FREM2
- Known as:
- FREM2
- Catalog number:
- Y214428
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FREM2
Related genes to: FREM2
- Gene:
- FREM2 NIH gene
- Name:
- FRAS1 related extracellular matrix 2
- Previous symbol:
- -
- Synonyms:
- DKFZp686J0811
- Chromosome:
- 13q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-15
- Date modifiied:
- 2019-04-08
Related products to: FREM2
Related articles to: FREM2
- Posterior urethral valves (PUV) are the most common cause of lower urinary tract obstruction in male infants, occurring in 1 in 4000 live male births and constituting a significant cause of urinary obstruction, long-term complications and end-stage renal disease (ESRD) in children. PUV is a multifactorial pathology, involving both genetic and environmental contributions. Congenital anomalies of the kidney and urinary tract (CAKUT), such as renal agenesis, hypoplasia and vesicoureteral reflux, share etiological and phenotypic overlap with PUV. While CAKUT can arise from monogenic causes, the specific genetic factors remain poorly understood. - Source: PubMed
Publication date: 2026/03/13
Sharma JyotiKumar SourabhPandey HimaniMukherjee SampreetiJain VisheshYadav Devendra KumarDhua Anjan KumarAfroz MasarratDhikav VikasKumar NeetaLal DeviGoel Prabudh - Could follicular fluid-derived extracellular vesicles (ffEVs) benefit human oocyte rescue maturation (rIVM)? - Source: PubMed
Publication date: 2026/03/09
Makieva SofiaSaenz-de-Juano Mara DAlmiñana CarmenBauersachs StefanBernal-Ulloa SandraXie MinVelasco Ana GCervantes NataliaSachs MaikeUlbrich Susanne ELeeners Brigitte - To characterize the prenatal phenotypic spectrum, genetic findings, and pregnancy outcomes of fetal renal agenesis (RA), and to clarify the complementary roles of chromosomal microarray analysis (CMA) and whole exome sequencing (WES) in phenotype-stratified prenatal evaluation. - Source: PubMed
Publication date: 2026/01/31
Zhang NaHuang RuibinFu FangZhou HangLi RuLiao Can - Fraser syndrome (FS) is an autosomal recessive inherited malformation disorder characterized by cryptophthalmos, syndactyly, and abnormalities of the respiratory and urogenital tracts. Variants in the FRAS1-related extracellular matrix 2 (FREM2) gene are the major genetic cause. However, clinical diagnosis remains challenging due to phenotypic heterogeneity. - Source: PubMed
Publication date: 2025/12/04
Wei WeidongFan YinanSong JiaqiLou YedanZhang TaoYuan HuaJin JieyuanZhang SinanJin Xin - The mechanisms regulating organ size remain poorly understood. Here, we show that FREM2 is a critical modulator of lung size. Frem2 mutant mice exhibit defects in the formation of elastic fibers around mesothelial cells, which compromises phosphorylated myosin light chain (pMLC) signaling and mesothelial cell polarization, leading to lung growth inhibition. These processes are regulated in part through inhibition of p38-mediated upregulation of matrix metalloproteinase-2, as pharmacological decrease of p38 phosphorylation or MMP activity partially attenuates the Frem2 mutant lung phenotypes. Disruption of ROCK function also leads to defects in elastic fiber organization and mesothelial cell polarity, while inhibition of Vangl2-regulated mesothelial cell polarity causes defects in pMLC abundance and elastic fiber structure. Collectively, these processes constitute a positive feedback loop to regulate lung size. Notably, Frem2 mutant mice also display defects in the formation of the mesothelium and reduced growth of other internal organs. Importantly, patients with FREM2 mutations exhibit smaller lungs. These results reveal a shared role and mechanism for the mesothelium in organ size control. - Source: PubMed
Publication date: 2025/10/30
Liu XinyuanLin BingyingLi PeiyiCai ZhiqiangCao WeitaoYang WeipingZeng JiahangLi LeZhou YuminHuang DanpingStainier Didier Y RRan PixinYin Wenguang