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Our results suggest that relatively common genetic variants in stearoyl CoA desaturase (show SCD ELISA Kits) and SREBF1 attenuated the positive associations between intake of a traditional diet rich in n-3 polyunsaturated fatty acids and increases in fasting cholesterol and HbA1c levels, as well as the waist-to-hip ratio among Yup'ik participants.
changes in distinct lipid ratios may converge on ARF1 (show ARF1 ELISA Kits) to increase SBP-1 (show MEGF8 ELISA Kits)/SREBP-1 activity.
Variants in the TOM1L2/SREBF1 locus exert opposing effects of total-body lean mass (TB-LM) and total-body less head bone mineral density (TBLH-BMD) .
Date indicate that sterol regulatory element-binding proteins Srebp1 and Srebp2 (show SREBF2 ELISA Kits) are essential for the metabolic reprogramming of NK cells and for the attainment of elevated glycolysis and oxidative phosphorylation.
Study identified a novel human specific lncRNA, lncHR1, as a negative regulator of SREBP-1c expression. Overexpression of lncHR1 inhibit (show FAS ELISA Kits)ed expression of SREBP-1c and (show ACACA ELISA Kits)fatty acid synthase (FAS) and then repressed oleic acid-induced hepatic cell triglyceride (TG) and lipid droplet (LD) accumulation.
Glucose adsorption to chitosan membranes increases proliferation of human chondrocytes via mammalian target of rapamycin (show FRAP1 ELISA Kits) complex 1 and sterol regulatory element-binding protein-1 signaling.
miR (show MLXIP ELISA Kits)-185 negatively regulates the differentiation of 3T3-L1 cells by targeting SREBP-1
The authors further demonstrated that the upregulation of sterol regulatory element-binding protein (show CNBP ELISA Kits) (SREBP)-1c by activation of the Akt (show AKT1 ELISA Kits) and p70S6K (show RPS6KB1 ELISA Kits) pathways is critical for high-glucose-treated Porphyromonas gingivalis-induced NLRP3 (show NLRP3 ELISA Kits) expression.
Results show that PPARalpha (show PPARA ELISA Kits) is downregulated and SREBP-1c is upregulated in steatosis L-02 cells. These changes increase lipid synthesis and reduce lipid disposal, which ultimately lead to hepatic steatosis.
SREBP-1 and SREBP-2 (show SREBF2 ELISA Kits) mRNA expression levels were measured in EAT from 49 patients with CAD (show CAD ELISA Kits) (26 with diabetes) and 23 controls without CAD (show CAD ELISA Kits) or diabetes.SREBP expression was associated as cardiovascular risk factor for the severity of CAD (show CAD ELISA Kits) and the poor lipid control.
a novel role for SREBP-1 as a cell surface retention factor for TbetaRI (show TGFBR1 ELISA Kits) in mesangial cells, is reported.
Srebp1c is a key regulator of metabolic remodeling leading to the beneficial effects of caloric restriction.
The present study indicates a requirement for C/EBPbeta (show CEBPB ELISA Kits) in the insulin (show INS ELISA Kits)-mediated induction of SREBP-1c mRNA expression in rodent liver. Coupled with previous data showing that this induction requires LXRalpha (show NR1H3 ELISA Kits), our data reported herein indicate a requirement for both transcription factors.
The deletion of Srebf-2 (show SREBF2 ELISA Kits) and subsequent lower sterol synthesis in hepatocytes eliminated the production of an endogenous sterol ligand required for LXR (show NR1H3 ELISA Kits) activity and SREBP-1c expression.
The fasting-induced (show C10orf10 ELISA Kits) transcription factor KLF15 (show KLF15 ELISA Kits), a key regulator of gluconeogenesis, forms a complex with LXR (show NR1H3 ELISA Kits)/RXR, specifically on the Srebf1 promoter.
Exposure to a xenobiotic during early development induced persistent fat accumulation via hypomethylation of lipogenic genes. Moreover, increased Nrf2 (show NFE2L2 ELISA Kits) recruitment to the Srebp-1c promoter in livers of BPA (show DST ELISA Kits)-exposed mice was observed.
suggesting a specific effect of sterol regulatory element binding protein (show CNBP ELISA Kits)-1c on neurosteroidogenesis
Transforming growth factor-beta activated kinase 1 (TAK1 (show MAP3K7 ELISA Kits)) regulation of sterol-regulatory element-binding proteins (SREBPs) critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) development.
SREBP1 pathway plays an important role in hepatocellular carcinoma pathogenesis.
In vivo, the data of established transgenic animals showed that mice with lncHR1 expression had less hepatic expression of SREBP-1c, FAS (show FAS ELISA Kits), Acetyl-CoA carboxylase alpha (show ACACA ELISA Kits) (ACCalpha), and less hepatic and plasma TG after being fed a high-fat diet.
dysregulation of SIRT1 (show SIRT1 ELISA Kits)-AMPK (show PRKAA1 ELISA Kits)-SREBP and stimulation of NLRP3 (show NLRP3 ELISA Kits) inflammasome may contribute to vascular lipid deposition and inflammation in atherosclerosis
Polymorphisms of the ACACA (show ACACA ELISA Kits) and SREBF1 genes are promising markers for pig carcass and performance traits.
IL-4 induced activation of Akt/SREBP-1/lipid biosynthesis in EC, resulting in protection against membrane attack complex and melittin, in association with mitochondrial protection.
Basal transcription and supra-additive stimulation of porcine LDLR (show LDLR ELISA Kits) gene transcription by LH and insulin (show INS ELISA Kits) in granulosa-luteal cells require SREBP-1a and Sp1 (show SP1 ELISA Kits)/Sp3 (show SP3 ELISA Kits)-binding elements.
Results of associated analysis show that the polymorphism of ADD1 gene was associated traits of Intramuscular fat content (IMF (show MDFI ELISA Kits)) and back fat thickness (BF).
SREBF1 might play an important role in regulation of muscle fat deposition during postnatal growth of pigs.
SREBP1a activated while C/EBP (show CEBPA ELISA Kits) factors downregulated the activity of the SCD1 (show SCD ELISA Kits) promoter.
These results suggest that increased expression of hepatic CD36 (show CD36 ELISA Kits) and SREBP-1 is relevant in the obesity-driven lipid accumulation in the liver of dairy cows during late gestation.
Hepatic SREBP-1c-mediated lipid synthesis and the NF-kappaB (show NFKB1 ELISA Kits) inflammatory pathway were both overinduced in cows with fatty liver.
SREBP1 was found to be a key positive regulator of milk fat synthesis and was shown to be regulated by stearic acid and serum.
data suggest that low SREBP-1c expression can decrease lipid synthesis, increase lipid oxidation, and decrease the TG and VLDL content in bovine hepatocytes
84-bp indel in intron 5 was significantly associated with palmitoleic acid, stearic acid, saturated fatty acids, triglycerides and the C16 index in Simmental bulls.
genetic polymorphisms in sterol regulatory element binding transcription factor 1 (SREBF1)can be used to develop genetic tools for the selection of animals producing milk with healthier fatty acid composition
The results of this study demonstrated the existence of the polymorphisms in the SCD1 (show SCD ELISA Kits) and SREBP-1 genes in the population of Fleckvieh cattle and their associations with the concentrations of several muscle fat and subscutaneous fat fatty acids.
These results provide detailed genetic information for the SREBP1 signalling pathway and SCD (show SCD ELISA Kits) that can be used to change milk fat composition by marker-assisted breeding.
The SREBP1-9 SNP showed a significant effect on marbling score, monounsaturated fatty acids and C18:1n-9 in the muscle fat of commercial Korean cattle.
the ability of Pu-erh (show ERH ELISA Kits) tea in promoting inhibition of food uptake and the biosynthesis of fat via SBP-1 and SCD (show SCD ELISA Kits), thereby reducing fat storage.
SBP-1/SREBP-1 is part of a conserved feedback loop responding to phosphatidylcholine (show SGMS1 ELISA Kits) levels to regulate expression of one-carbon cycle biogenesis genes and ensure adequate S-adenosylmethionine levels for phosphatidylcholine (show SGMS1 ELISA Kits) production.
elo-5 and elo-6 may be transcriptional targets of LPD (show ACSBG1 ELISA Kits)-1
both SBP-1 and MDT-15 control transcription of genes governing desaturation of stearic acid to oleic acid
Essential role of sbp-1 activation in oxygen deprivation induced lipid accumulation and increase in body width/length ratio in Caenorhabditis elegans.
This gene encodes a transcription factor that binds to the sterol regulatory element-1 (SRE1), which is a decamer flanking the low density lipoprotein receptor gene and some genes involved in sterol biosynthesis. The protein is synthesized as a precursor that is attached to the nuclear membrane and endoplasmic reticulum. Following cleavage, the mature protein translocates to the nucleus and activates transcription by binding to the SRE1. Sterols inhibit the cleavage of the precursor, and the mature nuclear form is rapidly catabolized, thereby reducing transcription. The protein is a member of the basic helix-loop-helix-leucine zipper (bHLH-Zip) transcription factor family. This gene is located within the Smith-Magenis syndrome region on chromosome 17. Two transcript variants encoding different isoforms have been found for this gene.
, class D basic helix-loop-helix protein 1
, sterol regulatory element-binding protein 1
, adipocyte determination- and differentiation-dependent factor 1
, sterol regulatory element binding protein 1
, adipocyte determination and differentiation-dependent factor 1
, sterol regulatory binding transcription factor 1
, sterol regulatory element-binding transcription factor 1
, sterol regulatory element binding-protein 1
, sterol regulatory element binding transcription factor 1
, sterol response element binding protein 1
, similar to sterol regulatory element binding transcription factor 1 isoform b
, sterol regulatory element binding protein-1
, sterol regulatory element-binding protein 1-like
, Sterol regulatory element Binding Protein family member (sbp-1)
, Sterol regulatory element-binding transcription factor 1