GO curators for mouse genes have assigned the following annotations to the gene product of Lfng. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene is a member of the fringe gene family which also includes radical and manic fringe genes. They all encode evolutionarily conserved glycosyltransferases that act in the Notch signaling pathway to define boundaries during embryonic development. While their genomic structure is distinct from other glycosyltransferases, fringe proteins have a fucose-specific beta-1,3-N-acetylglucosaminyltransferase activity that leads to elongation of O-linked fucose residues on Notch, which alters Notch signaling. This gene product is predicted to be a single-pass type II Golgi membrane protein but it may also be secreted and proteolytically processed like the related proteins in mouse and Drosophila (PMID: 9187150). Mutations in this gene have been associated with autosomal recessive spondylocostal dysostosis 3. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2009]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Lfng
participates in the following biological processes:
Hahn KL et al. (2005) Lunatic fringe null female mice are infertile due to defects in meiotic maturation. Development, 132:817-28. (PubMed:15659488)
Yang LT et al. (2005) Fringe glycosyltransferases differentially modulate Notch1 proteolysis induced by Delta1 and Jagged1. Mol Biol Cell, 16:927-42. (PubMed:15574878)
Zhang N et al. (2002) Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice. Genesis, 33:21-8. (PubMed:12001066)
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