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a potent tumor-suppressive function for Lfng
TGFBR2 (显示 TGFBR2 ELISA试剂盒) signaling can affect Notch1 (显示 NOTCH1 ELISA试剂盒) glycosylation via regulation of glycosyltransferase LFNG expression and provide a first mechanistic example for altered glycosylation in microsatellite instability colorectal tumor cells.
LFNG expression correlates with expansion of cancer stem cell populations and NKX3.1 (显示 NKX3-1 ELISA试剂盒) expression in human prostate cancer.
Reduced LFNG expression facilitates JAG/NOTCH (显示 NOTCH1 ELISA试剂盒) luminal progenitor signaling and cooperates with MET/CAVEOLIN basal-type signaling to promote basal-like breast cancer.
Mutation of the LFNG gene causes spondylocostal dysostosis with a severe vertebral phenotype, reinforcing the hypothesis that proper regulation of the Notch (显示 NOTCH1 ELISA试剂盒) signaling pathway is an absolute requirement for the correct patterning of the axial skeleton.
These results show that Notch (显示 NOTCH1 ELISA试剂盒) signaling is finely calibrated in the cochlea via Lfng and Mfng (显示 MFNG ELISA试剂盒) to produce precisely tuned levels of signaling that first set the boundary of the organ of Corti and later regulate hair cell development.
Fringe modifications at EGF8 and EGF12 enhanced Notch1 binding to and activation from Delta-like 1, while modifications at EGF6 and EGF36 (added by Manic and Lunatic but not Radical) inhibited Notch1 activation from Jagged1.
LFNG protein may have context-dependent effects on Notch (显示 NOTCH1 ELISA试剂盒) activity; somitogenesis is disrupted by a novel dominant allele of Lfng
Lfng expression and activity is normal in mice whose Lfng is lengthened by 10 kb, and no effects on segmentation are evident.
suggest that modulation of the Notch (显示 NOTCH1 ELISA试剂盒) signaling by Lfng affects the clock period during development
STAT5 (显示 STAT5A ELISA试剂盒)-dependent amplification of Notch (显示 NOTCH1 ELISA试剂盒)-modifying Lfng augments Th2 response via Dll4 (显示 DLL4 ELISA试剂盒) and is critical for amplifying viral exacerbation during allergic airway disease.
The repressive effect of Lfng against Notch (显示 NOTCH1 ELISA试剂盒) activities in neighbouring cells can sufficiently explain the synchronization in vivo.
Intriguing changes are observed in the cranio-caudal (显示 CAD ELISA试剂盒) borders of multifidus muscle in mutant Dll3 (显示 DLL3 ELISA试剂盒) and Lfng models of idiopathic scoliosis.
lfng regulates delta-notch (显示 NOTCH1 ELISA试剂盒) induction of hypochord.
The sequence and embryonic expression of lfng were studied.
Lfng acts in a feedback loop downstream of proneural genes.
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.
, beta-1,3-N-acetylglucosaminyltransferase lunatic fringe
, O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase
, lunatic fringe gene homolog
, lunatic fringe homolog