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Validated All-in-One™ qPCR Primer for IRS1(NM_005544.2) Search again
Product ID:
HQP054298
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HIRS-1
Gene Description:
insulin receptor substrate 1
Target Gene Accession:
NM_005544.2(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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Gene References into function
- association between the Gly972Arg polymorphism in insulin receptor substrate-1 (IRS-1) and birth weight in a population-based sample of Brazilian newborns
- Insulin receptor substrate 1 translocation to the nucleus by the human JC virus T-antigen
- Nitric oxide regulates oestrogen-activated signalling pathways at multiple levels through cyclic GMP-dependent recruitment of insulin receptor substrate 1 in human breast cancer cells.
- insulin sensitivity of glucose disposal and lipolysis: no influence of common genetic variants
- Relationship of genotypes to phenotypic features of polycystic ovary syndrome
- IRS-1 is a novel direct substrate for IKK and that phosphorylation of IRS-1 at Ser(312) (and other sites) by IKK may contribute to the insulin resistance mediated by activation of inflammatory pathways
- PTPL1/FAP-1 has a key role in the apoptotic process in human breast cancer cells independent of Fas but associated with an early inhibition of the insulin receptor substrate-1/phosphatidylinositol 3-kinase pathway
- genetic variants in the gene appear not to have a major role as modifier genes in familial combined hyperlipidemia
- Data suggest that salicylic acid can reverse the inhibitory effects of TNFalpha on insulin signaling via insulin receptor substrate 1
- Constitutive IRS-1 activation is a common phenomenon in tumors.
- In two cohorts ofobese Caucasian children, we measured insulin sensitivity and genotyped insulin receptor substrate IRS-1 and IRS-2 genes for the Arg972Gly and the Asp1057Gly variants, respectively.
- Increased frequency of the G972R variant of the insulin receptor substrate-1 (irs-1) gene among girls with a history of precocious pubarche. Sex hormone-binding globulin concentrations were lower among girls heterozygous for G972R variant.
- inhibition of insulin-stimulated insulin receptor substrate (IRS)-phosphatidylinositol 3-kinase/Akt signaling pathway by Grb10
- role in modulating insulin-stimulated degradation by serine 312 phosphorylation
- concluded that the IRS-1 protein is involved in the signalling pathway of the BCR-ABL tyrosine kinase
- Data describe the expression of peroxisome proliferator-activated receptor gamma (PPAR gamma) co-activator 1, PPAR gamma, insulin receptor substrate-1, glucose transporter isoform-4, and mitochondrial uncoupling protein-1 in adipose tissue.
- findings suggest a role for Arg(972) IRS-1 in conferring risk for the development of type 1 diabetes
- Increased growth caused by IRS-1 over-expression is balanced by constitutive activation of pro-death mechanisms.
- there is an increase of serine 636 phosphorylation of insulin receptor substrate-1 in primary culture of skeletal muscle cells from patients with type 2 diabetes.
- Carriers of the Gly972Arg variant of the IRS-1 gene are at a 25% increased risk of having Type 2 diabetes compared with non-carriers.
- IRS-1 is stabilized in tumor cells, the IRS-1/Akt/GSK-3 pathway is upregulated, and improved cell survival is seen in the presence of IGF-I
- the Arg(972) IRS-1 variant could contribute to the risk for atherosclerotic cardiovascular diseases associated with type 2 diabetes by producing a cluster of insulin resistance-related metabolic abnormalities.
- Protein kinase C delta modulates the ability of the insulin receptor kinase to tyrosine-phosphorylate IRS-1.
- IRS-1 has a role in insulin attenuation of platelet functions by interfering with cAMP suppression along with Gi
- Both of the IRS proteins modulate VPF/VEGF expression in pancreatic cancer cells by different mechanistic pathways.
- The association of variants in IRS1 with type 2 diabetes and type 2 diabetes-related phenotypes and the differential expression of IRS1 in adipocytes and skeletal muscle suggest a role of this gene in the pathogenesis of type 2 diabetes in Pima Indians.
- The IRS-1 Gly972Arg polymorphism relates to higher fasting insulin levels and lower triglyceride levels. The impact of this genotype and its modification by overweight may be smaller than suggested previously.
- ETV6-NTRK3.IRS-1 complex formation through the NTRK3 C terminus is essential for ETV6-NTRK3 transformation
- None of the polymorphisms in INSR or IRS1 was associated with metabolic syndrome findings.
- G972R IRS-1 polymorphism impairs insulin regulation of endothelial nitric oxide synthase in vascular endothelial cells.
- These data indicate that both insulin receptor substrate (IRS)-1 and -3, but not IRS-2 or IRS-4, play key roles in the differentiation of brown adipocytes.
- Association of this gene's single nucleotide polymorphism with type 2 diabetes.
- Activation of hexosamine pathway affects glucose-induced phosphorylation of IRS-1. Impairs coupling of IRS-1 and PI 3-kinase and activativates Akt/mammalian target of rapamycin/phosphorylated heat- and acid-stable protein-1/p70S6 kinase pathway.
- AII, acting via the type 1 receptor, increases IRS-1 phosphorylation at Ser312 and Ser616 via JNK and ERK1/2, respectively, thus impairing the vasodilator effects of insulin mediated by the IRS-1/PI 3-kinase/Akt/eNOS pathway.
- phosphorylation of Ser(318) by PKC-zeta might contribute to the inhibitory effect of prolonged hyperinsulinemia on IRS-1 function.
- data demonstrate cell-specific alterations in IRS protein concentrations in theca cells from polycystic ovaries consistent with exaggerated amplification of the insulin signal & which may play a role in ovarian hyperandrogenism & thecal hyperplasia
- Data show that in adipocytes the insulin receptor is localized to caveolae,and that part of insulin receptor substrate 1 (IRS1), the immediate downstream signal mediator, colocalizes with the insulin receptor in the plasma membrane and caveolae.
- a lack of the Arg972 IRS1 polymorphism was found in the Parakana Indian population
- By inducing endothelial dysfunction, the Arg(972) IRS-1 polymorphism may contribute to the genetic predisposition to develop cardiovascular disease.
- Having at least one R allele (GR or RR) for IRS1 G972R was associated with an increased risk of colon cancer [odds ratio 1.4, 95% confidence interval (95% CI) 1.1-1.9]
- SH2-B dramatically enhanced leptin-stimulated tyrosine phosphorylation of IRS1 and IRS2 in human and mouse cells.
- nuclear IRS-1 interacts with ERalpha and that this interaction might influence ERalpha transcriptional activity
- unable to replicate the association of the IRS-1 G972R polymorphism with type 2 diabetes
- Estimate of the overall contribution of IRS1 variation to type 2 diabetes susceptibility, but current study suggests that previous studies have overestimated the magnitude of this effect.
- the G972R naturally occurring polymorphism of IRS-1 not only reduces phosphorylation of the substrate but allows IRS-1 to act as an inhibitor of the insulin receptor kinase, producing global insulin resistance
- mTOR/S6K1 overactivation contributes to elevated serine phosphorylation of IRS-1, leading to impaired insulin signaling to Akt in liver and muscle
- pinpoint the signalling dysregulation in type 2 diabetes to be the insulin-stimulated phosphorylation of IRS1 in human adipocytes
- IRS1 G972R GR/RR genotypes were associated with a 2.8-fold increased risk for prostate cancer and also associated with a more advanced Gleason score and AJCC stage.
- IRS1 variant and CYP21 mutations seem to play a limited role in the development of polycystic ovary syndrome in the population studied.
- the PPARgamma and IRS-1 genes have a possible interaction in their effects on adiponectin concentration in blood
- IRS-1 is a novel physiological substrate for pelle-like kinase
- Carriers of Pro allele compared with carriers of Ala allele of PPARG2 gene had higher frequency of insulin resistance. No association was found between insulin resistance and alleles and genotypes of PPAR and IRS1 genes.
- Data show that JC polyomavirus T-antigen inhibits homologous recombination DNA repair by binding insulin receptor substrate 1, which then translocates to the nucleus and binds Rad51 at the site of damaged DNA.
- Phosphorylation of Ser1223 dampens association of IRS-1 with Src homology domain 2 (SH2)-containing phosphatase-2 (SHP-2).
- The Gly972Arg variant of IRS-1 may modulate reproduction by lowering sex hormone-binding globulin in both healthy women and women with polycystic ovary syndrome.
- Insulin induces IRS1 protein levels in humans and rodents
- Ser(318) phosphorylation of IRS-1 is an early physiological event in insulin-stimulated signal transduction, which attenuates the continuing action of insulin
- IRS-1 serine 307 phosphorylation is attenuated in insulin resistance of type 2 diabetes
- Variations in various codons among African Pygmies and Bantus.
- IRS-1 serine phosphorylation in muscle has a role in insulin resistance
- Raptor directly binds to and serves as a scaffold for mTOR-mediated phosphorylation of IRS-1 on Ser636/639.
- interleukin-6 has a role in insulin signal transduction via insulin receptor substrate-1 in skeletal muscle cells
- Negative feedback phosphorylation of serine 312 required relatively high concentrations of insulin (EC(50)=3 nM) for a long time (t(1/2) ca. 30 min) and reduced the steady-state tyrosine phosphorylation, without affecting the concentration, of IRS1.
- These studies suggest that, through serine phosphorylation, Raptor-mTOR and S6K1 promote the depletion of IRS1 from specific intracellular pools in pathological states of insulin and IGF-I resistance and in lesions associated with tuberous sclerosis.
- Ser24 is a negative regulatory phosphorylation site in IRS-1.
- IRS-1 is selectively inactivated in metastatic breast cancer in transgenic mice.
- Transgenic mice overexpressing IRS1 in the mammary gland show progressive mammary hyperplasia, tumorigenesis and metastasis.
- Genetic variation in IRS1 is associated with breast cancer risk
- phosphorylation is a mechanism for regulation of insulin receptor substrate-1/2, Akt, and ERK1/2
- Polymorphism of the insulin receptor substate-1 gene at codon 972, especially Gly/Arg variant, appears to be associated with occurrence of obstructive sleep apnea syndromes in male patients, whereas this polymorphism is not related to severity of OSAS
- IRS-1 gene polymorphisms do not associate with obesity.
- hypoxia-mediated suppression of Akt may induce caspase-mediated IRS-1 cleavage.
- We showed that clearance of HCV improves insulin resistance, beta-cell function, and hepatic IRS1/2 expression.
- Overexpression of IRS1 and IRS2 but not of Shc induced DNA synthesis in starved CHO-IR cells independent of exogenous growth factors.
- CRP may cause insulin resistance by increasing IRS-1 phosphorylation at Ser(307) and Ser(612) via JNK and ERK1/2, respectively, leading to impaired insulin-stimulated glucose uptake, GLUT4 translocation, and glycogen synthesis
- IRS-1 activates promoters involved in cell growth and cell proliferation, resulting in a more transformed phenotype.
- Assessment of IRS-1 phosphorylation in vivo shows that insulin has profound effects on IRS-1 serine/threonine phosphorylation in healthy humans.
- This review points out that IRS-1, which is inactivated in metastatic mammary tumors, may be a novel predictive indicator of metastasis.
- This review discusses the roles of IRS-1 and IRS-2 in oncogenic transformation and cancer progression.
- Data do not support an association of common variants in IRS1 with type 2 diabetes in populations of European descent.
- insulin-stimulated IRS kinases such as PKCzeta overlap with IRS kinases triggered by inducers of insulin resistance, such as IKKbeta, to phosphorylate IRS-1 on common Ser si
- phosphatidylinositol 3-kinase/Akt signaling and induces apoptosis is inhibited by energy depletion via AMP-activated protein kinase-dependent phosphorylation of IRS-1 at Ser-794
- Despite the small sequence divergence of the hepatitis C virus core proteins of genotypes 3a and 1b, the 2 proteins appear to interfere with insulin receptor substrate 1 using genotype-specific mechanisms
- phosphorylation is inhibited by RBP4 in diabetic adipocytes
- IRS-1 may act as a repressor of liganded estrogen receptor (ER)alpha and coactivator of unliganded ERalpha.
- PTPN13/PTPL1 induces apoptosis through insulin receptor substrate-1 dephosphorylation
- Understanding the complex phosphorylation patterns of IRS-1 is crucial to elucidating the factors contributing to insulin resistance and, ultimately, the pathogenesis of type 2 diabetes.
- PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells.
- IRS-1 Gly972Arg polymorphism is associated with polycystic ovary syndrome in the Japanese population.
- Overexpression of Akt1 upregulates glycogen synthase activity and phosphorylation of mTOR in IRS-1 knockdown HepG2 cells.(
- identify miR145 as a micro RNA that down-regulates the IRS-1 protein, and inhibits the growth of human cancer cells
- IGF-1 activates the IGF receptor/IRS/PI3K/PKB pathway, and that PI3Kalpha is essential for the potentiatory effect of IGF-1 on platelet responses
- The results of this study show that triglyceride is a central feature of peripheral insulin resistance, and also suggest that triglyceride-induced ER stress influences insulin resistance.
- Chimeric IRS1, consisting of the conserved N-terminus of rat IRS1 with the variable C-terminal of human IRS1, did not target the plasma membrane, indicating that subtle sequence differences direct human IRS1 to the plasma membrane.
- Rapamycin inhibits S6K1-dependent IRS-1 serine phosphorylation, increases IRS-1 protein levels, and promotes association of tyrosine-phosphorylated IRS-1 with PI3K.
- Carrying the variant allele of the IRS1 Gly972Arg SNP further decreased the risk for colorectal cancer among the INSR-603G allele carriers.
- Transgenic mice overexpressing IRS1 show impaired insulin action and insulin secretion.
- nondiabetic carriers of the G972R IRS-1 variant showed increased expression of prothrombotic genes and a decreased expression of fibrinolytic genes
- agents that block IRS-1 potentiate the effect of mTOR inhibition in the growth of prostate cancer cell xenografts.
- phosphorylation of IRS-1 Ser(357) mediates at least in part the adverse effects of PKC-delta activation on insulin action
- the K1 mutation within the retinoblastoma protein (Rb) binding motif of TAg disrupts not only Rb binding but also IRS1 binding, contributing to the loss of activation of PI3K/Akt signaling.
- Results demonstrate a key role for the CUL7 E3 in targeting IRS-1 for degradation, a process that may contribute to the regulation of cellular senescence.
- Gly972Arg genotype is associated with lower birth weight, body length and head circumference in neonates with adequate gestational age.Gly972Arg polymorphism in the IRS-1 gene was genotyped.
- None of the components in the IGF-1 pathway including IGFBP3, PI3k, and PTEN influence the relation between IRS-1 genotype and prostate cancer risk. Ther is no association between carriage of the variant IRS-1 gene and prostate cancer risk.
- results indicate that IRS-1 plays a significant role in Simian Virus 40 large T antigen activation of cell cycle progression genes
- ApoCIII activates PKCbeta, which inhibits the IRS-1/PI3K/Akt/eNOS pathway and induces endothelial dysfunction.
- mir-126, a cell growth suppressor, targets IRS-1.
- IRS-1 may have a more general role in cancer, and could be considered as a protein having the opposite effect of tumor suppressors.
- S6K1 directly phosphorylates IRS-1 on Ser-270 to promote insulin resistance in response to TNF-(alpha) signaling through IKK2.
- There are significant changes in dynamics within the phosphotyrosine-binding domain of IRS1 that have significant consequences for stability and function.
- the nucleus, nuclear interaction between IRS-1 and Rad51, and the inhibition of recombination.