SREBF1

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SREBF1

A gene on chromosome 17p11.2 that encodes a basic helix-loop-helix-leucine zipper (bHLH-Zip) transcription factor, which binds to the sterol regulatory element-1 (SRE1), a decamer flanking the low-density lipoprotein receptor gene and genes involved in sterol biosynthesis. The protein is synthesised as a precursor attached to the nuclear membrane and endoplasmic reticulum; once cleaved, the mature protein translocates to the nucleus and activates transcription by binding to the SRE1. Sterols inhibit precursor cleavage; the mature nuclear form is rapidly catabolised, reducing transcription.
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Altered hepatic expression of SREBP-1 and PPAR gamma is associated with liver injury in insulin-resistant lipodystrophic HIV-infected patients.
Polyunsaturated fatty acids ameliorate hepatic steatosis in obese mice SREBP-1 suppression.
SREBP-1 is found naturally in cells throughout the body and is involved with cholesterol and other fat production.
lthough the scientists implicated a gene known as SREBP-1, a master regulator of lipids' manufacture in the liver, not much was known about the underlying molecular connections between fructose and those metabolic disorders.
Broadly speaking, activation of PPARs enhances conversion of lipids into energy, whereas activation of SREBP-1 induces an opposing effect.
This includes normalization of the levels of NOX4, p67phox, TGF-[beta], CTGF, osteopontin, vimentin, desmin, SREBP-1, iNOS, synaptopodin, connexin 43, erythropoietin, p300, and extracellular matrix proteins [227, 233, 234].
Association analyses of DNA polymorphisms in bovine SREBP-1 LXRa FADS1 genes with fatty acid composition in Canadian commercial crossbred beef steers.
Rutin has been shown to increase phosphorylation of AMPK and reduce SREBP-1 expression thereby inhibiting hepatic lipogenesis (Wu et al.
Furthermore, CPP and 5-CQA decreased the nuclear active form of SREBP-1, acetyl-CoA carboxylase activity, and cellular malonyl-CoA levels.
The expression and activities of the genes involved in fatty acids metabolism, such as FAS, ACC, and ME, are closely related to the metabolism of fatty acids (Fang and Hillgartner, 1998), and their transcription has a common control element, which is directly affected by SREBP-1 (Richards et al.
A recent study has demonstrated that Sch B dose-dependently suppresses free fatty acid-induced steatosis in cultured L02 hepatocytes, in part via the inhibition of adipose differentiation-related protein (ADRP) and SREBP-1 [75].