index as follows: negative, weakly positive, moderately positive, and strongly positive. p values were calculated by a Chi-squared test performed using SPSS statistical 18.0 software. p < 0.001. F Proposed model for ADT-induced PKLR drives hormone-refractory PCa. Hormone-sensitive PCa activates AR signaling by increasing ZBTB10 leading to increased binding to the PKLR regulatory sequence and mediation of its transcriptional suppression. ADT induced inactivation of the AR-ZBTB10 pathway, leading to an abundance of PKLR through ZBTB10 loss of function. Overexpression of PKLR may upregulate glucose metabolism and NED progression of PCa cells. Targeting PKLR by potential PKLR inhibitors may reduce the PKLR-driven glycolysis and NED of ADT-resistant PCa.
    Figure Legend Snippet: A , B IHC staining of PKLR and ZBTB10 on consecutive sections of a PCa TMA (CA4) in two selected cases. Scale bars, 100 μm. C Correlation analysis of the intensities of PKLR and ZBTB10 of the PCa TMA ( n = 49). PKLR expression was negatively associated with ZBTB10-expressing PCa samples. R , correlation coefficient; p , two-tailed p value. Significance was determined by correlation XY analyses in GraphPad Prism. D , E Tumor grade association analysis using a Chi-squared test of the CA9 PCa TMA. Intensities of PKLR ( D ) and ZBTB10 ( E ) staining were semiquantitatively scored using the H-index as follows: negative, weakly positive, moderately positive, and strongly positive. p values were calculated by a Chi-squared test performed using SPSS statistical 18.0 software. p < 0.001. F Proposed model for ADT-induced PKLR drives hormone-refractory PCa. Hormone-sensitive PCa activates AR signaling by increasing ZBTB10 leading to increased binding to the PKLR regulatory sequence and mediation of its transcriptional suppression. ADT induced inactivation of the AR-ZBTB10 pathway, leading to an abundance of PKLR through ZBTB10 loss of function. Overexpression of PKLR may upregulate glucose metabolism and NED progression of PCa cells. Targeting PKLR by potential PKLR inhibitors may reduce the PKLR-driven glycolysis and NED of ADT-resistant PCa.

    Techniques Used: Immunohistochemistry, Expressing, Two Tailed Test, Staining, Software, Binding Assay, Sequencing, Over Expression



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    candidate pklr inhibitors  (MedChemExpress)
    94
    MedChemExpress candidate pklr inhibitors
    A , B IHC staining of <t>PKLR</t> and ZBTB10 on consecutive sections of a PCa TMA (CA4) in two selected cases. Scale bars, 100 μm. C Correlation analysis of the intensities of PKLR and ZBTB10 of the PCa TMA ( n = 49). PKLR expression was negatively associated with ZBTB10-expressing PCa samples. R , correlation coefficient; p , two-tailed p value. Significance was determined by correlation XY analyses in GraphPad Prism. D , E Tumor grade association analysis using a Chi-squared test of the CA9 PCa TMA. Intensities of PKLR ( D ) and ZBTB10 ( E ) staining were semiquantitatively scored using the H-index as follows: negative, weakly positive, moderately positive, and strongly positive. p values were calculated by a Chi-squared test performed using SPSS statistical 18.0 software. p < 0.001. F Proposed model for ADT-induced PKLR drives hormone-refractory PCa. Hormone-sensitive PCa activates AR signaling by increasing ZBTB10 leading to increased binding to the PKLR regulatory sequence and mediation of its transcriptional suppression. ADT induced inactivation of the AR-ZBTB10 pathway, leading to an abundance of PKLR through ZBTB10 loss of function. Overexpression of PKLR may upregulate glucose metabolism and NED progression of PCa cells. Targeting PKLR by potential PKLR <t>inhibitors</t> may reduce the PKLR-driven glycolysis and NED of ADT-resistant PCa.
    Candidate Pklr Inhibitors, supplied by MedChemExpress, 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/product/candidate+pklr+inhibitors/Fosinopril/pmc08934352-325-47-58
    Average 94 stars, based on 1 article reviews
    candidate pklr inhibitors - by Bioz Stars, 2026-09
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    A , B IHC staining of PKLR and ZBTB10 on consecutive sections of a PCa TMA (CA4) in two selected cases. Scale bars, 100 μm. C Correlation analysis of the intensities of PKLR and ZBTB10 of the PCa TMA ( n = 49). PKLR expression was negatively associated with ZBTB10-expressing PCa samples. R , correlation coefficient; p , two-tailed p value. Significance was determined by correlation XY analyses in GraphPad Prism. D , E Tumor grade association analysis using a Chi-squared test of the CA9 PCa TMA. Intensities of PKLR ( D ) and ZBTB10 ( E ) staining were semiquantitatively scored using the H-index as follows: negative, weakly positive, moderately positive, and strongly positive. p values were calculated by a Chi-squared test performed using SPSS statistical 18.0 software. p < 0.001. F Proposed model for ADT-induced PKLR drives hormone-refractory PCa. Hormone-sensitive PCa activates AR signaling by increasing ZBTB10 leading to increased binding to the PKLR regulatory sequence and mediation of its transcriptional suppression. ADT induced inactivation of the AR-ZBTB10 pathway, leading to an abundance of PKLR through ZBTB10 loss of function. Overexpression of PKLR may upregulate glucose metabolism and NED progression of PCa cells. Targeting PKLR by potential PKLR inhibitors may reduce the PKLR-driven glycolysis and NED of ADT-resistant PCa.

    Journal: Cell Death & Disease

    Article Title: Pyruvate kinase L/R links metabolism dysfunction to neuroendocrine differentiation of prostate cancer by ZBTB10 deficiency

    doi: 10.1038/s41419-022-04694-z

    Figure Lengend Snippet: A , B IHC staining of PKLR and ZBTB10 on consecutive sections of a PCa TMA (CA4) in two selected cases. Scale bars, 100 μm. C Correlation analysis of the intensities of PKLR and ZBTB10 of the PCa TMA ( n = 49). PKLR expression was negatively associated with ZBTB10-expressing PCa samples. R , correlation coefficient; p , two-tailed p value. Significance was determined by correlation XY analyses in GraphPad Prism. D , E Tumor grade association analysis using a Chi-squared test of the CA9 PCa TMA. Intensities of PKLR ( D ) and ZBTB10 ( E ) staining were semiquantitatively scored using the H-index as follows: negative, weakly positive, moderately positive, and strongly positive. p values were calculated by a Chi-squared test performed using SPSS statistical 18.0 software. p < 0.001. F Proposed model for ADT-induced PKLR drives hormone-refractory PCa. Hormone-sensitive PCa activates AR signaling by increasing ZBTB10 leading to increased binding to the PKLR regulatory sequence and mediation of its transcriptional suppression. ADT induced inactivation of the AR-ZBTB10 pathway, leading to an abundance of PKLR through ZBTB10 loss of function. Overexpression of PKLR may upregulate glucose metabolism and NED progression of PCa cells. Targeting PKLR by potential PKLR inhibitors may reduce the PKLR-driven glycolysis and NED of ADT-resistant PCa.

    Article Snippet: To mimic ADT, cells were cultured in RPMI-1640 medium with 5% CSS (ThermoFisher, 12676-029)-containing medium for 48 h or treated with 10 μM MDV3100 (Selleckchem, S1250) under standard culture conditions for 48 h. The AR ligand was treated with 10 nM DHT (Sigma-Aldrich) for 24 h. The candidate PKLR inhibitors (vilanterol, saquinavir, fosinopril, and salmeterol) were purchased from MedChemExpress (HY-14300, HY-17007, HY-B0382, and HY-14302), and the concentrations of each candidate drug for cell viability were treated with 0, 1, 5, 10, 25, and 50 μM for 24 h.

    Techniques: Immunohistochemistry, Expressing, Two Tailed Test, Staining, Software, Binding Assay, Sequencing, Over Expression