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Study shows that the lipogenic pathway is a key mediator of oncogenic BRAF and that its constitutive activation, which is mediated by SREBP-1, contributes to melanoma therapy resistance.
results reveal that nBP1a/PKM2 interaction activates lipid metabolism genes in cancer cells and that Thr-59 phosphorylation of SREBP-1a plays an important role in cancer cell proliferation.
GTEE also downregulated the expression of AR and prostate-specific antigen (PSA) in both androgen-responsive and castration-resistant PCa cells. By blocking the SREBP-1/AR axis, GTEE suppressed cell growth and progressive behaviors, as well as activating the caspase-dependent apoptotic pathway in PCa cells
SREBP1 trans-activates CYP24A1 expression through SREBP binding elements present in the promoter.
Berberine (BBR), an effective suppressor of SREBP1 and lipogenesis regulated through reactive oxygen species (ROS)/AMPK pathway, selectively inhibited the growth of G-R nonsmall cell lung cancer cells and rheumatoid arthritis patiens but not that of normal cells
These findings suggest that SREBP-1c serves as a molecular bridge between lipid metabolism and cell cycle control inclear cell renal cell carcinoma tumorigenesis.
findings showed that PTEN inhibits HBV replication as well as HBV HCV co-replication. SREBP-1 is involved in HBV HCV replication inhibition by PTEN
FTO increased the lipid accumulation in hepatocytes by increasing nuclear translocation of SREBP1c and SREBP1c maturation, thus improving the transcriptional activity of lipid droplet-associated protein CIDEC.
common SNPs (rs62064119, rs2297508, rs11868035 and rs13306741) in the SREBP-1c gene were selected and genotyped in 593 Han patients with NAFLD and 593 healthy controls. No significant differences in genotype and allele frequencies of these four SNPs were found between cases and controls, suggesting that the SNPs are not associated with risk of NAFLD in the Chinese Han population.
Data suggests that expression of CYP4F2 is down-regulated in liver of mice with non-alcoholic fatty liver disease after high-fat/Western diet and in human hepatocyte cell line exposed to excess palmitic acid, oleic acid, or fructose. Two other genes are down-regulated, PPAR gamma and SREBP-1. (CYP4F2 = cytochrome P450 family 4 subfamily F member 2; PPAR = peroxisome proliferator-activated receptor )
LncARSR promotes hepatic lipogenesis via Akt/SREBP-1c pathway and contributes to the pathogenesis of nonalcoholic steatohepatitis.
CpG sites located in SREBF2 gene showed differential methylation in association with lipid traits. The expression of SREBF1 gene was inversely associated with methylation of its corresponding CpGs. Genetic variants in SREBF1 were also associated with lipid profile. SREBF1 expression was directly associated with HDL cholesterol.
Epidermal growth factor receptor (EGFR) signaling enhances miR-29 expression in glioblastoma cells via upregulation of Sterol regulatory element binding protein
Intracranial GBM xenografts were used to determine the effects of genetically silencing SOAT1 and SREBP-1 on tumor growth.
Our finding reveals a crucial roles for SREBP1 in lipid desaturation of ccRCC through regulation of NF-kappaB signaling, which provides not only new insights in regulatory mode of NF-kappaB signaling but also a novel target for potential metabolic therapies.
Our results suggest that relatively common genetic variants in stearoyl CoA desaturase 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 to increase SBP-1/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 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 inhibited expression of SREBP-1c and fatty acid synthase (FAS) and then repressed oleic acid-induced hepatic cell triglyceride (TG) and lipid droplet (LD) accumulation.
Adenosine 2A receptor (AZAR) can directly suppress hepatocyte fat deposition, which is attributable to the effects of A2AR on repressing SREBP1c expression under fasted states and on suppressing SREBP1c transcription activity.
Study using conditional Brg1 knockout mice showed that Brg1 interacted with and was recruited by SREBP1c to the promoters of SREBP target genes and optimized the chromatin structure to facilitate SREBP1c binding. Therefore, a previously unrecognized role for Brg1 in hepatic lipid metabolism by portraying Brg1 as an essential epigenetic co-factor for SREBP1c was identified.
our findings suggest that Cidea is highly associated with alcoholic fatty liver disease and Cidea expression is specifically induced by acetaldehyde, and this up-regulation is most likely mediated by SREBP1c.
disruption of SREBP-1a phosphorylation resulted in massive alteration of cellular processes, including signs for loss of targeting lipid pathways.
Depletion of SREBP-1 had no impact on liver IRS1Y612, AktS473, and downstream effectors GSK3alphaS21 and FoxO1S256 during the fed state. Reduced levels of these molecules were observed under fasting conditions. The contribution of SREBP-1 to maintain insulin signal transduction in liver is modest.
Data (including data from studies in transgenic/knockout mice) suggest that Kdm1a-mediated attenuation of Srebf1 transcriptional activities functions as underlying mechanism for suppression of de novo lipogenesis by oxidative stress in white adipose tissue. [Kdm1a = lysine (K)-specific demethylase-1A; Srebf1 = sterol-regulatory element-binding transcription factor-1]
Tlr4-mutant mice are resistant to acute alcohol-induced hepatic SREBP-1 activation and hepatic lipid accumulation.
Results showed that Glrx(-/-) mice exhibited decreased SirT1 activity that leads to hyperacetylation and activation of SREBP-1 and upregulation of key hepatic enzymes involved in lipid synthesis.
Inhibition of NAMPT aggravates high fat diet-induced hepatic steatosis in mice through regulating Sirt1/AMPKalpha/SREBP1 signaling pathway.
SREBP1 is dramatically reduced in dysbindin-1 knockout mice; possibly related to cognitive deficits.
Epidermal growth factor receptor (EGFR) signaling enhances miR-29 expression in glioblastoma cells via upregulation of Sterol regulatory element binding protein 1
The expression of hHL promoted hepatic triglyceride accumulation and de novo lipogenesis without affecting triglyceride secretion, and this was associated with an upregulation of Srebf1 as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL-mediated FFA influx into the WAT without affecting glucose tolerance
Data show that miR-200b and miR-200c could directly bind the 3' UTR of JUN, and JUN activated the transcription of srebp1 to increase lipid accumulation.
a novel role for SREBP-1 as a cell surface retention factor for TbetaRI 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 in the insulin-mediated induction of SREBP-1c mRNA expression in rodent liver. Coupled with previous data showing that this induction requires LXRalpha, our data reported herein indicate a requirement for both transcription factors.
The deletion of Srebf-2 and subsequent lower sterol synthesis in hepatocytes eliminated the production of an endogenous sterol ligand required for LXR activity and SREBP-1c expression.
The fasting-induced transcription factor KLF15, a key regulator of gluconeogenesis, forms a complex with LXR/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 recruitment to the Srebp-1c promoter in livers of BPA-exposed mice was observed.
In vivo, the data of established transgenic animals showed that mice with lncHR1 expression had less hepatic expression of SREBP-1c, FAS, Acetyl-CoA carboxylase alpha (ACCalpha), and less hepatic and plasma TG after being fed a high-fat diet.
Polymorphisms of the ACACA and SREBF1 genes are promising markers for pig carcass and performance traits.
Results of associated analysis show that the polymorphism of ADD1 gene was associated traits of Intramuscular fat content (IMF) and back fat thickness (BF).
SREBF1 might play an important role in regulation of muscle fat deposition during postnatal growth of pigs.
Expression of SCD1 was downregulated through reduced transcription and abundance of the transcription factor sterol regulatory element-binding protein 1 (SREBP1c).This effect was augmented by local chromatin tightening and DNA methylation at and around the SREBP1c binding site in the SCD1 promoter
SREBP1a activated while C/EBP factors downregulated the activity of the SCD1 promoter.
These results suggest that increased expression of hepatic CD36 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 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 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 that can be used to change milk fat composition by marker-assisted breeding.
role in integrated regulation of lipid synthesis in mammary epithelial cells through regulation of key enzymes
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.
role in transcriptional regulation of lipid synthesis in a mammary epithelial cell line
An association was found between five single sequence variants and 38 possible SREBP-1c combined genotypes with growth traits in cattle.
These results suggest that the indel mutation of bovine ADD1/SREBP1c gene may influence the growth traits in cattle.[SREBP1c]
SREBP-1 polymorphism was not associated with milk FA composition
Study provides strong support for a central role of sterol response element binding protein 1(SREBP1) and S14 in the regulation of milk fat synthesis.
Genotyping of bovine SREBP-1 is considered to reflect a genetic variation which is associated with physiologic characteristics of fat tissue in Japanese black cattle.
the ability of Pu-erh tea in promoting inhibition of food uptake and the biosynthesis of fat via SBP-1 and SCD, thereby reducing fat storage.
SBP-1/SREBP-1 is part of a conserved feedback loop responding to phosphatidylcholine levels to regulate expression of one-carbon cycle biogenesis genes and ensure adequate S-adenosylmethionine levels for phosphatidylcholine production.
elo-5 and elo-6 may be transcriptional targets of LPD-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