mouse monoclonal antibody against hif 1a (Novus Biologicals)
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Novus Biologicals
mouse monoclonal antibody against hif 1a
Mouse Monoclonal Antibody Against Hif 1a, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 96/100, based on 812 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+monoclonal+antibody+against+hif+1a/pm35847503-80-11-16?v=Novus+Biologicals
Average 96 stars, based on 812 article reviews
Mouse Monoclonal Antibody Against Hif 1a, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 96/100, based on 812 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+monoclonal+antibody+against+hif+1a/pm35847503-80-11-16?v=Novus+Biologicals
Average 96 stars, based on 812 article reviews
mouse monoclonal antibody against hif 1a - by Bioz Stars,
2026-08
96/100 stars
Images
1) Product Images from "Disruption of adipocyte HIF-1 α improves atherosclerosis through the inhibition of ceramide generation."
Article Title: Disruption of adipocyte HIF-1 α improves atherosclerosis through the inhibition of ceramide generation.
Journal: Acta pharmaceutica Sinica. B
doi: 10.1016/j.apsb.2021.10.001
Figure Legend Snippet: Figure 1 HIF-1a deficiency in adipocytes alleviates WD-induced atherosclerosis. Eight-week-old Hif1afl/flApoEe/e and Hif1aDAdipo ApoEe/e
Techniques Used:
Figure Legend Snippet: Figure 2 Adipocyte-specific HIF-1a ablation decreases ceramide generation. Eight-week-old Hif1afl/flApoEe/e and Hif1aDAdipo ApoEe/e mice were fed a WD for 8 weeks. (A) PLS-DA analysis of lipid metabolites in eWAT between the Hif1afl/flApoEe/e (green circle) and Hif1aDAdipo
Techniques Used:
Figure Legend Snippet: Figure 3 The ceramide-generation-related gene Smpd3 is a novel target gene of adipocyte HIF-1a. (A) The mRNA levels of genes related to ceramide metabolism, including synthesis, transportation and elimination in the eWAT of the AdHif1aLSL/LSL and Hif1aþ/þ mice (n Z 6 per group). Two-tailed Student’s t-test: **P < 0.01 compared to the Hif1aþ/þ mice. (B) The protein levels of HIF-1a and SMPD3 in the eWAT of the AdHif1aLSL/LSL and Hif1aþ/þ mice (n Z 3 per group). (C) The mRNA levels of genes related to ceramide metabolism, including synthesis, transportation and elimination in the eWAT of the Hif1afl/flApoEe/e and Hif1aDAdipo ApoEe/e mice fed a WD for 8 weeks (n Z 6 per group). Two-tailed Student’s t-test: **P < 0.01 compared to the Hif1afl/flApoEe/e mice. (D) The protein levels of HIF-1a and SMPD3 in the eWAT of the Hif1afl/flApoEe/e and Hif1aDAdipo ApoEe/e mice mice fed a WD for 8 weeks (n Z 3 per group). (E) Schematic diagram of the mouse Smpd3 promoter illustrating the predicted HRE in the regulatory region. The upstream regions are numbered in relation to the transcription initiation site, which is designated þ1. (F) ChIP assays of 3T3-L1 adipocytes treated with CoCl2 (200 mmol/L) for 12 h (n Z 4 per group). One-way ANOVA with Tukey’s post hoc test: **P < 0.01 compared to the IgG-Ab group. (G) Luciferase reporter gene assay of Smpd3 promoter activity (n Z 4 per group). One-way ANOVA with Dunnett’s T3 post hoc test: **P < 0.01 compared to the Smpd3 promoter plasmid with vector group; ##P < 0.01 compared to the Smpd3 promoter plasmid with HIF-1a TM group.
Techniques Used: Two Tailed Test, Luciferase, Reporter Gene Assay, Activity Assay, Plasmid Preparation
Figure Legend Snippet: Figure 6 Administration of ceramide reverses the protective effects of adipose HIF-1a deficiency on atherosclerosis through increased inflammation and cholesterol. Eight-week-old Hif1afl/flApoEe/e and Hif1aDAdipo ApoEe/e mice were injected with ceramide C16:0 or vehicle and were fed a WD for 6 weeks. (A) Schematic diagram of the mouse model illustrating the concept of mouse injection with ceramide C16:0 or vehicle. (B, C) Quantitation of ceramide concentrations in plasma (B) and eWAT (C), n Z 6 per group. (D, E) The levels of plasma total cholesterol (D) and triglyceride (E), n Z 6e7 per group. (F) FPLC analysis of plasma cholesterol levels in mice. (G) Left, representative oil red O staining of cross- sections of aortic roots. Scale bar, 500 mm. Right, quantification of aortic root lesion areas. n Z 6e7 per group. (H) Immunofluorescence stain- ing of atherosclerotic lesions with MAC-2 antibody and calculated MAC-2 positive areas in the plaques (n Z 3 per group). Scale bar, 500 mm. All data are presented as the mean SEM. One-way ANOVA with Tukey’s post hoc test (B, D, E, H) and KruskaleWallis test (C and G): *P < 0.05, **P < 0.01 compared to the Hif1afl/flApoEe/e þ vehicle group; #P < 0.05, ##P < 0.01 compared to the Hif1aDAdipo ApoEe/e
Techniques Used: Injection, Quantitation Assay, Clinical Proteomics, Staining
Figure Legend Snippet: Figure 7 Inhibition of HIF-1a by PX-478 improves atherosclerosis through the SMPD3eceramide axis. Eight-week-old ApoEe/e mice were administered with PX-478 (5 mg/kg) or vehicle every other day and fed a WD for 8 weeks. (A) Schematic diagram of the mouse model illustrating the concept of mouse injection with PX-478. (B) Left, representative oil red O staining of cross-sections of aortic roots. Scale bar, 500 mm. Right, quantification of aortic root lesion areas. n Z 7 per group. (C, D) Quantitation of ceramide concentrations in plasma (C) and eWAT (D), n Z 6 per group. (E, F) The levels of plasma total cholesterol (E) and triglyceride (F), n Z 7 per group. (G) FPLC analysis of plasma cholesterol levels in mice. (H) Immunofluorescence staining of atherosclerotic lesions with MAC-2 antibody and calculated MAC-2 positive areas in the plaques (n Z 3 per group). Scale bar, 500 mm. All data are presented as the mean SEM. ManneWhitney U test (B, D), Two-tailed Student’s t-test (C, E, F, H): *P < 0.05, **P < 0.01 compared to the vehicle group. See also Fig. S5.
Techniques Used: Inhibition, Injection, Staining, Quantitation Assay, Clinical Proteomics, Two Tailed Test