SH3BGR Mouse Monoclonal Antibody
- Known as:
- SH3BGR Mouse Monoclonal Antibody
- Catalog number:
- ENZ-006450-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SH3BGR Mouse Monoclonal Antibody
Related genes to: SH3BGR Mouse Monoclonal Antibody
- Gene:
- SH3BGR NIH gene
- Name:
- SH3 domain binding glutamate rich protein
- Previous symbol:
- -
- Synonyms:
- 21-GARP
- Chromosome:
- 21q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2016-10-05
Related products to: SH3BGR Mouse Monoclonal Antibody
Related articles to: SH3BGR Mouse Monoclonal Antibody
- Total congenital cataract (TCC), a leading cause of childhood visual impairment. We analyzed transcriptome profiles of lens epithelial cells (LECs) and lens fiber cells (LFCs) in pediatric patients with TCC to identify differentially expressed genes (DEGs) and potential pathogenic pathways. - Source: PubMed
Publication date: 2026/05/26
Lin XiaoleiChen HuiyuLiu XinFan FanWang YulanLuo Yi - Non-suicidal self-injury (NSSI) is highly prevalent in recent years, but the genetic architecture remains unknown. We perform a multitrait analysis of genome-wide association study on NSSI, incorporating self-harm and suicide attempt. Common genetic variants account for 6.03% of NSSI variance. Three risk loci are associated with NSSI at 7q31.2 (rs62474683), DCC (rs4372758), and LCA5L/GET1/GET1-SH3BGR (rs2837022). Increased expression levels of GET1/SH3BGR in hippocampus relates to NSSI risk. Fine-mapping identifies seven likely causal variants, and colocalization with rs4281987 and rs2837022 evidences SH3BGR/GET1 expression in hippocampus to NSSI. In an independent sample, polygenic risk score for NSSI is associated with children's NSSI behavior, suicidal ideation, and suicide attempt (odds ratios [ORs]: 1.14-1.37). Reduction in right temporal pole volume mediates NSSI genetic liability for children's NSSI behavior. Walking for pleasure and exercises like swimming and bowling reduces NSSI risk, whereas smoking increases it. This study elucidates the NSSI genetic basis and its impact on children's emotions, behavior, and brain structure. - Source: PubMed
Publication date: 2025/05/09
Sun YaoyaoZhao GuoruiZhang YuyananLu ZheKang ZheweiSun JunyuanFeng XiaoyangGuo JingLiao YundanGuo LiangkunYang YangZhang DaiBi WenjianChen RunsenYue Weihua - The Sahiwal are among the most prominent international transboundary dairy cattle distributed in large numbers between India and Pakistan. With the elapse of more than seven decades after the independence and limited cross-border exchange of Sahiwal germplasm, one thought-provoking question arises as to whether natural and artificial selection could alter the genomic signature patterns in the Sahiwal, reared for different purposes in these two countries. Deciphering the genetic mechanisms that underlie economic traits is essential for advancement and long-term breeding plans that are reflected in the distinct selection signatures they carry. To identify these genomic signatures, three medium-density SNP datasets of Sahiwal from three geographical locations of India and Pakistan were analyzed, using De-Correlated Composite of Multiple Selection Signals technique to identify the major candidate genes. In the genome of Sahiwal, a total of 70 genomic regions with 261 protein-coding genes were found. Milk production (NEK11, HMGCS1, BTN1A1,KCNH3), reproduction (SH3BGR, PSMG1, BRWD1,B3GALT5) and immune response genes (BPIFB1, MCOLN2) were more closely related to the Indian Sahiwal. Pakistani Sahiwal had genes closely linked with the dual-purpose meat (RALGAPA2, RIN2, CFAP61), and milk (SLC24A3 GALNT17, BACH2) traits. Our findings revealed differential patterns of selection signatures in transboundary Sahiwal cattle. - Source: PubMed
Publication date: 2025/05/05
Muansangi LalTiwari JigyashaIlayaraja IrusappanKumar IshmeetVyas JayeshChitra AnilSingh Sanchit PalPal PritamGowane GopalMishra A KMukherjee AnupamaMukherjee Sabyasachi - Down syndrome (DS), caused by an additional chromosome 21, has a high risk of congenital heart defects (CHD), one of the primary causes of mortality in DS newborns. To elucidate the pathogenetic mechanisms underlying this condition, we explored the role of RNA m6A methylation, regulated by METTL3, in DS cardiac development and its impact on the expression of SH3BGR, a gene located at Down syndrome congenital heart disease (DS-CHD) minimal region. We analyzed DS fetal cardiac tissues to assess RNA m6A methylation levels and identify potential contributors. RNA sequencing was performed to detect differentially expressed genes in the same tissues. To further understand METTL3's function in heart development, we inactivated Mettl3 in the developing mouse heart to mimic the significantly reduced METTL3 observed in DS cardiac development. Additionally, human cardiomyocyte AC16 cells were used to investigate the molecular mechanism by which METTL3 regulates SH3BGR expression. Apoptosis was analyzed to evaluate METTL3's effect on heart development through SH3BGR regulation. Reduced m6A modification and decreased METTL3 expression were observed in human DS fetal hearts, along with a significant increase of SH3BGR expression. METTL3, through m6A modification, was found to regulate SH3BGR expression, by influencing mRNA stability. METTL3-deficient mouse embryos exhibited heart malformation with increased apoptosis, emphasizing its role in heart development. In DS hearts, METTL3 downregulation and SH3BGR upregulation, potentially orchestrated by abnormal m6A modification, contribute to gene dysregulation and apoptosis. This study reveals novel insights into DS cardiac pathology, highlighting the intricate role of METTL3 in DS congenital heart defects and presenting the m6A modification of SH3BGR as a potential therapeutic target. - Source: PubMed
Publication date: 2024/09/06
Shi WeiliChen RuiZhou MingjieLi YunianZhang YuweiWang JikuiHao BingtaoLiao Shixiu - The aim of the present work was to find an efficient method for safe and reliable expansion of human dental pulp cells (hDPCs) in vitro. Here, we examined the effect of a novel recombinant E8 fragment of Laminin-511 (iMatrix-511) in hDPCs regarding viability and cell spreading. Further, we investigated the underlying mechanisms governing its effects in hDPCs using RNA sequencing (RNA-seq). - Source: PubMed
Publication date: 2024/06/18
Tang JiaHuang Xiaofeng