IRS_1 Antibody (S636)
- Known as:
- IRS_1 Antibody (S636)
- Catalog number:
- AE1018a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- IRS_1 Antibody (S636)
Related genes to: IRS_1 Antibody (S636)
- Gene:
- IL20RB NIH gene
- Name:
- interleukin 20 receptor subunit beta
- Previous symbol:
- FNDC6
- Synonyms:
- DIRS1, IL-20R2, MGC34923
- Chromosome:
- 3q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2015-12-11
- Gene:
- IRS1 NIH gene
- Name:
- insulin receptor substrate 1
- Previous symbol:
- -
- Synonyms:
- HIRS-1
- Chromosome:
- 2q36.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-24
- Date modifiied:
- 2016-10-05
- Gene:
- KRT71 NIH gene
- Name:
- keratin 71
- Previous symbol:
- -
- Synonyms:
- KRT6IRS, KRT6IRS1, K6IRS1
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-17
- Date modifiied:
- 2016-03-09
Related products to: IRS_1 Antibody (S636)
Related articles to: IRS_1 Antibody (S636)
- Activating mutations in PI3K are one of the most frequent mutations in breast cancer and are associated with worse patient outcomes in many breast cancer subtypes. Despite intense interest, cancer treatments that target the PI3K pathway have been only modestly effective due to intrinsic and acquired resistance mechanisms which reactivate PI3K signaling. Here, we characterize a feedback mechanism by which PI3K pathway inhibitors increase insulin receptor substrate 2 (IRS2) abundance and demonstrate the role of IRS2 in promoting resistance to these drugs. In mutant breast tumors and cell lines, there is a significant reduction in IRS2 mRNA and protein abundance which is reversed by PI3K pathway inhibition and mediated by the transcription factor FOXO3. mutations do not alter IRS1 expression. IRS2 confers resistance to PI3K pathway inhibition by sustaining PI3K signaling in mutant, but not wild-type breast cancer cells. Increased IRS2 abundance also correlates with PI3K pathway inhibitor resistance across PI3K mutant cancer cell lines from a variety of tissues. The clinical relevance of these findings is highlighted by the frequency of PI3K mutations in cancer and the identification of a new target to address the challenges associated with prior efforts to block the reactivation of PI3K signaling during PI3K inhibition. - Source: PubMed
Publication date: 2026/04/28
Lero Michael WMorgan Jennifer SCard Michael-AnthonyZhu Lihua JulieLi JunhuiLi RuiBui Quyen ThuMohlmann EmmaShaw Leslie M - Molecular mechanisms in frontotemporal dementia (FTD) and Alzheimer's disease (AD) are obscure. FTD can result from loss-of-function progranulin mutations, although pathogenetic consequences are uncertain. Progranulin insufficiency also increases human AD risk, and progranulin treatment improves mouse AD. Furthermore, AD and FTD risks are abetted by obesity/diabetes-induced hyperinsulinemia and hyperactivation of brain insulin signaling, and progranulin deficiency activates insulin signaling in fat and liver. Here, we found progranulin deletion in mouse brain increased activation of IRS-1 and activities of downstream PKC-λ/ι, NF-κB and mTOR, but diminished IRS-2 and Akt. Similarly, in microglial cells, progranulin deletion increased, and progranulin treatment diminished, activation of IRS-1, PKC-λ/ι, NF-κB, and mTOR. These progranulin-related changes in IRS-1 activation were due to JNK-mediated phosphorylation of inhibitory serine-302/307 residues in IRS-1. Progranulin deficiency in brain selectively activates an IRS-1-dependent insulin signaling pathway, and the resultant increases in inflammation and impaired autophagy/lysosomal function may augment progranulin deficiency-related neuropathology. - Source: PubMed
Publication date: 2026/04/12
Sajan Mini PAggarwal GeetikaHwang Joel JihwanSmith Denise MCooper Denise RDuncan Mildred AcevedoHansen Barbara CNguyen Andrew DFarese Robert V - Childhood obesity is tightly linked to dyslipidemia, chronic low-grade inflammation, and insulin resistance (IR). CD36 has been implicated in metabolic disease, yet its pediatric mechanisms remain unclear. This study aims to investigate the CD36/ANXA1/TLR4/NF-κB axis as a potential therapeutic target for lipid metabolism and IR in childhood obesity. - Source: PubMed
Publication date: 2026/05/04
Yao YiqingYang WeimingCheng FengMao Shunfeng - High-fat diets (HFDs) are a key contributor to obesity and promote oxidative stress and inflammation, which are associated with muscle atrophy and insulin resistance (IR). Passiflora edulis exhibits anti-obesity, antioxidant, and anti-inflammatory effects. The study aimed to investigate the potential benefit of P. edulis f. flavicarpa (PF) extract in preventing obesity-associated muscle atrophy and IR. The PF extract effectively inhibited cholesterol micelle solubility with an IC of 3431 µg/mL and decreased fat accumulation in 3T3-L1 adipocytes. Furthermore, this study investigated a model of HFD-induced IR and muscle atrophy in rats. Thirty-five male Sprague-Dawley (SD) rats were induced with obesity by HFD and were administered 250 and 500 mg/kg/day of PF extract. Rats fed with an HFD were associated with fat accumulation and oxidative stress, which promoted inflammation, muscle damage, muscle atrophy, and IR in obese rats. However, administration of PF extract effectively mitigated these effects. The PF extract decreased fat accumulation in white adipose tissues and gastrocnemius (GAS) muscle by inhibiting fat absorption and synthesis, particularly Cd36 and Hmgcr. The PF extract also notably reduced oxidative stress-induced muscle inflammation and damage via elevating nuclear factor erythroid 2-related factor 2 (Nrf2) and reducing nuclear factor kappa B (NF-κB) expressions. Additionally, PF extract was found to mechanistically prevent muscle atrophy by inhibiting Fbxo32, Trim63, and B-cell lymphoma 2 (BCL2)-associated X (Bax) expressions, while enhancing Bcl2 expression. We also found that PF extract mitigated muscle IR by upregulation of the insulin receptor substrate-1/phosphatidylinositol-3 kinase/protein kinase B (IRS-1/PI3K/AKT) pathway and Slc2a4 expression. The findings indicate that PF extract can prevent skeletal muscle loss and IR in obesity by modulating oxidative stress, inflammation, and activating IRS-1/PI3K/AKT signaling pathway. - Source: PubMed
Chobsuay NraratChonpathompikunlert PennapaSrivilai JukkarinMalakul WachirawadeeLimpeanchob NanteetipAimjongjun SathidTunsophon Sakara - In Uganda, where malaria transmission is high, insecticide treated nets (ITNs) have been distributed nationwide every 3 years since 2013. In West Nile, northern Uganda, indoor residual spraying (IRS) was first implemented with clothianidin-deltamethrin (Fludora Fusion®) in 2022, followed by pirimiphos-methyl (Actellic® 300CS) in 2023. We utilised a quasi-experimental study to assess the impact of IRS + ITNs on malaria incidence in West Nile. - Source: PubMed
Publication date: 2026/05/05
Namuganga Jane FMcDermott Daniel PEpstein AdrienneNankabirwa Joaniter IGonahasa SamuelOpigo JimmyNabende IsaiahMaiteki-Sebuguzi CatherineKamya Moses RDonnelly Martin JDorsey GrantStaedke Sarah G