anti-Insulin Receptor Substrate 1 (IRS1) Antikörper

Human Insulin Receptor Substrate 1 (IRS1) Interaktionspartner

1. The protein-protein docking study of SOCS1 with its natural substrates, IRS1 and IRS2, and subsequent solvent accessible surface area analysis gave insight into the binding region of the SOCS1 protein.

2. The report the association between common variants in IRS1 gene with insulin resistance, glucose, and HbA1c levels in Bosnia and Herzegovina's population.

3. The decreased hepatic expression of IRS1 and beta-catenin in nonalcoholic fatty liver disease is linked to histological progression such as ballooning, and might lead to diabetes as a result of impaired glucose metabolism.

4. the expression level of miR-466 was significantly downregulated in tumor tissues and cell lines, and its overexpression was able to inhibit cell proliferation and invasion. The tumor-suppressive roles of miR-466 in OS cells were mediated by the silencing of IRS1.

5. Studied insulin resistance in human nonalcoholic fatty liver disease patients and controls by analyzing gene expression levels of molecules involved in insulin signaling including insulin receptor substrate 1(IRS-1) and insulin receptor substrate 2(IRS-2).

6. miR-30e blocked the activation of AKT and ERK1/2 pathways, and the expression of HIF-1alpha and VEGF via directly targeting IRS1.

7. Adipose tissue DNA promoter methylation correlated negatively with insulin receptor substrate 1 IRS-1 (IRS1) gene expression in obese subjects.

8. The presence of AA genotype in both CCR5 59029 and IRS1 rs10498210 is associated with type 2 diabetes.

9. This study establishes a new role for IRS-1 as an endocytic regulator of IGF-IR that ensures sustained IGF bioactivity, independent of its classic role as an adaptor in IGF-IR signaling.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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 .

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

17. 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.

18. 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

19. 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.

20. 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

Mouse (Murine) Insulin Receptor Substrate 1 (IRS1) Interaktionspartner

1. Our studies highlight that IRS-1, by regulating BMAL1, is an important regulator of Kir4.1 in Muller cells and the dysfunctional signaling mediated by IRS-1 may be detrimental to Kir4.1.

2. Through dual targeting of IRS-1 and AMPK.

3. The associated genes of the IRS1/PI3K/Akt pathway were significantly downregulated by HFD.

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

5. 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.

6. 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.

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

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

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

10. 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

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

12. 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.

13. 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.

14. 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.

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

16. 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

17. 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

18. 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

19. 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.

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

Rabbit Insulin Receptor Substrate 1 (IRS1) Interaktionspartner

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) Interaktionspartner

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) Interaktionspartner

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.