نتایج جستجو برای: sterol regulatory element‑binding transcription factor 1
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background: metabolic syndrome (mets) is a prevalent disorder in pediatric age groups, described by a combination of genetic and environmental factors. sterol regulatory element‑binding transcription factor 1 (srebf‑1) induces the expression of a family of genes involved in fatty acid synthesis. moreover, dysregulation of mir‑33b, which is located within the intron 17 of the srebf‑1 gene, disru...
Dietary PUFAs (polyunsaturated fatty acids) co-ordinately suppress transcription of a group of hepatic genes encoding glycolytic and lipogenic enzymes. Suppression of Fasn (fatty acid synthase) transcription involves two PUFA-responsive regions, but the majority of PUFA sensitivity maps to a region within the proximal promoter containing binding sites for NF-Y (nuclear factor-Y), Sp1 (stimulato...
Insulin-induced gene 2 (INSIG2) and its homolog INSIG1 encode closely related endoplasmic reticulumproteins that regulate the proteolytic activation of sterol regulatory elementbinding proteins, transcription factors that activate the synthesis of cholesterol and fatty acids in animal cells. Several studies have been carried out to identify INSIG2 genetic variants associated with metabolic dise...
Sterol-regulatory-element-binding protein 1c (SREBP-1c) is one member of the family of transcription factors that stimulate sterol and fatty-acid biosynthesis in animal cells. Human SREBP-1c, mapped to chromosome 17p11.2, is expressed in liver, intestine, skeletal muscle and adipocytes. A section of genomic sequence from a chromosome 17 library, thought to contain the SREBP-1c promoter, was clo...
There is a genetic susceptibility for nonalcoholic fatty liver disease (NAFLD). To examine the role of genetic factors in the disease, a Bayesian analysis was performed to model gene relationships in NAFLD pathogenesis. The Bayesian analysis indicated a potential gene interaction between the TM6SF2 and PNPLA3 genes. Next, to explore the underlying mechanism at the cellular level, we evaluated t...
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