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SREBPSterol Regulatory Element Binding Protein
SREBPSterol Response Element Binding Protein
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This regulation was supported by the expression of downstream genes controlled by FXR, including SHP-1 as the nuclear receptor induced by FXR and involved in bile acid biosynthesis (19), SREBP-1, which is associated with lipid metabolism and negatively regulated by FXR (20), PPARa, which controls SREBP activity and lipid synthesis (21), CYP7A1, which acts as another important regulator of bile acid metabolism inhibited by both FXR and SHP (19,22), and also PEPCK, which regulates the rate-limiting step of hepatic gluconeogenesis and is activated by FXR (23).
When the cholesterol or lanosterol level is high in the cell, the SSDs of HMG-CoA reductase and SREBP cleavage activating protein (SCAP) sense the sterol and cause those proteins to bind to Insig in the ER membrane [106].
An increase of ER cholesterol above ~5 mol% results in the appearance of PFO-accessible cholesterol and in the disappearance of SREBP-2 in the nucleus controlled by SREBP cleavage-activating protein (SCAP).
Adipogenesis is a well-orchestrated process, in which preadipocyte proliferation, differentiation, and lipid biosynthesis are regulated by a set of factors that include signal transducer and activator of transcription 5A (STAT5A), sterol-regulatory-element-binding protein 1c (SREBP 1c), and peroxisome proliferator-activated receptor gamma (PPAR[gamma]).
Moreover, PI3K/Akt/ mTORC1 signaling conversely exerts crucial effects on the maintaining integrity of lipid rafts by modulating SREBP activation and subsequent cholesterogenesis [6].
oil red O staining; PBS, phosphate buffered saline; PPAR[gamma], peroxisome proliferator-activated receptor [gamma]; PTP1B, protein-tyrosine phosphatase; RIPA buffer, radioimmunoprecipitation assay buffer; SDS, sodium dodecyl sulphate; SREBP, sterol regulatory element-binding protein: TAG, triglycerides.
It is an oral small molecule that modulates the SREBP pathway.
[3] Nonstandard abbreviations: PCSK, proprotein convertase subtilisin/kexin proprotein; FH, familial hypercholesterolemia; LDL-R, LDL receptor; FH, familial hypercholesterolemia; ER, endoplasmic reticulum; EGF, epidermal growth factor; LDL-C, LDL cholesterol; SREBP, sterol responsive element binding protein; HMG CoA R, hydroxymethylglutaryl coenzyme A reductase; TGN, trans Golgi network; SRE, sterol regulatory element; GWAS, genome-wide association studies; TG, transgenic; KO, knockout; APP, amyloid precursor protein; BACE1, [beta]-site APP-cleaving enzyme 1; HCV, hepatitis C virus; mAb, monoclonal antibody.
To safely make the trip to the Golgi, says Espenshade, cells give each SREBP a chauffeur - the protein SCAP - which binds to SREBP before they both make their way to the Golgi.
The mTORC2 substrate GSK3 (glycogen synthase kinase 3) connects AKT to lipid synthesis since GSK phosphorylates lipogenic transcription factor SREBP (sterol responsive element binding protein) and targets it for protein degradation which is opposed by AKT mediated phosphorylation and inactivation of GSK.
Consistent with these data, it has been previously shown in Ob/Ob mice that increased rates of hepatic fatty acid synthesis are associated with increased nuclear SREBP-1c protein and mRNA levels for known SREBP target genes involved in fatty acid biosynthesis [26].
Primer Sequences (5; to 3;) Size (bp) SREBP-1c GCT ACC GTT CCT CTA TCA ATG ACA A 81 CAG ATT TAT TCA GCT TTG CCT CAG T SCD-1 TTC TTG AGA TAC ACT CTG GTG CTC A 97 GAG ATT GAA TGT TCT TGT CGT AGG G chREBP CAG TAT GTG GCT TCG TAA CTC CTC T 89 CCA GTA ATT ACC CTC CAA GAC AAC A FAS TCC ACA GCT CTT ACA GTG AGA ATC A 99 CTT CTC CAG GGT GGG GAC CAG ACC AGA GTG AGT GCT CTC AAT TCT GTC C 97 GTC CTT CTT CTT TCC CGA TAA TGT C GAPDH CCT TCT CTT GTG ACA AAG TGG ACA T 96 CGT GGG TAG AGT CAT ACT GGA ACA T SREBP: sterol regulatory element-binding protein; SCD: stearoyl-CoA; chREBP: carbohydrate response element-binding protein; FAS: fatty acid synthase; ACC: acetyl-CoA carboxylase; GAPDH: glyceraldehyde-3- phosphate dehydrogenase.