anti-Insulin Receptor Substrate 1 (IRS1) 抗体产品概述

Human Insulin Receptor Substrate 1 (IRS1) interaction partners

1. Overexpression of IRS-1 protein is associated with expression of p-Akt, and could be an independent biomarker for poor prognosis in breast invasive ductal carcinoma.

2. miR-664 is downregulated in BC tissues and cell lines. In addition, miR-664 restricts proliferation and migration of BC cells. Moreover, IRS1 is validated as a direct target of miR-664 in BC.

3. Neither the PPARgamma nor the IRS-1 polymorphism was associated with mortality outcome in breast-cancer patients. The TNF-alfa -308 G > A polymorphism was associated with reduced breast-cancer-specific and all-cause mortality.

4. Results show that ectopic expression of SH2B1 in lung adenocarcinoma (LADC) cell line H1299 cells increased IRS1 expression level. Reduced expression of IRS1 considerably inhibited H1299 cell proliferation, migration, and invasion. These findings suggest that IRS1 plays a role in LADC carcinogenesis.

5. Axl binds to and phosphorylates TNS2 and that Axl/TNS2/IRS-1 cross-talk may potentially play a critical role in glucose metabolism of cancer cells.

6. our present data point to IRS1 rs1801278 as a potential biomarker for pursuing the goal of stratified medicine in the field of antihyperglycemic treatment in type 2 diabetes .

7. IRS-1 gene polymorphism Gly972Arg was found a significant risk factor for ischemic stroke in Indonesian subjects.

8. ER and IRS-1 subgroups appear to be critical factors for the prediction of breast cancer recurrence. In particular, we suggest that the patients who have ER-positive and IRS-1-negative breast cancer undergo more aggressive treatment because they have poorer prognoses.

9. our findings suggested that the overexpression of LncRNA H19 could inhibit cell proliferation and promoted apoptosis via downregulation of IRS-1 in thyroid cancer cells in vitro. These findings might provide important clues for the establishment of LncRNA H19 functional network in thyroid cancer. Long noncoding RNA H19 might be a potential new target for antitumor therapy of thyroid cancer

10. Acute loss of IRS1/IRS2 or inhibition of IR/IGF1R in KRAS-mutant human NSCLC cells decreases the uptake and lowers the intracellular levels of amino acids, while enhancing basal autophagy and sensitivity to autophagy and proteasome inhibitors.

11. S6K1-dependent IRS-1pSer suppresses insulin signaling leading to insulin resistance, which is frequently observed in AD brains. Notably, miR-200b/c transfection of SH-SY5Y cells reduced the levels of IRS-1pSer. This finding indicates that miR-200b/c has the potential to alleviate insulin resistance via modulation of S6K1

12. Together, miR-145 mimics suppress cell proliferation by targeting and inhibiting IRS1 expression to inhibit MAPK/ERK signaling pathways.

13. Data suggest that Y537S/D538G ESR1 mutant breast cancer cell lines exhibit enhanced proliferation in response to IGF1/IGF1R signaling; mechanism involves IRS1; here, knockdown of IRS1 attenuates enhanced IGF1/IGF1R signaling response in ESR1 mutant cells. (ESR1 = estrogen receptor 1; IGF1 = insulin like growth factor 1; IGF1R = IGF1 receptor; IRS1 = insulin receptor substrate 1)

14. The effect of PF may be associated with its role in inhibiting de novo lipid synthesis and in regulating the ROCK/IRS/Akt signalling pathways.

15. Gene expression for insulin receptor substrate 1 (IRS-1), protein kinase B (Akt-2) and glucose transporter 4 (GLUT-4) genes were evaluated by real time PCR.

16. Reduced insulin receptor substrate-1 (IRS-1) staining in lung adenocarcinoma tissue microarray displayed a significant survival disadvantage, especially within the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutant subgroup.

17. This study examined the normal regional brain expression of IRS-1 and found a significant correlation with the volumetric associated with regional atrophy in Alzheimer's disease.

18. Data show that MIR126 induces autophagic flux in malignant mesothelioma (MM) cells by downregulating insulin receptor substrate-1 (IRS1) and disrupting the IRS1 signaling pathway.

19. IRS1/beta-Catenin Axis Is Activated and Induces MYC Expression in Acute Lymphoblastic Leukemia Cells

20. These effects were exerted by changes on the phosphorylation of IRS-1.

Mouse (Murine) Insulin Receptor Substrate 1 (IRS1) interaction partners

1. Hyperglycemia- or insulin resistance-induced IRS-1 down-regulation decreases the p53/KLF4 association and enhances dedifferentiation and proliferation.

2. MID-00935 disrupted the molecular interaction of MG53 and IRS-1, abrogated MG53-induced IRS-1 ubiquitination and degradation and improved insulin signaling in C2C12 myotubes.

3. Autophagy through p62 plays an important role in regulating insulin receptor substrate 1 protein levels in response to nutritional deficiency. The present findings suggest that autophagy might function as energy depletion-sensing machinery that finely tunes insulin signal transduction.

4. CD36 functioned through ubiquitination-dependent binding to IRS1 and inhibiting its interaction with cullin 7.

5. this study shows that microRNA-126 deficiency enhanced the activation and function of CD4(+) T cells by elevating IRS-1 pathway

6. The data suggest that upregulated Irs1 by Wnt3a/beta-catenin signaling plays a crucial role in the progression of hepatocellular carcinoma.

7. DPP-4 inhibitor sitagliptin has effects on cardiac function, glycemia, and beta-cell function together with reducing S6K1 activation and IRS-1 and IRS-2 degradation in the obesity female mouse model

8. 'selective insulin resistance' is caused by the differential expression of Irs1 and Irs2 in different zones of the liver

9. Lung-specific dual ablation of insulin receptor substrates 1/2 (succumb to tumor burdenIrs1/Irs2) strongly suppresses tumor initiation and dramatically extends the survival of a mouse model of lung cancer with Kras activation and p53 loss. Mice with Irs1/Irs2 loss eventually.

10. Noise exposure led to enhanced JNK phosphorylation and IRS1 serine phosphorylation as well as reduced Akt phosphorylation in skeletal muscles in response to exogenous insulin stimulation.

11. The data, therefore, suggest that 1,25(OH)2D3 increases glucose consumption by inducing SIRT1 activation, which in turn increases IRS1 phosphorylation and GLUT4 translocation in myotubes.

12. Results show that lack of IRS1 prevents beta-cell apoptosis induced by ER stress, and promotes XBP-1 instability secondary to proteasomal degradation.

13. Using two long-lived IIS models, namely Drosophila lacking three insulin-like peptides (dilp2-3,5(-/-)) and mice lacking insulin receptor substrate 1 (Irs1(-/-)), and two independent translation assays, polysome profiling and radiolabeled amino acid incorporation, we show that reduced IIS lowers translation in these organisms

14. findings suggest that up-regulation of miR-222 followed by reduction in IRS-1 expression may be a viable mechanism of insulin resistance in the liver

15. These results demonstrate the cooperative interaction between RPTPbeta and the IGF-I receptor leading to a coordinated series of signaling events that are required for osteoblast differentiation. Our findings emphasize the important role IRS-1 plays in modulating these signaling events and confirm its essential role in facilitating osteoblast differentiation

16. EGCG significantly ameliorated insulin resistance and cognitive disorder by up-regulating the insulin receptor substrate-1 (IRS-1)/AKT and ERK/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathways.

17. Pit1 deletion inhibited USP7/IRS1 dissociation upon insulin stimulation.

18. TSH improves insulin sensitivity in skeletal muscle by increasing Irs1 gene expression.

19. Insulin receptor substrate-1 time-dependently regulates bone formation by controlling collagen Ialpha2 expression via miR-342

20. Irs1 was downregulated in the arcuate nucleus of type 2 diabetic mice.

Rabbit Insulin Receptor Substrate 1 (IRS1) interaction partners

1. IRS1 gene was associated with growth traits in rabbits.Association between the IRS1 and FTO genes regulates body weight in rabbits.

Pig (Porcine) Insulin Receptor Substrate 1 (IRS1) interaction partners

1. miR-146a-5p targets porcine insulin receptor and could inhibit its protein expression.

2. TBC1D4, insulin receptor and GLUT4 showed altered expression in some tissues in pre-diabetic pigs.

3. Association analysis of genotypes with growth traits, anatomy traits, meat quality traits and physiological biochemical indexes traits showed that different genotypes at locus 3,257 of IRS-1 have significant differences in carcass straight length in pigs.

Xenopus laevis Insulin Receptor Substrate 1 (IRS1) interaction partners

1. Knock down of IRS-1 in neural tissue by specific antisense morpholino oligonucleotides (MO) resulted in abnormal eye formation accompanied by reduction of the eye-specific marker genes Rx1 and Pax6 and a decreased cell proliferation.