Ask about this productRelated genes to: Sh3gl3 antibody
- Gene:
- SH3GL3 NIH gene
- Name:
- SH3 domain containing GRB2 like 3, endophilin A3
- Previous symbol:
- -
- Synonyms:
- SH3D2C, SH3P13, CNSA3, EEN-B2, HsT19371
- Chromosome:
- 15q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2016-10-05
Related products to: Sh3gl3 antibody
Related articles to: Sh3gl3 antibody
- Insight into the conformational dynamics of proteins is essential toward understanding their function at a molecular level. The motions experienced by individual atoms in the protein can be precisely quantified through NMR relaxation rates, but their measurement requires well-resolved spectral responses. Two-dimensional H-N correlation spectra are the standard approach to resolve amide signals in protein NMR, but come with an excessive cost in experimental time when spectra are heavily congested due to limited N chemical shift dispersions. This limitation often thwarts the characterization of dynamics for intrinsically disordered proteins, especially when they feature low-complexity or homopolymer regions, or short sample life-times. Here, we introduce a fast, ultra-selective H-N 1D NMR method that allows high-quality measurement of individual N spin-relaxation constants, even when N resonances are merely 6-8 Hz apart. We demonstrate the new experiment by characterizing, for the first time, pico- to nanosecond dynamics along a 16-residue polyglutamine stretch within the protein huntingtin, the causal agent of Huntington's disease, as well as millisecond conformational exchange in the SH3GL3 protein. The new experiment will find wide application in the study of conformational dynamics of intrinsically disordered proteins or any other biomacromolecule that features highly dense H-N 2D spectra. - Source: PubMed
Publication date: 2026/02/17
Adamski WiktorLevy Geraldine RCantrelle François-XavierSinnaeve Davy - Ambient air pollution contributes to chronic obstructive pulmonary disease (COPD), but the genetic factors that may influence susceptibility remain poorly defined. We conducted a genome-wide interaction analysis to identify genetic markers that may modify the association between air pollution and COPD. We analyzed data from 16,839 Canadian Longitudinal Study of Aging participants, including spirometry, genome-wide genotype data (645,625 single-nucleotide polymorphisms [SNPs]), and air pollution exposure estimates. COPD was defined as a forced expiratory volume in 1 second to forced vital capacity ratio (FEV/FVC) below the lower limit of normal. Annual average concentrations of particulate matter (PM), nitrogen dioxide (NO), and ozone (O), representing multi-year exposure estimates (2012-2015), were assigned to participants' residential postal code. Logistic regression models with SNP-by-air-pollutant interaction terms were applied, with a significant interaction threshold set at p < 7.74 × 10 after Bonferroni correction. Significant interactions were observed between PM and rs3762953 in CEP72/TPPP (P = 4.82 × 10) and rs72802672 in WFDC1 (P5.62 × 10). For NO, significant interactions were observed with rs2585043 near ADAMTSL3/SH3GL3 (P4.01 × 10), rs6809120 in ADAMTS9 (P4.53 × 10), rs6761941 near EPCAM-DT/CALM2 (P5.12 × 10), rs113083358 in DLG2 (P6.44 × 10), and rs17801230 near FASTKD2/CPO (P4.69 × 10). These loci map to genes involved in microtubule and ciliary function, extracellular matrix remodeling and protease regulation, airway inflammation and smooth muscle contractility, and mitochondrial function. These findings highlight genetic modification of the association between air pollution and COPD susceptibility in low-exposure settings and offer mechanistic insight without implying direct clinical application. - Source: PubMed
Publication date: 2026/01/20
Odimba UgochukwuFarrell JamieSadatsafavi MohsenJiang XiantaGao Zhiwei - Endophilin A, a family of Bin-Amphoterisin-Rvs (BAR) domain-conserved proteins, is found in several tissues and is associated with disease pathogenesis. In patients with breast cancer, endophilin A expression pertains to boosted tumour cell endocytosis, migration, and invadopodia formation, potentially linked to a poor prognosis. - Source: PubMed
Publication date: 2025/10/08
Mehta VikrantIslam SohidulKasana HaritChander Harish - Egg weight is an economically important trait in the chicken, and affects the hatchability and chicks' performance in broiler breeding programs. Our comprehensive analysis of 22,375 chickens revealed that the hens' egg weight was linked to their body weight, egg production and hatchability, with higher egg weight potentially increasing the body weight and delaying the female sexual maturity. Egg weight is a dynamic trait, however, previous studies usually focused on single time point and overlooked the dynamic changes during egg-laying period. We performed both single and longitudinal genome-wide association studies in 2,350 hens, combining selective sweep analysis, to identify genetic variants. Then, we integrated multi-omics data of 40 chickens to determine key genes and metabolites. A multi-omics analysis identified 22 key candidate genes, such as ATF6, CSPG4, SH3GL3, C4, LMX1B, CDC34, and CCDC171, of which four (BSG, CFD, MAP2K2, and POLRMT) were associated with egg weights in the ChickenGTEx database. In particular, the SNP rs315726522 may regulate MAP2K2 and FSHB gene expression by modulating the binding of transcription factors, and the SNP rs738839430 caused amino acid change that affected function of CFD protein. This, in turn, affected gonadotropin expression within the GnRH signaling pathway, which ultimately influenced egg weights. Metabolomic analysis revealed 13 metabolites associated with oxidative stress and metabolism of fatty acids, which potentially influenced reproductive performance through stress reduction and hormonal regulation. This study comprehensively analyzed the effects of egg weight in broiler breeders and enhanced our understanding of the genetic mechanisms underlying egg weight in chickens. - Source: PubMed
Publication date: 2025/09/11
Ding JiqiangLiu XiangpingNawaz Ali HassanLeng DongLi NiGe DoudouLi DongfengFeng Chungang - In recent years, pulmonary infection caused by Klebsiella pneumoniae has been increasing in clinical practice, becoming one of the important pathogens threatening human health. Morukin, as a commonly used antibiotic, has a certain effect in the treatment of bacterial pneumonia, but the acute pulmonary inflammation caused by Morukin has also brought serious side effects to patients. Therefore, the aim of this study was to explore the molecular mechanism of SH3GL3 recombinant protein and investigate its effect on reducing acute pulmonary inflammation in the treatment of Klebsiella pneumoniae infection by modulating the STAT3/ROS signaling pathway. In this study, recombinant SH3GL3 protein was prepared by genetic engineering technology to establish an animal model of Klebsiella pneumoniae infection. The effect of recombinant SH3GL3 protein on acute pulmonary inflammation was evaluated by observing the pathological changes of lung tissue, inflammatory cell infiltration and expression levels of inflammatory factors in each group. Western blot, immunohistochemistry and other techniques were used to detect the expression and activity of STAT3 and ROS signaling pathway related proteins, in order to reveal the molecular mechanism of SH3GL3 recombinant protein in alleviating inflammation. In the SH3GL3 recombinant protein intervention group, the pathological changes of lung tissue were significantly reduced, the number of inflammatory cells was reduced, and the expression level of inflammatory factors was decreased. Further molecular mechanism studies have shown that SH3GL3 recombinant protein can significantly inhibit the phosphorylation and activation of STAT3 and reduce the production of ROS, thus inhibiting the activation of STAT3/ROS signaling pathway and alleviating pulmonary inflammation. The recombinant protein SH3GL3 effectively alleviates acute pulmonary inflammation in the treatment of Klebsiella pneumoniae infection with morukin by regulating the STAT3/ROS signaling pathway. - Source: PubMed
Publication date: 2025/03/20
Yueqing WangLei XuXu WangJiao WangLimin GuZhongbo Shang