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LFNG O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase

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] (from NCBI)
Top mentioned proteins: CLOCK, p300, delta1, Hes7, CAN
Papers on Lfng
Lunatic, Manic, and Radical Fringe Each Promote T and B Cell Development.
Stanley et al., New York City, United States. In J Immunol, Feb 2016
Lunatic, Manic, and Radical Fringe (LFNG, MFNG, and RFNG) are N-acetylglucosaminyltransferases that modify Notch receptors and regulate Notch signaling.
Hoxb6 can interfere with somitogenesis in the posterior embryo through a mechanism independent of its rib-promoting activity.
Mallo et al., Portugal. In Development, Jan 2016
In particular, Hoxb6 can disturb somitogenesis and anterior-posterior somite patterning by deregulating Lfng expression.
Lunatic Fringe is a potent tumor suppressor in Kras-initiated pancreatic cancer.
Xu et al., Jackson, United States. In Oncogene, Sep 2015
Here we report differential regulation of Notch receptors by Lunatic Fringe (Lfng), which encodes an O-fucosylpeptide 3-β-N-acetylglucosaminyltransferase known to modify epidermal growth factor repeats in the Notch extracellular domain, during pathogenesis of Kras-induced pancreatic ductal adenocarcinoma (PDAC).
O-fucosylation of DLL3 is required for its function during somitogenesis.
Gossler et al., Hannover, Germany. In Plos One, 2014
Loss of the DSL protein DLL3 in the mouse results in severe somite patterning defects, which are virtually indistinguishable from the defects in mice that lack lunatic fringe (LFNG), a glycosyltransferase involved in modifying Notch signaling.
On the origin of vertebrate somites.
Kuratani et al., Kōbe, Japan. In Zoological Lett, 2014
In vertebrates, the somite segmental boundary is determined by Notch signalling and the antagonistic relationship of the downstream targets of Notch, Lfng, and Delta1 in the anterior PSM.
Lunatic fringe deficiency cooperates with the Met/Caveolin gene amplicon to induce basal-like breast cancer.
Egan et al., Toronto, Canada. In Cancer Cell, 2012
Reduced LFNG expression facilitates JAG/NOTCH luminal progenitor signaling and cooperates with MET/CAVEOLIN basal-type signaling to promote basal-like breast cancer.
Galactose differentially modulates lunatic and manic fringe effects on Delta1-induced NOTCH signaling.
Stanley et al., New York City, United States. In J Biol Chem, 2012
the presence of Gal on O-fucose glycans differentially affects DLL1-induced NOTCH signaling modulated by LFNG versus MFNG
Mutations in the Notch pathway alter the patterning of multifidus.
Wilson-Rawls et al., Phoenix, United States. In Anat Rec (hoboken), 2012
Intriguing changes are observed in the cranio-caudal borders of multifidus muscle in mutant Dll3 and Lfng models of idiopathic scoliosis.
A multi-cell, multi-scale model of vertebrate segmentation and somite formation.
Glazier et al., Bloomington, United States. In Plos Comput Biol, 2011
For reasonable initial conditions, 2D simulations of our model robustly generate spatially and temporally regular somites, realistic dynamic morphologies and spontaneous emergence of anterior-traveling stripes of Lfng.
Lunatic Fringe prolongs Delta/Notch-induced self-renewal of committed αβ T-cell progenitors.
Guidos et al., Toronto, Canada. In Blood, 2011
Decreasing Lfng expression during the (TCR-CD4/CD8 double negative 3) DN3-DP (CD4/CD8 double positive) transition minimizes the potent leukemogenic potential of Notch1 signaling.
Lunatic fringe enhances competition for delta-like Notch ligands but does not overcome defective pre-TCR signaling during thymocyte beta-selection in vivo.
Guidos et al., Toronto, Canada. In J Immunol, 2010
data reveal that Lfng enhances CD4/CD8 double-negative 3b precursor competition for intrathymic Delta-like Notch ligands to maximize Notch-induced clonal expansion during the earliest stage of beta-selection.
The role of Notch in patterning the human vertebral column.
Dunwoodie, Sydney, Australia. In Curr Opin Genet Dev, 2009
More specifically it describes that mutations in genes encoding Notch pathway components (DLL3, MESP2, LFNG and HES7) cause severe congenital vertebral defects in humans.
Regulation of Notch signaling during T- and B-cell development by O-fucose glycans.
Guidos et al., New York City, United States. In Immunol Rev, 2009
The combined data show that Lfng and Mfng regulate T-cell development by enhancing the interactions of Notch1 in T-cell progenitors with Dll4 on thymic epithelial cells.
Lunatic and manic fringe cooperatively enhance marginal zone B cell precursor competition for delta-like 1 in splenic endothelial niches.
Guidos et al., Toronto, Canada. In Immunity, 2009
Lunatic Fringe (Lfng) and Manic Fringe (Mfng) cooperatively enhanced the DL1-Notch2 interaction to promote marginal zone B cell development
Mutation of the fucose-specific beta1,3 N-acetylglucosaminyltransferase LFNG results in abnormal formation of the spine.
Dunwoodie, Sydney, Australia. In Biochim Biophys Acta, 2009
Here, mutation in Notch pathway genes demonstrates that Notch signaling is also required for normal somite formation and vertebral column development in humans; of particular interest here is mutation of the LUNATIC FRINGE (LFNG) gene, which causes SCD type 3. LUNATIC FRINGE encodes for a fucose-specific beta1,3-N-acetylglucosaminyltransferase, which modifies Notch receptors and alters Notch signaling activity.
Oscillator mechanism of Notch pathway in the segmentation clock.
Niwa et al., Kyoto, Japan. In Dev Dyn, 2007
The basic helix-loop-helix factor Hes7, a Notch effector, is cyclically expressed by negative feedback and regulates cyclic expression of Lunatic fringe (Lfng), a Notch modulator.
Regulation of T lymphopoiesis by Notch1 and Lunatic fringe-mediated competition for intrathymic niches.
Guidos et al., Toronto, Canada. In Nat Immunol, 2006
The ability of Lfng and Notch1 to control progenitor competition for limiting cortical niches is an important mechanism for the homeostatic regulation of thymus size.
The Mesp2 transcription factor establishes segmental borders by suppressing Notch activity.
Saga et al., Mishima, Japan. In Nature, 2005
Genetic and biochemical studies indicate that this interface is generated by suppression of Notch activity by mesoderm posterior 2 (Mesp2) through induction of the lunatic fringe gene (Lfng).
Periodic notch inhibition by lunatic fringe underlies the chick segmentation clock.
Pourquie et al., Marseille, France. In Nature, 2003
Here we show that the protein product of the cyclic gene lunatic fringe (Lfng), which encodes a glycosyltransferase that can modify Notch activity, oscillates in the chick presomitic mesoderm.
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