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A Co-IP followed by western blotting analyses in PRAS40-overexpressed HT29 cells. Analyses of <t>PGK1</t> activity in HT29 cells with PRAS40 knockdown B or overexpression C . D – H HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector together with control or PGK1 shRNA. Glucose consumption analyses D , lactate production analyses E , flow cytometry analyses with anti-CD44 and anti-CD133 antibodies F were conducted. Representative images and quantification of tumor spheres were shown G , H . Data represent the mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.
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A Co-IP followed by western blotting analyses in PRAS40-overexpressed HT29 cells. Analyses of <t>PGK1</t> activity in HT29 cells with PRAS40 knockdown B or overexpression C . D – H HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector together with control or PGK1 shRNA. Glucose consumption analyses D , lactate production analyses E , flow cytometry analyses with anti-CD44 and anti-CD133 antibodies F were conducted. Representative images and quantification of tumor spheres were shown G , H . Data represent the mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.
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A Co-IP followed by western blotting analyses in PRAS40-overexpressed HT29 cells. Analyses of <t>PGK1</t> activity in HT29 cells with PRAS40 knockdown B or overexpression C . D – H HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector together with control or PGK1 shRNA. Glucose consumption analyses D , lactate production analyses E , flow cytometry analyses with anti-CD44 and anti-CD133 antibodies F were conducted. Representative images and quantification of tumor spheres were shown G , H . Data represent the mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.
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G-Rh2 reduced PIN1-dependent mitochondrial translocation of <t>PGK1.</t> ( A - D ) The effect of G-Rh2 on glucose uptake, lactate production, pyruvate production, and PDH activity was assessed following PIN1 interference; ( E ) The interaction between PIN1 and PGK1 before and after G-Rh2 treatment was analyzed by co-IP assay; ( F ) The interaction between PGK1 and TOM20 before and after G-Rh2 treatment was examined by co-IP assay; ( G ) PGK1 expression in total, cytoplasmic, and mitochondrial protein fractions after G-Rh2 treatment were analyzed by Western blot analysis; ( H ) Immunofluorescence analysis was performed to examine the co-localization of PGK1 with mitochondria following G-Rh2 treatment. Scale bar, 100 μm; ( I ) Western blot analysis was used to detect the expression of PDHK1, PDH, and their phosphorylated forms following G-Rh2 treatment; ( J ) Western blot analysis was performed to assess the effect of G-Rh2 on mitochondrial PGK1 levels following PGK1 mutation; ( K ) Western blot analysis was performed to examine changes in G-Rh2 expression and downstream PGK1-phosphorylated proteins, including PDHK1 and PDH after PGK1 mutation; ( L ) The effect of G-Rh2 on glucose consumption in NSCLC cells following PGK1 mutation was assessed by glucose uptake detection; Data are presented as mean ± SD ( n = 3 biological replicates). ns P > 0.05; *** P < 0.001. Co-IP, co-immunoprecipitation
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A Co-IP followed by western blotting analyses in PRAS40-overexpressed HT29 cells. Analyses of PGK1 activity in HT29 cells with PRAS40 knockdown B or overexpression C . D – H HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector together with control or PGK1 shRNA. Glucose consumption analyses D , lactate production analyses E , flow cytometry analyses with anti-CD44 and anti-CD133 antibodies F were conducted. Representative images and quantification of tumor spheres were shown G , H . Data represent the mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.

Journal: Oncogenesis

Article Title: PRAS40 promotes colorectal cancer stemness by enhancing glycolysis through triggering PGK1 acetylation

doi: 10.1038/s41389-025-00594-x

Figure Lengend Snippet: A Co-IP followed by western blotting analyses in PRAS40-overexpressed HT29 cells. Analyses of PGK1 activity in HT29 cells with PRAS40 knockdown B or overexpression C . D – H HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector together with control or PGK1 shRNA. Glucose consumption analyses D , lactate production analyses E , flow cytometry analyses with anti-CD44 and anti-CD133 antibodies F were conducted. Representative images and quantification of tumor spheres were shown G , H . Data represent the mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Antibodies were purchased for detection of PRAS40 (2691S), PCNA (13110), PCAF (3378 T) (Cell Signaling); PGK1 (17811-1-AP), CD133 (66666-1-Ig), α-Tubulin (66031-1-Ig), β-Actin (66009-1-Ig), CD44 (15675-1-AP) (Proteintech); SIRT7 (ab259968), anti-phosphotryosine (ab179530) (Abcam); and pan-Acetyl (sc-8649)(Santa Crus Biotechnology).

Techniques: Co-Immunoprecipitation Assay, Western Blot, Activity Assay, Knockdown, Over Expression, Plasmid Preparation, Expressing, Control, shRNA, Flow Cytometry

Co-IP followed by western blotting analyses in HT29 cells with PRAS40 knockdown A or overexpression B . C – I HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector, and treated with or without acetyltransferase inhibitors PU139 (20 μM) or Anacardic acid (5 or 10 μM). NC, negative control. Analyses of PGK1 activity C , representative images and quantification of tumor spheres were shown D , E , real time PCR analyses F , western blotting analyses G , and flow cytometry analyses with anti-CD44 and anti-CD133 antibodies H , I were performed. J Co-IP followed by western blotting analyses in HT29 cells. Co-IP followed by western blotting analyses in HT29 cells with PRAS40 knockdown K or overexpression L . Data represent the mean ± SD. ** P < 0.01; *** P < 0.001. The quantification results of the band density were labeled above the bands.

Journal: Oncogenesis

Article Title: PRAS40 promotes colorectal cancer stemness by enhancing glycolysis through triggering PGK1 acetylation

doi: 10.1038/s41389-025-00594-x

Figure Lengend Snippet: Co-IP followed by western blotting analyses in HT29 cells with PRAS40 knockdown A or overexpression B . C – I HT29 cells were introduced with empty vector or FLAG-PRAS40 expression vector, and treated with or without acetyltransferase inhibitors PU139 (20 μM) or Anacardic acid (5 or 10 μM). NC, negative control. Analyses of PGK1 activity C , representative images and quantification of tumor spheres were shown D , E , real time PCR analyses F , western blotting analyses G , and flow cytometry analyses with anti-CD44 and anti-CD133 antibodies H , I were performed. J Co-IP followed by western blotting analyses in HT29 cells. Co-IP followed by western blotting analyses in HT29 cells with PRAS40 knockdown K or overexpression L . Data represent the mean ± SD. ** P < 0.01; *** P < 0.001. The quantification results of the band density were labeled above the bands.

Article Snippet: Antibodies were purchased for detection of PRAS40 (2691S), PCNA (13110), PCAF (3378 T) (Cell Signaling); PGK1 (17811-1-AP), CD133 (66666-1-Ig), α-Tubulin (66031-1-Ig), β-Actin (66009-1-Ig), CD44 (15675-1-AP) (Proteintech); SIRT7 (ab259968), anti-phosphotryosine (ab179530) (Abcam); and pan-Acetyl (sc-8649)(Santa Crus Biotechnology).

Techniques: Co-Immunoprecipitation Assay, Western Blot, Knockdown, Over Expression, Plasmid Preparation, Expressing, Negative Control, Activity Assay, Real-time Polymerase Chain Reaction, Flow Cytometry, Labeling

G-Rh2 reduced PIN1-dependent mitochondrial translocation of PGK1. ( A - D ) The effect of G-Rh2 on glucose uptake, lactate production, pyruvate production, and PDH activity was assessed following PIN1 interference; ( E ) The interaction between PIN1 and PGK1 before and after G-Rh2 treatment was analyzed by co-IP assay; ( F ) The interaction between PGK1 and TOM20 before and after G-Rh2 treatment was examined by co-IP assay; ( G ) PGK1 expression in total, cytoplasmic, and mitochondrial protein fractions after G-Rh2 treatment were analyzed by Western blot analysis; ( H ) Immunofluorescence analysis was performed to examine the co-localization of PGK1 with mitochondria following G-Rh2 treatment. Scale bar, 100 μm; ( I ) Western blot analysis was used to detect the expression of PDHK1, PDH, and their phosphorylated forms following G-Rh2 treatment; ( J ) Western blot analysis was performed to assess the effect of G-Rh2 on mitochondrial PGK1 levels following PGK1 mutation; ( K ) Western blot analysis was performed to examine changes in G-Rh2 expression and downstream PGK1-phosphorylated proteins, including PDHK1 and PDH after PGK1 mutation; ( L ) The effect of G-Rh2 on glucose consumption in NSCLC cells following PGK1 mutation was assessed by glucose uptake detection; Data are presented as mean ± SD ( n = 3 biological replicates). ns P > 0.05; *** P < 0.001. Co-IP, co-immunoprecipitation

Journal: Journal of Translational Medicine

Article Title: Ginsenoside Rh2 as a novel PIN1 inhibitor disrupting the cancer stem cell-like phenotype in non-small cell lung cancer

doi: 10.1186/s12967-025-07318-0

Figure Lengend Snippet: G-Rh2 reduced PIN1-dependent mitochondrial translocation of PGK1. ( A - D ) The effect of G-Rh2 on glucose uptake, lactate production, pyruvate production, and PDH activity was assessed following PIN1 interference; ( E ) The interaction between PIN1 and PGK1 before and after G-Rh2 treatment was analyzed by co-IP assay; ( F ) The interaction between PGK1 and TOM20 before and after G-Rh2 treatment was examined by co-IP assay; ( G ) PGK1 expression in total, cytoplasmic, and mitochondrial protein fractions after G-Rh2 treatment were analyzed by Western blot analysis; ( H ) Immunofluorescence analysis was performed to examine the co-localization of PGK1 with mitochondria following G-Rh2 treatment. Scale bar, 100 μm; ( I ) Western blot analysis was used to detect the expression of PDHK1, PDH, and their phosphorylated forms following G-Rh2 treatment; ( J ) Western blot analysis was performed to assess the effect of G-Rh2 on mitochondrial PGK1 levels following PGK1 mutation; ( K ) Western blot analysis was performed to examine changes in G-Rh2 expression and downstream PGK1-phosphorylated proteins, including PDHK1 and PDH after PGK1 mutation; ( L ) The effect of G-Rh2 on glucose consumption in NSCLC cells following PGK1 mutation was assessed by glucose uptake detection; Data are presented as mean ± SD ( n = 3 biological replicates). ns P > 0.05; *** P < 0.001. Co-IP, co-immunoprecipitation

Article Snippet: After blocking with 5% skim milk (Beyotime Biotechnology, Shanghai, China) for 1 h, the membranes were incubated overnight at 4°C with the following primary antibodies: E-cad (Proteintech, Wuhan, China, Cat# 20874-1-AP), N-cad (Proteintech, Cat# 66219-1-Ig), β-tubulin (Proteintech, Cat# 10068-1-AP), β-actin (Proteintech, Cat# 66009-1-Ig), PIN1 (Proteintech, Cat# 10495-1-AP), PGK1 (Proteintech, Cat# 17811-1-AP), phospho-PGK1 (Ser203) (SAB, USA, Cat# SAB487P), PDHK1 (Proteintech, Cat# 18262-1-AP), PDH E1 (Proteintech, Cat# 18068-1-AP), phospho-PDH E1 (Ser293) (ABclonal, China, Cat# AP1250), TOM20 (Proteintech, Cat# 66777-1-Ig), COXIV (Proteintech, Cat# 11242-1-AP), TIM22 (Proteintech, Cat# 14927-1-AP), SOX2 (Proteintech, Cat# 11064-1-AP), OCT4 (Proteintech, Cat# 11263-1-AP), NANOG (Proteintech, Cat# 14295-1-AP), CD44 (ABclonal, China, Cat# A1351), and CD133 (ZEN-BIO, China).

Techniques: Translocation Assay, Activity Assay, Co-Immunoprecipitation Assay, Expressing, Western Blot, Immunofluorescence, Mutagenesis, Immunoprecipitation

G-Rh2 inhibited tumor metastasis and enhanced therapeutic sensitivity via the PGK1/PDHK1 pathway. ( A - C ) The effect of G-Rh2 on the migration capacity of A549 cells, following treatment with 72.3 nM API-1, 2.5 µM NG52, or 36.8 nM AZD7545, was assessed by wound healing assay; ( D ) The effect of 30 µg/mL G-Rh2 on the invasion ability of A549 cells, treated with 72.3 nM API-1, 2.5 µM NG52 or 36.8 nM AZD7545, was assessed by Transwell assay; ( E ) Western blot analysis was used to detect the effect of G-Rh2 on EMT markers in A549 cells treated with inhibitors API-1, NG52, and AZD7545; ( F ) Flow cytometry analysis was performed to detect the apoptosis in A549 cells treated with 72.3 nM API-1, 30 µg/mL G-Rh2, 5 µM DDP (or 10 µM GF) alone or in combination; ( G - H ) The effects of G-Rh2, chemotherapy alone, and combination treatment on A549 cell proliferation, following API-1 treatment, were assessed by CCK-8 assay; ( I ) Flow cytometry analysis was used to detect the apoptosis in A549 cells treated with 2.5 µM NG52, 30 µg/mL G-Rh2, 5 µM DDP (or 10 µM GF) alone or in combination; ( J - K ) The effects of NG52 treatment combined with G-Rh2, DDP (or GF), or both, on A549 cell proliferation, were measured by CCK-8 assay; ( M ) Flow cytometry analysis was used to detect the apoptosis in A549 cells following 36.8 nM AZD7545 treatment, with 30 µg/mL G-Rh2, 5 µM DDP (or 10 µM GF) alone or in combination. ( M - N ) The effects of AZD7545 treatment combined with G-Rh2, DDP (or GF), or both, on A549 cell proliferation, were assessed by CCK-8 assay; Data are presented as mean ± SD ( n = 3 biological replicates). ns P > 0.05; ** P < 0.01; *** P < 0.001. Scale bar, 200 μm

Journal: Journal of Translational Medicine

Article Title: Ginsenoside Rh2 as a novel PIN1 inhibitor disrupting the cancer stem cell-like phenotype in non-small cell lung cancer

doi: 10.1186/s12967-025-07318-0

Figure Lengend Snippet: G-Rh2 inhibited tumor metastasis and enhanced therapeutic sensitivity via the PGK1/PDHK1 pathway. ( A - C ) The effect of G-Rh2 on the migration capacity of A549 cells, following treatment with 72.3 nM API-1, 2.5 µM NG52, or 36.8 nM AZD7545, was assessed by wound healing assay; ( D ) The effect of 30 µg/mL G-Rh2 on the invasion ability of A549 cells, treated with 72.3 nM API-1, 2.5 µM NG52 or 36.8 nM AZD7545, was assessed by Transwell assay; ( E ) Western blot analysis was used to detect the effect of G-Rh2 on EMT markers in A549 cells treated with inhibitors API-1, NG52, and AZD7545; ( F ) Flow cytometry analysis was performed to detect the apoptosis in A549 cells treated with 72.3 nM API-1, 30 µg/mL G-Rh2, 5 µM DDP (or 10 µM GF) alone or in combination; ( G - H ) The effects of G-Rh2, chemotherapy alone, and combination treatment on A549 cell proliferation, following API-1 treatment, were assessed by CCK-8 assay; ( I ) Flow cytometry analysis was used to detect the apoptosis in A549 cells treated with 2.5 µM NG52, 30 µg/mL G-Rh2, 5 µM DDP (or 10 µM GF) alone or in combination; ( J - K ) The effects of NG52 treatment combined with G-Rh2, DDP (or GF), or both, on A549 cell proliferation, were measured by CCK-8 assay; ( M ) Flow cytometry analysis was used to detect the apoptosis in A549 cells following 36.8 nM AZD7545 treatment, with 30 µg/mL G-Rh2, 5 µM DDP (or 10 µM GF) alone or in combination. ( M - N ) The effects of AZD7545 treatment combined with G-Rh2, DDP (or GF), or both, on A549 cell proliferation, were assessed by CCK-8 assay; Data are presented as mean ± SD ( n = 3 biological replicates). ns P > 0.05; ** P < 0.01; *** P < 0.001. Scale bar, 200 μm

Article Snippet: After blocking with 5% skim milk (Beyotime Biotechnology, Shanghai, China) for 1 h, the membranes were incubated overnight at 4°C with the following primary antibodies: E-cad (Proteintech, Wuhan, China, Cat# 20874-1-AP), N-cad (Proteintech, Cat# 66219-1-Ig), β-tubulin (Proteintech, Cat# 10068-1-AP), β-actin (Proteintech, Cat# 66009-1-Ig), PIN1 (Proteintech, Cat# 10495-1-AP), PGK1 (Proteintech, Cat# 17811-1-AP), phospho-PGK1 (Ser203) (SAB, USA, Cat# SAB487P), PDHK1 (Proteintech, Cat# 18262-1-AP), PDH E1 (Proteintech, Cat# 18068-1-AP), phospho-PDH E1 (Ser293) (ABclonal, China, Cat# AP1250), TOM20 (Proteintech, Cat# 66777-1-Ig), COXIV (Proteintech, Cat# 11242-1-AP), TIM22 (Proteintech, Cat# 14927-1-AP), SOX2 (Proteintech, Cat# 11064-1-AP), OCT4 (Proteintech, Cat# 11263-1-AP), NANOG (Proteintech, Cat# 14295-1-AP), CD44 (ABclonal, China, Cat# A1351), and CD133 (ZEN-BIO, China).

Techniques: Migration, Wound Healing Assay, Transwell Assay, Western Blot, Flow Cytometry, CCK-8 Assay

G-Rh2 reduced tumor growth and the distribution of NSCLC stem cell-like cells in vivo. ( A ) The effect of 10 mg/kg G-Rh2 treatment on the growth of transplanted tumors at various LLC concentrations and tumor number statistics was assessed; ( B ) H&E staining was used to evaluate the number of tumor lesions after LLC tail vein lung metastasis following G-Rh2 treatment; ( C ) Immunohistochemistry was used to detect the expression of EMT-related markers before and after G-Rh2 treatment; ( D ) PIN1 expression analysis was performed in tumor and adjacent non-tumor tissues under G-Rh2 treatment; ( E ) The expression of stem cell-related markers was assessed by immunohistochemistry before and after G-Rh2 treatment; ( F ) The expression of PGK1, PDHK1, PDH, and their phosphorylated forms was assessed by immunohistochemistry before and after G-Rh2 treatment; ( G ) Tumor volumes were monitored during drug administration; ( H ) Changes in body weight of the mice during treatment; ( I ) The effects of 20 mg/kg G-Rh2, 50 mg/kg GF, and their combination (20 mg/kg G-Rh2 and 25 mg/kg GF) on LLC-luc derived tumor size were evaluated; ( J ) Tumor weight at the end of the treatment period was recorded for each group; ( K ) In vivo imaging was performed to monitor tumor size in each treatment group following administration; ( L - N ) Immunohistochemical analysis was used to assess the EMT process, tumor stem cell markers, and PGK1/PDHK1-related proteins in each treatment group; Data are presented as mean ± SD ( n = 5 biological replicates). * P < 0.05; *** P < 0.001. Scale bar, 100 μm

Journal: Journal of Translational Medicine

Article Title: Ginsenoside Rh2 as a novel PIN1 inhibitor disrupting the cancer stem cell-like phenotype in non-small cell lung cancer

doi: 10.1186/s12967-025-07318-0

Figure Lengend Snippet: G-Rh2 reduced tumor growth and the distribution of NSCLC stem cell-like cells in vivo. ( A ) The effect of 10 mg/kg G-Rh2 treatment on the growth of transplanted tumors at various LLC concentrations and tumor number statistics was assessed; ( B ) H&E staining was used to evaluate the number of tumor lesions after LLC tail vein lung metastasis following G-Rh2 treatment; ( C ) Immunohistochemistry was used to detect the expression of EMT-related markers before and after G-Rh2 treatment; ( D ) PIN1 expression analysis was performed in tumor and adjacent non-tumor tissues under G-Rh2 treatment; ( E ) The expression of stem cell-related markers was assessed by immunohistochemistry before and after G-Rh2 treatment; ( F ) The expression of PGK1, PDHK1, PDH, and their phosphorylated forms was assessed by immunohistochemistry before and after G-Rh2 treatment; ( G ) Tumor volumes were monitored during drug administration; ( H ) Changes in body weight of the mice during treatment; ( I ) The effects of 20 mg/kg G-Rh2, 50 mg/kg GF, and their combination (20 mg/kg G-Rh2 and 25 mg/kg GF) on LLC-luc derived tumor size were evaluated; ( J ) Tumor weight at the end of the treatment period was recorded for each group; ( K ) In vivo imaging was performed to monitor tumor size in each treatment group following administration; ( L - N ) Immunohistochemical analysis was used to assess the EMT process, tumor stem cell markers, and PGK1/PDHK1-related proteins in each treatment group; Data are presented as mean ± SD ( n = 5 biological replicates). * P < 0.05; *** P < 0.001. Scale bar, 100 μm

Article Snippet: After blocking with 5% skim milk (Beyotime Biotechnology, Shanghai, China) for 1 h, the membranes were incubated overnight at 4°C with the following primary antibodies: E-cad (Proteintech, Wuhan, China, Cat# 20874-1-AP), N-cad (Proteintech, Cat# 66219-1-Ig), β-tubulin (Proteintech, Cat# 10068-1-AP), β-actin (Proteintech, Cat# 66009-1-Ig), PIN1 (Proteintech, Cat# 10495-1-AP), PGK1 (Proteintech, Cat# 17811-1-AP), phospho-PGK1 (Ser203) (SAB, USA, Cat# SAB487P), PDHK1 (Proteintech, Cat# 18262-1-AP), PDH E1 (Proteintech, Cat# 18068-1-AP), phospho-PDH E1 (Ser293) (ABclonal, China, Cat# AP1250), TOM20 (Proteintech, Cat# 66777-1-Ig), COXIV (Proteintech, Cat# 11242-1-AP), TIM22 (Proteintech, Cat# 14927-1-AP), SOX2 (Proteintech, Cat# 11064-1-AP), OCT4 (Proteintech, Cat# 11263-1-AP), NANOG (Proteintech, Cat# 14295-1-AP), CD44 (ABclonal, China, Cat# A1351), and CD133 (ZEN-BIO, China).

Techniques: In Vivo, Staining, Immunohistochemistry, Expressing, Derivative Assay, In Vivo Imaging, Immunohistochemical staining

A schematic illustration depicting how G-Rh2 targets the PIN1/PGK1 cascade metabolic signaling pathway to enhance therapeutic sensitivity in NSCLC (Created in BioRender, https://BioRender.com/2s9laob)

Journal: Journal of Translational Medicine

Article Title: Ginsenoside Rh2 as a novel PIN1 inhibitor disrupting the cancer stem cell-like phenotype in non-small cell lung cancer

doi: 10.1186/s12967-025-07318-0

Figure Lengend Snippet: A schematic illustration depicting how G-Rh2 targets the PIN1/PGK1 cascade metabolic signaling pathway to enhance therapeutic sensitivity in NSCLC (Created in BioRender, https://BioRender.com/2s9laob)

Article Snippet: After blocking with 5% skim milk (Beyotime Biotechnology, Shanghai, China) for 1 h, the membranes were incubated overnight at 4°C with the following primary antibodies: E-cad (Proteintech, Wuhan, China, Cat# 20874-1-AP), N-cad (Proteintech, Cat# 66219-1-Ig), β-tubulin (Proteintech, Cat# 10068-1-AP), β-actin (Proteintech, Cat# 66009-1-Ig), PIN1 (Proteintech, Cat# 10495-1-AP), PGK1 (Proteintech, Cat# 17811-1-AP), phospho-PGK1 (Ser203) (SAB, USA, Cat# SAB487P), PDHK1 (Proteintech, Cat# 18262-1-AP), PDH E1 (Proteintech, Cat# 18068-1-AP), phospho-PDH E1 (Ser293) (ABclonal, China, Cat# AP1250), TOM20 (Proteintech, Cat# 66777-1-Ig), COXIV (Proteintech, Cat# 11242-1-AP), TIM22 (Proteintech, Cat# 14927-1-AP), SOX2 (Proteintech, Cat# 11064-1-AP), OCT4 (Proteintech, Cat# 11263-1-AP), NANOG (Proteintech, Cat# 14295-1-AP), CD44 (ABclonal, China, Cat# A1351), and CD133 (ZEN-BIO, China).

Techniques: