SREBF2

SREBF2

A gene on chromosome 22q13 that encodes a ubiquitously expressed transcription factor with a basic helix-loop-helix-leucine zipper (bHLH-Zip) domain, which controls cholesterol homeostasis by stimulating transcription of sterol-regulated genes. The cognate gene product is required for lipid homeostasis: it regulates transcription of the LDL receptor gene, cholesterol and the fatty acid synthesis pathway.
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G also enhanced the mRNAs encoding the LDL and VLDL receptors and reduced ACACA mRNA, without altering the transcription of the mRNA encoding the SREBF2.
2014): namely, HMGCR, -acetyl-CoA carboxylase (ACACA, catalyzing the rate-limiting step in fatty-acid biosynthesis), SREBF2, the low-density-lipoprotein (LDL) receptor, (mediating LDL-cholesterol internalization into the cell), and the very-low-density-lipoprotein (VLDL) receptor--it apparently playing an essential role in the uptake and degradation of fatty acids and TG-rich particles (Crawford et al.
05--indicated that ACSL1, ABCA1, DHCR24, ACAT2, ACACA, ABCG1, ACAD9, ACACB, IDI1, PPARG, SCD, SCARB1, HMGCS1, EBP, DHCR7, FASN, HMGCR, and GPAM were down-regulated upon G treatment; whereas NR1H2, PPARA, INSIG2, CPTP1, APOE, VLDLR, ABCC2, and SREBF2 were activated after exposure to G (Fig.
Regarding the regulation of HMGCR messenger levels, despite the indication by in-silico analysis that SREBF2 mRNA-which transcript modulates the expression of the HMGCR structural gene-was overexpressed in cultured G-treated cells, our work demonstrated that those regulatory-mRNA levels did not vary in the livers of mice treated with geraniol (Fig.
In order to gain a more complete understanding of the role of SREBF2 transcription in the modulation of cholesterol levels under these experimental conditions, we also evaluated the effect of G on LDL-receptor mRNA--its gene constituting another target of the mature SREBF2 (Sato 2009)-since one of the mechanisms that participates in cellular-cholesterol homeostasis is the uptake of cholesterol from the serum mainly through the internalization of LDL-cholesterol via the LDL receptor (Chang et al.
Accordingly, on the basis of the in-silico analyses presented here, we hypothesized that G induced a fundamental change in the expression of several key genes involved in lipid metabolism resulting in a significant decrease in lipogenic-gene expression, particularly those related to the synthesis of cholesterol, fatty acids, and the saponifiable lipids; all of those gene products being targets for SREBF2 and SREBFlc.
Abbreviations: ACACA, acetyl-CoA carboxylase; G, geraniol; HMG-CoA, 3-hydroxy-3-methylglutarylcoenzyme-A; HMGCR, 3-hydroxy-3-methylglutarylcoenzyme-A reductase; LDL, low-density-lipoprotein; LDLR, low-density-lipoprotein receptor; MP, mevalonate pathway; RT-PCR, reverse-transcriptase-polymerase-chain reaction; SREBF2, sterol-regulatory-element-binding transcription factor; TG, triglyceride; VLDL, very-low-density-lipoprotein; VLDLR, very-low-density-lipoprotein receptor.
The researchers uncovered three novel signals, from the genes TOMM40-APOE-APOC1, SREBF2 and NTRK2) that were significantly associated with BMI in adults.
The SREBF2 gene is in the same family as SREBF1, linked to type 2 diabetes in another CardioChip study.