IRS_1 (Phospho_Ser612) Antibody
- Known as:
- IRS_1 (Phospho_Ser612) Antibody
- Catalog number:
- E012093-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- IRS_1 (Phospho_Ser612) Antibody
Related genes to: IRS_1 (Phospho_Ser612) Antibody
- 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 (Phospho_Ser612) Antibody
Related articles to: IRS_1 (Phospho_Ser612) Antibody
- [This corrects the article DOI: 10.3892/ol.2018.9486.]. - Source: PubMed
Publication date: 2026/06/22
Jiang WenliMeng LinghongXu GuangmingLv CuitingWang HongliangTian HeChen RuohuaJiao BinghuaWang BinguiHuang Caiguo - Dysfunctional autophagy in ovarian granulosa cells (GCs) represents a key pathological feature of insulin resistance (IR) in polycystic ovary syndrome (PCOS), though regulatory roles of autophagy-associated lncRNAs remain poorly characterized. - Source: PubMed
Pan JingKurban RiyangulBo Xiaoli - Obesity that develops at different life stages may have distinct metabolic consequences, and the mechanisms distinguishing juvenile from adult-onset obesity remain incompletely defined. Thus, we examined how the timing of exposure to a high-fat diet (HFD) affects expansion, lipid metabolism, and insulin signaling in epididymal visceral adipose tissue (eVAT). - Source: PubMed
Publication date: 2026/06/30
Vratarić MilošAlempijević IsidoraBursać BiljanaTeofilović AnaVojnović Milutinović DanijelaDjordjevic Ana - Background Increasing evidence links metabolic dysregulation, insulin resistance, and endotoxin-induced inflammation to sporadic AD. A disruption of the PPARγ-adiponectin-AMPK-insulin pathway leads to neuroinflammation, Aβ buildup, tau hyperphosphorylation, and cognitive impairments. This study examined the neuroprotective effects of telmisartan and formononetin alone and in combination in metabolically primed AD-like rats. Methodology A two-hit model was employed to simulate metabolic endotoxemia-related sporadic Alzheimer's disease in male wistar rats. The model utilised chronic HFD feeding and systemic administration of LPS (250 µg/kg, i.p.). The animals received telmisartan, formonoetin, their combination, or a PPARγ inhibitor/ blocker. We evaluated metabolic parameters, cognitive performance, insulin resistance, inflammatory cytokines, adiponectin concentrations, cholinergic function, histopathology, and immunohistochemical markers of Aβ, tau, IRS-1, AMPK, and AKT signalling. Results The outcomes of HFD + LPS encompass weight gain, insulin resistance, inflammation, cholinergic dysfunction, neurotoxicity, elevated Aβ and tau pathology, and cognitive impairment. The therapy with telmisartan and formononetin enhanced these alterations in a dose-dependent manner, with the combination regimen demonstrating greater efficacy. The treatment reinstated adiponectin levels, enhanced AdipoR1-AMPK-AKT signalling, diminished pathogenic IRS-1 serine phosphorylation, reduced pro-inflammatory cytokines, maintained neuronal structure, and augmented recognition memory. The co-administration of PPARγ inhibitor/blocker abolished these protective effects, showing mediation reliance on PPARγ. Conclusion Telmisartan and formononetin have significant metabolic and neuroprotective advantages against AD generated by HFD and LPS through the activation of the PPARγ-adiponectin-AMPK-IRS-1-AKT signalling pathway. Targeting metabolic-inflammatory pathways using natural PPARγ modulators may aid in delaying or preventing sporadic AD associated with obesity, insulin resistance, and endotoxemia. - Source: PubMed
Publication date: 2026/06/30
Saini DigvijayaMujeeb MohdAkhtar MohammadHaque Syed EhtaishamulNajmi Abul Kalam - It is becoming more well acknowledged that type 2 diabetes mellitus (T2DM) is a metabolic and inflammatory condition linked to microbiota that involves interrelated disruptions in intestinal integrity, immune control, and insulin signalling. Butyrate-producing bacteria, such as Faecalibacterium prausnitzii and Roseburia spp., are reduced in gut dysbiosis in type 2 diabetes, whereas opportunistic Gram-negative pathobionts that cause endotoxemia and mucosal inflammation proliferate. Increased intestinal permeability makes it easier for lipopolysaccharide (LPS) to translocate and activate the TLR4/MyD88/IKKβ/NF-κB pathway. This increases the production of TNF-α, IL-6, MCP-1, and IL-1β, which disrupt insulin signalling by serine phosphorylation of IRS-1 and subsequent inhibition of PI3K/Akt/GLUT4 function. Concurrently, JNK and NLRP3 inflammasome pathway activation increases oxidative stress, caspase-1 activation, and inflammatory β-cell damage. Simultaneously, decreased microbial-derived short-chain fatty acid synthesis impairs GPR41/GPR43- and HDAC-mediated signalling, which in turn affects AMPK activation, mitochondrial function, and enteroendocrine release of GLP-1 and PYY. FXR-FGF19 and TGR5-cAMP signalling are further disrupted by altered bile acid biotransformation, which encourages hepatic gluconeogenesis, fat buildup, and insulin resistance. Moreover, dysregulated branched-chain amino acid metabolism and overactivation of the mTOR/S6K1 pathway lead to chronic low-grade inflammation and metabolic rigidity. When taken as a whole, these interrelated microbiota-host signalling pathways are significant mechanistic contributors to the pathophysiology of type 2 diabetes and new treatment targets. - Source: PubMed
Publication date: 2026/06/02
Chen YiJin DanruHan XueLiu XiaotingLiu YisiWang Li