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Validated All-in-One™ qPCR Primer for SREBF1(NM_004176.4) Search again
Product ID:
HQP055405
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HMD, IFAP2, SREBP1, bHLHd1
Gene Description:
sterol regulatory element binding transcription factor 1
Target Gene Accession:
NM_004176.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- expression altered in obesity and niddm
- SREBP-1a and the CRE-bound proteins are essential for the SREBP-dependent response
- transcriptional activities to different target promoters of lipogenic and cholesterogenic genes
- expression of SREBP-1 is affected by polyunsaturated fatty acids in human cells
- a strong graded interaction between SREBF-1a -36del/G genotypes and response of plasma apoA-I to treatment with fluvastatin.
- Regulation of fatty acid synthase expression in breast cancer by sterol regulatory element binding protein-1c.
- Sphinglipids in endocytic compartments serve as a "molecular trap" for cholesterol, leading to a reduction in cholesterol at the endoplasmic reticulum, induction of sterol regulatory element-binding protein-1 cleavage, and up-regulation of LDL receptors.
- may play discrete role in the regulation of the resistin gene expression
- SREBP1a and APOB have roles in total and low-density lipoprotein cholesterol levels in patients with coronary artery disease
- SREBP-1 not necessary for hepatic Akt-mediated hypoglycemic effect. Myr-Akt-induced hypertriglyceridemia and hepatic triglyceride accumulation mediated by Akt-induced SREBP-1 expression and mechanism involving fatty acid synthesis independent of SREBP-1.
- SREBP-1 has a novel role as negative regulator of gluconeogenic genes through a cross-talk with HNF-4alpha interference with PGC-1 recruitment
- results provide evidence that insulin action on sterol regulatory element binding protein (SREBP)-1c is dysregulated in adipose tissue from type 2 diabetic subjects
- SREBP-1c and Sp1 interact to regulate transcription of the gene for phosphoenolpyruvate carboxykinase (GTP) in the liver
- SREBP-1c is involved in the effect of insulin on HKII gene transcription.
- molecular cloning of promoter; studies suggest that PDX-1 and HNF-4 both stimulate SREBP-1c gene expression
- SREBP-1c gene is a candidate for human insulin resistance and a variant might influence diabetes risk.
- High levels of SREBP-1 protein is associted with during prostate cancer progression to androgen independence
- nSREBPs are essential for high levels of lipid synthesis in the liver and indicate that Insig's modulate nSREBP levels by binding and retaining SCAP in the ER.
- This review shows how SREBP-1 might play a role in the development of cellular features belonging to lipotoxicity and, possibly, syndrome X.
- SREBP-1 has a role in the species differential regulation of cholesterol and bile acid homeostasis via a novel mechanism of up-regulation of the hSHP gene expression
- Role of the SREBF-1 gene in genetic predisposition of metabolic diseases such as obesity, type 2 diabetes, and dyslipidemia.
- APOA5 gene expression is regulated by the LXR ligand T0901317 in a negative manner through SREBP-1c.
- While the SREBP-1a and -1c isoforms differentially activate transcription, the molecular basis of this difference is unknown. Here we define the differences between these proteins that confer the enhanced activity of SREBP-1a.
- EC nuclei showed strong SREBP staining in human atherosclerotic lesions, suggesting a role for SREBP. Endothelial cholesterol depletion & SREBP activation play a role in inflammatory processes in which phospholipid oxidation products accumulate.
- Tethered SREBP-1a and -2 homodimers, similar to the monomeric forms, activated target genes more robustly than tethered SREBP-1c homodimers.
- Transfected from humans into transgenic mice, SREBP-1c and endogenous lipogenesis could be involved in beta-cell dysfunction and diabetes.
- hCG and insulin cause a switch toward expression of the SREBP-1c isoform with consequent effects on fatty acid synthesis in culturred ganulosa cells (SRESBP-1c)
- effect of SREBP-1a expression on lipid metabolism at the level of the cellular protein network and the protein pattern of mitochondria
- SREBP-1 homodimers and heterodimers localize in the nucleus and activate transcription.
- Transgenic SHR overexpressing SREBP-1a is nonobese rat model of fatty liver, disordered glucose and lipid metabolism, and hypertension. Possible model for studying pathogenesis and treatment of metabolic syndrome associated with hepatic steatosis.
- 2 years after bilio-pancreatic diversion the degree of fat mass loss seems to interfere with regulatory binding protein 1c (SREBP-1c)gene suppression to preserve an adequate amount of fat storage
- muscle cholesterol (p=0.045) and lathosterol (p=0.054) concentrations were elevated in the CC homozygotes supporting the view that endogenous cholesterol synthesis rate is SREBF-1 genotype-dependent.
- activation of SREBP-1 by Akt leads to the induction of key enzymes of the cholesterol and fatty acid biosynthesis pathways, and thus membrane lipid biosynthesis
- the SREBP-1c.BETA2.E47 complex is in a DNA looping structure which is required for efficient recruitment of CREB-binding protein/p300
- Phagocytosis triggered the proteolytic activation of SREBP-1a and SREBP-2; upon overexpression of these proteins, phagocytosis-induced transcription and lipid synthesis were blocked; SREBPs are essential regulators of membrane biogenesis
- SREBP-1ac mRNA was detectable in all tissues studied, although at lower levels than the major SREBP-1a & -1c isoforms. Transcription of SREBP-1ac mRNA was detectable in all tissues studied, although at lower levels than the major SREBP-1a & -1c isoforms.
- fibroblast growth factor 7 requires both PI3K and JNK signaling pathways to induce SREBP-1
- SREBP-1c-mediated insulin regulation of acyl-CoA synthestase 5 expression indicate that ACS-5 is involved in the anabolic fate of fatty acids.
- LXRalpha is a negative modulator of Abcd2, acting through a novel regulatory mechanism involving overlapping SREBP and LXRalpha binding sites
- there is a role for sphingolipid metabolism and SREBP1 in ACTH-dependent CYP17 regulation and steroidogenesis
- the function of an additional SREBP-1 responsive element located in the first intron of caspase-2 gene
- Adenoviral mediated overexpression of SREBP-1c transcription factor confirms its implication in insulin-mediated stimulation of proprotein convertase subtilisin kexin 9 (PCSK9) expression
- the threonine residue and/or surrounding region play an important role in the SREBP-1 function
- SREBP1, activated by atorvastatin, suppressed vascular endothelial growth factor expression through the indirect interaction with the proximal tandem Sp1 sites in vascular smooth muscle cells
- Knockout of sterol regulatory element-binding protein (SREBP)-1c, had no effect on the ability of leptin to decrease either stearoyl-CoA desaturase transcript or activity.
- Our results demonstrate cell-specific mechanisms for the processing and storage of cytotoxic PUFAs in closely related cell lines, and suggest downregulation of nSREBP1 as a possible contributor to the growth inhibitory effect of DHA.
- analysis of phosphorylation and ubiquitination of the transcription factor sterol regulatory element-binding protein-1 in response to DNA binding
- Cdk1-mediated phosphorylation of S439 stabilizes mature SREBP1 during mitosis, thereby preserving a critical pool of active transcription factors to support lipid synthesis.
- FOXO1 and SREBP-1c have roles in insulin regulation of cholesterol 7alpha-hydroxylase expression
- Evidence for single nucleotide polymorphism in the 5'utr region of this gene is associated with type 2 diabetes and blood glucose levels.
- These results indicate that positional and geometrical isomers of CLAs have specific effects on gene expression of human macrophages and that t9,t11-CLA activates ABCG1 by a SREBP-1c-dependent mechanism.
- associations of rs2297508 with type 2 diabetes prevalence and plasma adiponectin
- SREBP transcription factors play an important role in disturbed lipid metabolism in renal failure.
- LXRalpha is regulated not only by oxysterol derivatives but also by PKA-mediated phosphorylation, which suggests that nutritional regulation of SREBP-1c and lipogenesis could be regulated at least partially through modulation of LXR
- hepatitis C virus core protein enhanced the transcriptional activity of SREBP1
- SREBP-1c could participate to the hepatic steatosis observed in humans and related to alcohol consumption and hyperhomocysteinaemia, two pathologies which are concomitant with a stress of the endoplasmic reticulum and an insulin activation.
- We have identified novel nonclassical mediators of the SREBP-1 response, including HMOX1 & p55gamma, supporting the hypothesis that SREBP-1 regulates stress response and signaling genes.
- SREBP-1 is involved in the early regulation of delta5 desaturase gene by simvastatin, in THP-1 cells.
- treatment of macrophages with urokinase increased sterol regulatory element-binding protein-1(SREBP-1) processing, and mature SEREBP-1 content (by 5.7-fold) in the nucleus.
- inhibition of the PI3-K pathway also blocked the IGF-1-induced transcription of SREBP target genes and sebocyte lipogenesis
- Upregulation of sterol response element-binding protein (SREBP), known to induce PPARgamma expression, can increase PTEN expression.
- mapped the minimal human SREBP-1a promoter region to 75bp upstream of the translation start site where we discovered a functional role for the 3 GC-boxes containing overlapping sites for the Sp1 and EGR-1 transcription factors
- SREBP-1 may be implicated in ezetimibe's mechanism of action.
- Because sterol regulatory element-binding protein-1c is a mediator of insulin action, findings of variations in SREBF1are consistent with the presence of a yet undefined subtle loss-of-function in type 2 diabetes.
- The ratio of SREBP-1Delta expression to total SREBP-1 expression in HepG2 cells was not affected by either insulin or high glucose treatment.
- Transport of LDL-derived cholesterol from late endosomes/lysosomes to the sterol-regulatory pool is regulated by the NPC1 protein and promotes feedback inhibition of the SREBP pathway.
- FAS gene is up-regulated by hypoxia via activation of the Akt and HIF1 followed by the induction of the SREBP-1 gene, and that hypoxia-induced chemoresistance is partly due to the up-regulation of FAS.
- SREBP-1 blocks the interaction of pregnane X receptor and constitutive androstane receptor and impairs mRNA induction of cytochromes P450 by drugs and other xenochemicals
- in nonalcoholic fatty liver disease, insulin signaling via IRS-1 causes the up-regulation of SREBP1-c, leading to the increased synthesis of fatty acids
- growth factors inhibit sumoylation of SREBPs through their phosphorylation, thus avoiding the recruitment of an HDAC3 corepressor complex and stimulating the lipid uptake and synthesis required for cell growth.
- Taken together, results suggest that HCV NS2 can upregulate the transcription of SREBP-1c and FAS, and thus is probably a contributing factor for HCV-associated steatosis.
- Tumor necrosis factor-alpha can provoke cleavage and activation of sterol regulatory element-binding protein in ethanol-exposed cells via a caspase-dependent pathway that is cholesterol insensitive
- Genome-wide occupancy of SREBP1 and its partners NFY and SP1 reveals novel functional roles and combinatorial regulation of distinct classes of genes.
- Proto-oncogene FBI-1 (Pokemon) and SREBP-1 synergistically activate transcription of fatty-acid synthase gene
- Findings indicate that the SREBP-1c SNPs rs2297508 and rs11868035 are associated with a significantly increased risk of T2DM and dyslipidemia in the Chinese population.
- Lipid accumulation and levels of the nuclear form of SREBP1c increased in H2O2-stimulated HepG2 cells. ROS may stimulate lipid accumulation in HepG2 cells via SREBP1c activation.
- SREBP-1c may not play a prominent role in the pathogenesis of hepatitic C-related steatosis
- Results suggest that the FASN gene is activated by the synergistic action of KLF5 and SREBP-1, which was induced by androgen in androgen-dependent prostate cancer cells.
- Unsaturated fatty acid-mediated stabilization of Insig-1 enhances the ability of sterols to inhibit proteolytic activation of SREBP-1, which activates transcription of genes involved in fatty acid synthesis
- 25-Hydroxycholesterol-3-sulfate regulates macrophage lipid metabolism via the LXR/SREBP-1 signaling pathway.
- SREBF1 protein expression was evaluated in 54 hepatocellular carcinoma samples by immunohistochemistry, and Kaplan-Meier survival analysis indicated that SREBF1-high hepatocellular carcinoma correlated with high mortality.
- Polymorphism of the SREBF1 gene is associated with the risk of osteonecrosis of the femoral head in the Korean population.
- The islets isolated from the transgenic mice with overexpressed human SREBP-1a were fewer and smaller, and had decreased insulin content and unaltered glucagon staining.