WebApr 9, 2024 · Insulin receptor substrate 2 (IRS2) belongs to the member of IRS family that regulates cell proliferation, apoptosis, and metabolism by functioning as a molecular adaptor to integrate and coordinate extracellular signals from insulin and other ligands to mitochondria (Dearth et al. 2007 ). WebThe IR of any CVC-related complication was numerically higher in patients with SBS with cancer vs without cancer (3.44 vs 1.86 cases per 1,000 catheter-days, respectively). Conclusion: Our study quantifies the incidence of complications in patients with CVCs, including those with SBS, in Japan. Keywords: database, epidemiology, prevalence ...
IRS4 induces mammary tumorigenesis and confers …
WebIRS2 - Explore an overview of IRS2, with a histogram displaying coding mutations, full tabulated details of all associated variants, tissue distribution and any drug resistance data. Projects COSMIC WebBreast cancer stem cells (BSCSs) are a subtype of tumor cells that have properties similar to normal, tissue stem cells such as the ability to divide slowly and give rise to differentiated cellular lineages. Furthermore, BCSCs have been implicated in tumor initiation, therapy resistance and metastasis to distant organs. maverick estate winery
IRS2 is a candidate driver oncogene on 13q34 in colorectal
WebAug 8, 2024 · The insulin-like growth factor-1 (IGF-1) signaling pathway has been implicated in non-small cell lung cancer (NSCLC) outcomes and resistance to targeted therapies. However, little is known regarding the molecular mechanisms by which this pathway contributes to the biology of NSCLC. The insulin receptor substrate (IRS) proteins are … WebMar 18, 2024 · Breast cancers that do not express the estrogen receptor (ER) or the progesterone receptor (PR) and have no ERBB2 (commonly referred to as human epidermal growth factor receptor 2 [HER2]) amplification are categorized as triple-negative breast cancers (TNBCs) and comprise 10%–20% of all breast cancers ( Dent et al., 2007, … WebApr 2, 2024 · These results indicate that Irs1 and Irs2 are required for Kras -driven lung tumor initiation and that Kras -transformed cells can eventually bypass Irs1 / Irs2 loss, developing more aggressive tumors at a highly variable and extended latency. Fig. 1. Loss of Irs1 and Irs2 significantly delays Kras -driven lung tumorigenesis. maverick estate winery oliver