14.3.3 sigma antibody
- Known as:
- 14.3.3 sigma (anti-)
- Catalog number:
- 70r-7629
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- 14.3.3 sigma antibody
Related genes to: 14.3.3 sigma antibody
- Gene:
- AP3S2 NIH gene
- Name:
- adaptor related protein complex 3 subunit sigma 2
- Previous symbol:
- -
- Synonyms:
- sigma3b
- Chromosome:
- 15q26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2018-05-03
- Gene:
- PPP1R16A NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 16A
- Previous symbol:
- -
- Synonyms:
- MGC14333, MYPT3
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-29
- Date modifiied:
- 2015-11-18
Related products to: 14.3.3 sigma antibody
Related articles to: 14.3.3 sigma antibody
- Gestational diabetes mellitus (GDM) is hyperglycaemia first identified during pregnancy. Because GDM and type 2 diabetes mellitus (T2DM) share insulin resistance and β-cell dysfunction, T2DM variants may also influence the risk of GDM. This study examined the association of three genome-wide association study (GWAS)-identified T2DM variants, AP3S2 rs2028299 (C>A), ST6GAL1 rs16861329 (C>T), and VPS26A rs1802295 (C>T), with GDM susceptibility in pregnant women from North India. - Source: PubMed
Publication date: 2026/01/18
Shakir ZoyaPandey AmitaA Alsayegh AbdulrahmanFahad Alshahrani AbrarAshfaq FauziaKhan MohammadAli Wahid - This study investigated the interventional effects of dietary itaconic acid (ITA) on high-fat diet (HFD)-induced lipid deposition in largemouth bass () and the underlying mechanisms. Results showed that ITA supplementation significantly alleviated HFD-induced growth performance inhibition, as indicated by increased weight gain rate, increased specific growth rate, and reduced feed conversion ratio. ITA supplementation effectively reversed the HFD-induced increase in the hepatosomatic index, intraperitoneal fat ratio, serum triglycerides, total cholesterol, low-density lipoprotein/high-density lipoprotein ratio, hepatic lipid droplet accumulation, and hepatocyte vacuolation. Importantly, ITA ameliorated HFD-induced impairment of antioxidant capacity and reduced liver alanine aminotransferase and aspartate aminotransferase activities. Liver metabolomics revealed that ITA reduced levels of 20 fatty acids, 14 acylcarnitines, and 13 glycerides, suggesting enhanced fatty acid oxidation and reduced lipid esterification. Transcriptome sequencing and q-PCR validation demonstrated that ITA activated the AMPK/mTOR pathway, upregulating autophagy-related genes (, , , ) and lysosomal biogenesis-related genes (, , , ), thereby enhancing autophagic-lysosomal flux and promoting lipid degradation. In conclusion, ITA reduces hepatic lipid accumulation by synergistically activating autophagy and lysosomal biogenesis, thereby facilitating the oxidative degradation of fatty acids within lysosomes. This study provides a theoretical basis for the application of ITA as a functional feed additive in aquaculture. - Source: PubMed
Publication date: 2025/12/20
Li XueWang ShidongZhang MuziLi MingChen Chao - This case-control study investigated the association of three novel South Asian genome-wide association studies (GWAS)-derived type 2 diabetes mellitus (T2DM) susceptibility gene polymorphisms in the North Indian population. - Source: PubMed
Publication date: 2025/05/02
Shakir ZoyaSiddiqui Kauser UHimanshu DanduAli Wahid - The biological function of lysosomes has been increasingly appreciated in cancer. However, the relationship between lysosome and lung adenocarcinoma (LUAD) was not well understood. In this study, a lysosome-related signature was developed for LUAD risk stratification and prognosis prediction. - Source: PubMed
Publication date: 2024/12/04
Ye WeiSun LinFu CongDong HuajieZhou Tong - Aberrant activation of tropomyosin receptor kinases (TRKs) is a well-defined oncogenic driver for neurotrophic tropomyosin receptor kinase (NTRK)-fusion cancers, and acquired resistant mutations have emerged with clinical use of the first-generation TRK inhibitors. Here we present BPI-28592, a novel second-generation TRK inhibitor with efficacy against TRK fusion-positive cancers, including those with resistant mutations. Docking simulations indicated no steric hindrance between BPI-28592 and TRK mutants, suggesting its potential to overcome drug resistance. Biochemical assays showed strong inhibition and high selectivity against TRKA, TRKB, and TRKC. The inhibitor significantly reduced cell proliferation and blocked TRK signaling. In vivo studies demonstrated effective tumor suppression in xenograft models harboring TRK fusions with or without resistant mutations. Clinically, BPI-28592 achieved a complete response in a patient with malignant melanoma carrying an AP3S2-NTRK3 fusion (Clinicaltrials. gov identifier: NCT05302843). - Source: PubMed
Publication date: 2024/09/11
Sheng JinChen HongFu BangPan HongmingWang JiabingHan Weidong