Browse our anti-Insulin Receptor Substrate 1 (IRS1) Antibodies

Human Insulin Receptor Substrate 1 (IRS1) interaction partners

1. Together, miR (show MLXIP Antibodies)-145 mimics suppress cell proliferation by targeting and inhibiting IRS1 expression to inhibit MAPK/ERK (show MAPK1 Antibodies) signaling pathways.

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

3. The effect of PF may be associated with its role in inhibiting de novo lipid synthesis and in regulating the ROCK/IRS (show IARS Antibodies)/Akt (show AKT1 Antibodies) signalling pathways.

4. Gene expression for insulin receptor substrate 1 (IRS-1), protein kinase B (Akt-2) and glucose transporter 4 (GLUT-4 (show SLC2A4 Antibodies)) genes were evaluated by real time PCR.

5. 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 (show RAB1A Antibodies) homolog (KRAS) mutant subgroup.

6. 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.

7. 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.

8. IRS1/beta-Catenin (show CTNNB1 Antibodies) Axis Is Activated and Induces MYC (show MYC Antibodies) Expression in Acute Lymphoblastic Leukemia Cells

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

10. Allele and genotype frequencies of rs1801278 in IRS1 showed significant differences between cases and controls for obstructive sleep apnea risk in Chinese Han population.

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

1. Results show that lack of IRS1 prevents beta-cell apoptosis induced by ER stress, and promotes XBP-1 (show XBP1 Antibodies) instability secondary to proteasomal degradation.

2. Using two long-lived IIS models, namely Drosophila lacking three insulin (show INS Antibodies)-like peptides (dilp2 (show FLNA Antibodies)-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

3. findings suggest that up-regulation of miR (show MLXIP Antibodies)-222 followed by reduction in IRS-1 expression may be a viable mechanism of insulin (show INS Antibodies) resistance in the liver

4. These results demonstrate the cooperative interaction between RPTPbeta (show PTPRZ1 Antibodies) and the IGF-I receptor (show IGF1R Antibodies) 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

5. EGCG significantly ameliorated insulin (show INS Antibodies) resistance and cognitive disorder by up-regulating the insulin receptor substrate-1 (IRS-1)/AKT (show AKT1 Antibodies) and ERK (show EPHB2 Antibodies)/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF (show BDNF Antibodies)) signaling pathways.

6. Pit1 (show POU1F1 Antibodies) deletion inhibited USP7 (show USP7 Antibodies)/IRS1 dissociation upon insulin (show INS Antibodies) stimulation.

7. TSH improves insulin (show INS Antibodies) sensitivity in skeletal muscle by increasing Irs1 gene expression.

8. Insulin receptor substrate-1 time-dependently regulates bone formation by controlling collagen Ialpha2 expression via miR (show MLXIP Antibodies)-342

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

10. In conclusion, we have identified that ARL15 acts as an insulin (show INS Antibodies)-sensitizing effector molecule to upregulate the phosphorylation of members of the canonical IR/IRS1/PDPK1 (show PDPK1 Antibodies)/AKT (show AKT1 Antibodies) insulin (show INS Antibodies) pathway by interacting with its GAP ASAP2 (show ASAP2 Antibodies) and activating PDPK1 (show PDPK1 Antibodies). This research may provide new insights into GTPase (show RACGAP1 Antibodies)-mediated insulin (show INS Antibodies) signalling regulation and facilitate the development of new pharmacotherapeutic targets for insulin (show INS Antibodies) sensitizati

Rabbit Insulin Receptor Substrate 1 (IRS1) interaction partners

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

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

1. miR (show MYLIP Antibodies)-146a-5p targets porcine insulin receptor (show INSR Antibodies) and could inhibit its protein expression.

2. TBC1D4 (show TBC1D4 Antibodies), insulin receptor (show INSR Antibodies) and GLUT4 (show SLC2A4 Antibodies) 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 (show PAX6 Antibodies) and a decreased cell proliferation.