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Study demonstrated that the type II keratin topological associating domain undergoes epigenetic reprogramming in aromatase inhibitors-resistant ER-alpha positive breast cancer cells, leading to KRT80 upregulation. KRT80 expression is driven by de novo enhancer activation by SREBP1. KRT80 levels correlate with stiffer tumors and associates with poor survival in ER-alpha positive breast cancer patients.
Silencing GK5 in PC9R cells induced mitochondrial damage, caspase activation, cell cycle arrest, and apoptosis via SREBP1/SCD1 signaling pathway.
SREBF1 DNA methylation was associated with body mass index and low-density lipoprotein cholesterol at mid-gestation.
LINC01138 interacts with PRMT5 to increase arginine methylation and protein stability of SREBP1, promoting lipid desaturation and cell proliferation in Clear cell renal cell carcinoma.
High SREBP1 expression is associated with gastric adenocarcinoma.
Insulin suppression of gluconeogenic enzyme expression is facilitated by coordinated inactivation of FoxO1 and PGC-1alpha by WD40/ProF-associated Akt; but this coordination also increases vulnerability to aPKC hyperactivity, which is abetted by SREBP-1c-induced increases in PGC-1alpha and PKC-iota.
Data indicate a general mechanism centered on Lipin-1 and sterol regulatory element-binding protein (SREBP) that links the physical cell microenvironment to a key metabolic pathway.
These results unveil an unpredicted and evolutionary conserved role of SREBP1 in rewiring cell metabolism in response to mechanical cues.
TD26 is a positive regulator on SREBP1 transactivity, and the interaction between TD26 and SREBP1 can serve as a potential therapeutic target for hepatocellular carcinoma treatment.
beta-Conglycinin and fish oil are effective at preventing alcoholic fatty liver because beta-conglycinin decreases the function of SREBP-1c and PPARgamma2, and fish oil decreases the function of SREBP-1c and increases that of PPARalpha
Our results suggested that rs11868035 is likely to be associated with amyotrophic lateral sclerosis in early-onset or female patients but not with Parkinson's disease or Parkinson's disease in the Chinese population.
TGF-beta1 can downregulate the mRNA expression of SOCS-3 and upregulate the mRNA expression of SREBP-1c.
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.
CRTC2 modulates hepatic SREBP1c cleavage by controlling Insig2a expression during fasting
It findings demonstrate that BAP31-deletion induces SREBP activation and promotes hepatic lipid accumulation, reduces insulin signaling, impairs glucose/insulin tolerance, and increases ER stress and hepatic inflammation, explaining the protective roles of BAP31 in the development of liver steatosis and insulin resistance in HFD-induced obesity in animal models.
These results suggest that PPARalpha is a trans-acting factor that enhances Insig2a gene expression, thereby suppressing SREBP-1c processing during fasting.
stimulates mitochondrial permeability transition pore excessive opening, causing endoplasmic reticulum stress through p38 mitogen-activated protein kinase activation, resulting in enhanced sterol regulatory element-binding protein-1c transcription and hepatic steatosis
TLR4-dependent stimulation of macrophage phagocytosis requires mTORC1-directed SREBP-1a-dependent lipid synthesis.
BHLHE40 is required for insulin induction of SREBP-1c mRNA in rodent liver.
The "fat steal"-like lipodystrophy phenotype of the Tg-1a;ob/ob model demonstrates that hepatic SREBP-1a activation has a strong impact on the partition of TG accumulation, resulting in adipose-tissue remodeling by inflammation and fibrosis and insulin resistance.
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.
LncARSR promotes hepatic lipogenesis via Akt/SREBP-1c pathway and contributes to the pathogenesis of nonalcoholic steatohepatitis.
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
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.
U2AF65 functions as a positive regulator of milk synthesis in and proliferation of bovine mammary epithelial cells via the mTOR-SREBP-1c signalling pathway.
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