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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.
miR-33a and miR-33b are found in the introns of SREBF2 and SREBF1 transcription factors, respectively, and work in concert with their host genes to regulate cholesterol and fatty acid synthesis.
microRNA-33a and b (miR-33a/b), which differ by only two nucleotides, are intronic microRNAs located within the sterol response element binding protein genes SREBF2 and SREBF1, respectively, which code for transcription factors that regulate cholesterol homeostasis and fatty acid metabolism.
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