Ask about this productRelated genes to: LFNG antibody
- Gene:
- LFNG NIH gene
- Name:
- LFNG O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase
- Previous symbol:
- -
- Synonyms:
- SCDO3
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-07
- Date modifiied:
- 2014-11-19
Related products to: LFNG antibody
Related articles to: LFNG antibody
- A distinct form of chronic kidney disease of unknown etiology (CKDu) has emerged in tropical regions of Sri Lanka, predominantly affecting individuals aged 30-60 years in the North Central Province. Unlike conventional chronic kidney disease (CKD), CKDu occurs independently of diabetes or hypertension and is characterized by tubulointerstitial damage, including tubular atrophy, interstitial inflammation, and fibrosis. Epidemiological studies showed familial clustering, suggesting an underlying genetic predisposition. This study aimed to identify genetic variants associated with CKDu in Sri Lankan populations using whole-exome sequencing (WES). Eighty-six individuals (47 CKDu patients and 39 controls) were recruited from endemic and non-endemic regions. Physiological, biochemical, and geographic parameters were recorded. DNA extracted from blood was subjected to WES to identify variants associated with CKDu. Results: A total of 171 unique variants across 121 genes were identified. Among the most prevalent genes were , , , , and . In the case-control comparison, only showed statistically significant enrichment in affected individuals, whereas signals in , , and were not statistically significant, but have an association with renal dysfunction, and thus are included as hypothesis-generating variant observations. variants showed trends toward a protective haplotype. showed the greatest prevalence in affected individuals (71.7%), followed by (63%), (56%), (41%), and (32%). Conclusion: Findings suggest genetic variants in combination with environmental factors may contribute to CKDu susceptibility in the Sri Lankan population. We underscore the multi-factorial nature of CKDu and highlight the need for integrative genomic and environmental research to elucidate disease mechanisms and inform targeted prevention strategies. - Source: PubMed
Publication date: 2026/04/09
Tom WesleyWeerakoon ChiranFernando NirmaleeHasantha IsuruBandara ManojKrzyzanowski GaryNanayakkara ShanikaCosgrove DominicNanayakkara NishanthaFernando M Rohan - Centrosome amplification (CA) contributes to cancer but remains poorly characterized in non-neoplastic conditions such as pressure injuries (PI). This study investigated CA-related genes (CARGs) in PI to identify potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/09
Li SenShen HaoweiLi KunlinWang XinSun ZhaofeiLi YanpingYuan Yuhuan - Spondylocostal dysostosis (SCDO) is a rare disorder characterized by congenital malformations of the spine and ribs. SCDO affects 1 in 40,000 human births, with rare cases also reported in dogs. Mutations in , encoding a critical Notch signaling pathway ligand, account for a majority of human SCDO cases. The remaining cases have variants in , , , , and , which code for proteins in the Notch pathway. A mixed-breed litter of three dogs presented with varying degrees of spinal malformations and underwent comprehensive phenotyping including radiographic and neurologic examination. Two littermates demonstrated classic SCDO features including shortened torsos, vertebral malformations, and rib abnormalities, while a third showed only caudal vertebral truncation. - Source: PubMed
Publication date: 2026/01/26
Varney ScarlettVernau KarenBrown CraigToedebusch ChristineVo JuliaBannasch Danika - Identifying biological roles for glycosyltransferases is a continuing challenge and important for defining morbidities associated with congenital disorders of glycosylation. Here we investigate the consequences to intestinal development of conditionally deleting alone or and together in a mixed or -null genetic background. Each Fringe transfers N-acetylglucosamine (GlcNAc) to fucose (Fuc) attached to Ser or Thr by POFUT1 in a consensus sequence found in certain epithelial growth factor-like (EGF) repeats. EOGT transfers GlcNAc directly to Ser/Thr in a separate consensus sequence of the EGF repeat. Notch receptors and Notch ligands contain the largest number of EGF repeats with consensus sites for these O-glycans. Conditional deletion of in mouse intestine causes similar developmental defects to deletion of and or and . LFNG also contributes to optimal Notch signaling in mouse intestine. In this work, we generated [F/F]: -Cre and [F/F] [-/-] [-/-]: -Cre mice in which extension of O-Fuc on EGF repeats was inhibited or prevented in intestinal epithelium. Conditional deletion of either alone or all three Fringe activities together led to defective intestinal development with a marked increase in goblet and Paneth cells, increased crypt width and reduced villus length. Unexpectedly, in mice globally lacking EOGT, conditional inactivation of the three Fringe genes did not lead to defective intestinal development. Thus, the absence of EOGT prevented disruption of development in Fringe-null intestine, identifying a novel role for EOGT in regulating intestinal development. - Source: PubMed
Publication date: 2026/02/11
Nauman MohdStanley Pamela - Sprouting angiogenesis and blood vessel stabilization require precise coordination between endothelial cells (ECs) and pericytes. Bone Morphogenic Protein 9 (Bmp9), whose signaling through activin receptor-like kinase 1 (Alk1) is dysregulated in several diseases, was thought to regulate these processes by independently activating Notch target genes in an additive fashion with canonical Notch signaling. Here, through predictive computational modeling validated in mice, zebrafish, and human cell lines, we uncover that Bmp9 enhances Notch activity synergistically by upregulating Lunatic Fringe (Lfng) in ECs. Specifically, Bmp9-induced Lfng enhances Notch receptor activation, most strongly when Delta-like ligand 4 (Dll4) is also present. This Lfng regulation alters vessel branching by modulating the timing of EC phenotype selection and rearrangement during angiogenesis. Lfng also contributes to pericyte-driven vessel stabilization by mediating Jagged1 upregulation in Bmp9-stimulated ECs. In summary, Bmp9-upregulated Lfng enhances Dll4-Notch1 signaling in ECs and Jag1-Notch3 activation in pericytes, shaping angiogenic sprouting and stabilization outcomes. - Source: PubMed
Publication date: 2026/02/05
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