rabbit polyclonal anti hnf4α  (Cell Signaling Technology Inc)

Journal: eLife

Article Title: TAZ inhibits glucocorticoid receptor and coordinates hepatic glucose homeostasis in normal physiological states

doi: 10.7554/eLife.57462

Figure Lengend Snippet:

Article Snippet: Antibody , (Rabbit polyclonal) anti-HNF4α , Santa Cruz Biotechnology , Cat. #: sc-8987 RRID: AB_2116913 , PMID: 29937200 IB (1:000).

Techniques: Blocking Assay, Plasmid Preparation, Expressing, Enzyme-linked Immunosorbent Assay, Reporter Assay, Mutagenesis, cDNA Synthesis, Extraction, Glucose Oxidase Assay, Recombinant, Construct, Control, Knockdown, Generated, Sequencing, Cell Culture, In Vivo, Protease Inhibitor, SYBR Green Assay, Membrane, Transfection

Journal: Experimental and Therapeutic Medicine

Article Title: Functional inhibition of Oct leads to HNF4α upregulation

doi: 10.3892/etm.2021.9780

Figure Lengend Snippet: Gene expression analysis. (A) Hnf4α network in Oct3 -/- (n=3) mice. Network shapes: Double circle, complex/group; diamond, enzyme; square, growth factor; box, ion channel; triangle, kinase; circle, other; green, upregulated genes; red, downregulated genes; line, direct interaction; dashed line, indirect interaction; arrow, causation. (B) Hnf4α dependent genes in Oct3 -/- (n=3) mice. The majority of Hnf4α dependent genes in Oct3 -/- mice is upregulated. (C) Activation status (z-score) of the three top upstream regulators in Oct3 -/- mice (n=3); while myc and kras are significantly upregulated, tp53 is significantly downregulated in Oct3 -/- compared to WT mice. Results were normalized to WT results. **** P<0.0001 vs. WT mice. Hnf4α, hepatocyte nuclear factor 4α; Oct3 -/- , Oct3-knockout (FVB.Slc22a3tm10pb); N.s., not significant.

Article Snippet: Primary murine hepatocytes were incubated with rabbit-polyclonal-anti Hnf4α (Bioss Antibodies Inc.) as the primary antibody after preincubation with hydrogen peroxide for blocking of endogenous peroxidase.

Techniques: Expressing, Activation Assay, Knock-Out

Journal: Experimental and Therapeutic Medicine

Article Title: Functional inhibition of Oct leads to HNF4α upregulation

doi: 10.3892/etm.2021.9780

Figure Lengend Snippet: Hnf4α downregulation in cholestasis and fibrosis. (A) Hnf4α mRNA expression in 4 weeks old untreated Oct3 -/- (n=5) and WT mice (n=5); no significant difference was detected. (B) Hnf4α mRNA expression in Oct3 -/- (n=6) and WT mice (n=6) 7 days after BDL; Hnf4α mRNA expression was significantly downregulated in Oct3 -/- mice. Sham operation served as control. Values are expressed as fold expression relative to the control. (C) Hnf4α mRNA expression in Oct3 -/- (n=7) and WT mice (n=9) after 6 weeks of CCl 4 treatment: Hnf4α mRNA expression was significantly downregulated in Oct3 -/- mice. Oral gavage of mineral oil served as the control. Values are expressed as fold expression relative to the control. (D) Results of Hnf4α mRNA expression after induction of fibrosis with TAA for 6 weeks and after reversal for one and four weeks in C57BL/6 mice (n=5). Placebo intraperitoneal injection and oral gavage of mineral oil served as the control. (E) Results of Hnf4α mRNA expression after induction of fibrosis with CCl 4 for 6 weeks and after reversal for one and four weeks in C57BL/6 mice (n=5). Placebo intraperitoneal injection and oral gavage of mineral oil served as the control. (F) Correlation of Hnf4α and Oct1 mRNA expression after induction of fibrosis with TAA and CCl 4 for 6 weeks and after reversal for one and four weeks in C57BL/6 mice (n=5). * P<0.05, ** P<0.01; *** P<0.001; **** P<0.00001 vs. Control. Hnf4α, hepatocyte nuclear factor 4α; Oct3 -/- , Oct3-knockout (FVB.Slc22a3tm10pb); WT, wild type; TAA, thioacetamide; CCl 4 , carbon tetrachloride; BDL, bile duct ligation; n.s., not significant; w, weeks; rev, reversal.

Article Snippet: Primary murine hepatocytes were incubated with rabbit-polyclonal-anti Hnf4α (Bioss Antibodies Inc.) as the primary antibody after preincubation with hydrogen peroxide for blocking of endogenous peroxidase.

Techniques: Expressing, Injection, Knock-Out, Ligation

Journal: Experimental and Therapeutic Medicine

Article Title: Functional inhibition of Oct leads to HNF4α upregulation

doi: 10.3892/etm.2021.9780

Figure Lengend Snippet: Oct inhibition leads to Hnf4α upregulation. (A) Hnf4α mRNA expression in stably OCT1 (pcDNAOCT1)- and OCT3 (pcDNAOCT3)-transfected HepG2 (n=4) and HuH7 (n=4) cells after 48 h of treatment with 250 µM of the non-selective OCT inhibitor quinine: OCT inhibition leads to Hnf4α mRNA upregulation. Values are expressed as fold expression relative to empty vector in transfected tumour cell lines. Control groups were HepG2 and HuH7 cells transfected with the empty vector. (B) Hnf4α mRNA expression in primary murine hepatocytes (Oct3 -/- ): n=4, WT: n=6) after 48 h of treatment with 250 µM of the non-selective OCT inhibitor quinine: OCT inhibition leads to Hnf4α mRNA upregulation. Untreated primary murine hepatocytes served as control. (C) Representative western blots including densitometry and immunofluorescence (magnification, x10) in primary murine hepatocytes of two Oct3 -/- and WT mice after 48 h treatment with escalating quinine doses (0, 50, 100 and 150 µM). * P<0.05; ** P<0.01; **** P<0.0001 vs. 0 µM quinine. n.s., not significant; Hnf4α, hepatocyte nuclear factor 4α; Oct3 -/- , Oct3-knockout (FVB.Slc22a3tm10pb), WT, wild-type.

Article Snippet: Primary murine hepatocytes were incubated with rabbit-polyclonal-anti Hnf4α (Bioss Antibodies Inc.) as the primary antibody after preincubation with hydrogen peroxide for blocking of endogenous peroxidase.

Techniques: Inhibition, Expressing, Stable Transfection, Transfection, Plasmid Preparation, Western Blot, Immunofluorescence, Knock-Out