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anti hnf4a p1 k9218  (Perseus Proteomics)
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Perseus Proteomics anti hnf4a p1 k9218
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Anti Hnf4a P1 K9218, supplied by Perseus Proteomics, 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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na4 p2 o7 ⋅ 10h2 o  (Shanghai Macklin Biochemical)
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Shanghai Macklin Biochemical na4 p2 o7 ⋅ 10h2 o
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Na4 P2 O7 ⋅ 10h2 O, supplied by Shanghai Macklin Biochemical, 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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p2 adapters  (Solexa)
86
Solexa p2 adapters
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
P2 Adapters, supplied by Solexa, 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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cd19 cre b6 129 p2 c cd19tm1 cre cgn j  (Jackson Laboratory)
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Jackson Laboratory cd19 cre b6 129 p2 c cd19tm1 cre cgn j
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Cd19 Cre B6 129 P2 C Cd19tm1 Cre Cgn J, supplied by Jackson Laboratory, 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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cd19 cre b6 129 p2 c cd19tm1 cre cgn j - by Bioz Stars, 2026-07
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biotin labeled rna p2  (Sangon Biotech)
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Sangon Biotech biotin labeled rna p2
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Biotin Labeled Rna P2, supplied by Sangon Biotech, 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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fragment ca p2 nes  (Twist Bioscience)
86
Twist Bioscience fragment ca p2 nes
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Fragment Ca P2 Nes, supplied by Twist Bioscience, 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/product/p1+or+p2/pmc13191288-38-24-28?v=Twist+Bioscience
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fragment ca p2 nes - by Bioz Stars, 2026-07
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baidu index p2  (Baidu Inc)
86
Baidu Inc baidu index p2
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Baidu Index P2, supplied by Baidu 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/product/p1+or+p2/pm42249461-207-5-5?v=Baidu+Inc
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baidu index p2 - by Bioz Stars, 2026-07
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pi 4 5 p 2 powder  (Croda International Plc)
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Croda International Plc pi 4 5 p 2 powder
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Pi 4 5 P 2 Powder, supplied by Croda International Plc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p1+or+p2/pmc12771316-77-11-16?v=Croda+International+Plc
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qiagen p2 lysis buffer  (Qiagen)
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Qiagen qiagen p2 lysis buffer
Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of <t>HNF4A</t> bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using <t>an</t> <t>anti-HNF4A</t> antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.
Qiagen P2 Lysis Buffer, supplied by Qiagen, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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qiagen p2 lysis buffer - by Bioz Stars, 2026-07
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Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using an anti-HNF4A antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.

Journal: Molecular Therapy Oncology

Article Title: Ligand-dependent reprogramming of HNF4A expression and function suppresses multistep hepatocarcinogenesis

doi: 10.1016/j.omton.2026.201246

Figure Lengend Snippet: Antitumor effect of PA is enhanced by fatty acids (A) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells with no treatment or treated with LA (20 μM), PA (20 μM), ATRA (20 μM), or 9-cis RA (20 μM) for 72 h using ELISA ( n = 3). (B) Quantitation of HNF4A bound to HBEs in DN-like primary HCC cells treated with the indicated concentration of PA for 72 h using ELISA ( n = 3). (C) Quantitation of HNF4A bound to HBEs in PA-treated HLF cells transfected with wild-type (WT) or V255M mutant HNF4A (80 μM, 48 h) using ELISA ( n = 3). (D) Immunoblotting protein levels of HNF4A, RXRα, RXRα ΔN197, RARα, and ACTB in HCC cell lines Huh7, HLE, and HLF. (D) Quantitative reverse transcription polymerase chain reaction analysis of selected genes in DN-like primary HCC cells treated with siRNA control, siRNA HNF4A , or siRNA RXRα for 48 h ( n = 3). (E) Cell proliferation of KH cells transfected with small interfering RNAs treated with PA (40 μM) or ATRA (40 μM) for 96 h ( n = 4). (F) mRNA levels of HNF4A P1 , P2 , ALB , and TTR in DN-like primary HCC cells treated with PA (20 μM) for 1, 3, 6, and 12 h. (G) Protein levels of HNF4A P1 and P2 following treatment with PA (20 μM). (H) H4-Luciferase following 12 h of treatment with PA. (I) Chromatin immunoprecipitation followed by sequencing analysis using an anti-HNF4A antibody in DN-like primary HCC cells treated with 40 μM PA for 12 h, integrated with the RNA sequencing results. (J) Hallmark pathway enrichment analysis of genes activated by HNF4A binding and transcription following treatment with PA. Data are presented as the mean (SD) (in A–B, D–F, and H). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, as determined using one-way analysis of variance. HCC, hepatocellular carcinoma; HBEs, HNF4A-binding elements; RA, retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor; HNF4A, hepatocyte nuclear factor 4 alpha; TTR, transthyretin.

Article Snippet: Antibodies used included anti-HNF4A P1 K9218 (Perseus Proteomics Inc., Tokyo, Japan), anti-HNF4A P2 H6939 (Perseus Proteomics Inc.), anti-HNF4A All H1415 (Perseus Proteomics Inc.), anti RXRα (Cell Signaling Technology), anti-RXRα ΔN197 (Santa Cruz), anti-RARα C-20 (Santa Cruz), anti-Lamin A/C (Cell Signaling Technology), and anti-ACTB (Santa Cruz).

Techniques: Quantitation Assay, Enzyme-linked Immunosorbent Assay, Concentration Assay, Transfection, Mutagenesis, Western Blot, Reverse Transcription, Polymerase Chain Reaction, Control, Luciferase, Chromatin Immunoprecipitation, Sequencing, RNA Sequencing, Binding Assay