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MFNG O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase

This gene is a member of the fringe gene family which also includes radical and lunatic fringe genes. They all encode evolutionarily conserved secreted proteins that act in the Notch receptor pathway to demarcate 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. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: Lfng, p300, delta1, Ags, Epidermal Growth Factor
Papers on Mfng
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.
Sequential Notch activation regulates ventricular chamber development.
de la Pompa et al., Madrid, Spain. In Nat Cell Biol, Jan 2016
We show that Notch signalling first connects chamber endocardium and myocardium to sustain trabeculation, and later coordinates ventricular patterning and compaction with coronary vessel development to generate the mature chamber, through a temporal sequence of ligand signalling determined by the glycosyltransferase manic fringe (MFng).
A 10-gene expression signature of Notch pathway predicts recurrence in ovarian carcinoma.
Liu et al., Weifang, China. In Oncol Lett, Sep 2015
A 10-gene signature (FZD4, HES1, PSEN2, JAG2, PPARG, FOS, HEY1, CDC16, MFNG, and EP300) was identified and validated that is associated with recurrence-free survival time, but not with overall survival time, in the TCGA dataset and in other two independent datasets, GSE9891 and GSE30161.
Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.
Xu et al., Changsha, China. In Cancer Res, Jun 2015
Here, we report that Manic Fringe (Mfng), which encodes an O-fucosylpeptide 3-β-N-acetylglucosaminyltransferase known to modify EGF repeats in the Notch extracellular domain, is highly expressed in CLBC and functions as an oncogene in this context.
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
Fringe controls naïve CD4(+)T cells differentiation through modulating notch signaling in asthmatic rat models.
Guo et al., Shanghai, China. In Plos One, 2011
We found that Radical Fringe (Rfng) was highly expressed, whereas both Lunatic Fringe (Lfng) and Manic Fringe (Mfng) were expressed at low levels.
Identification and validation of genes involved in gastric tumorigenesis.
Ramakrishnan et al., Chennai, India. In Cancer Cell Int, 2009
RESULTS: Seventeen genes (ASPN, CCL15/MIP-1δ, MMP3, SPON2, PRSS2, CCL3, TMEPAI/PMEPAI, SIX3, MFNG, SOSTDC1, SGNE1, SST, IGHA1, AKR1B10, FCGBP, ATP4B, NCAPH2) were shown to be differentially expressed between the tumours and the paired normal, for the first time.
Jagged1 is a competitive inhibitor of Notch signaling in the embryonic pancreas.
Kaestner et al., Philadelphia, United States. In Mech Dev, 2009
Expression of the Notch modifier Manic Fringe (Mfng) is limited to endocrine precursors, providing a possible explanation for the inhibition of Notch signaling by Jag1 during mid-gestation embryonic pancreas development.
Manic fringe is not required for embryonic development, and fringe family members do not exhibit redundant functions in the axial skeleton, limb, or hindbrain.
Cole et al., Princeton, United States. In Dev Dyn, 2009
Manic fringe is not required for embryonic development.
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.
MFng is dispensable for mouse pancreas development and function.
Edlund et al., Umeå, Sweden. In Mol Cell Biol, 2009
MFng colocalized with the proendocrine transcription factor Ngn3 in the developing mouse pancreas between embryonic days 9 and 14
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
Bile duct proliferation in Jag1/fringe heterozygous mice identifies candidate modifiers of the Alagille syndrome hepatic phenotype.
Loomes et al., Philadelphia, United States. In Hepatology, 2008
Jag1/fringe genes (Lfng, Rfng, and Mfng) may regulate postnatal bile duct growth and remodeling, and serve as candidate modifiers of the hepatic phenotype in Alagille syndrome.
The fringe molecules induce endocrine differentiation in embryonic endoderm by activating cMyt1/cMyt3.
Gu et al., Nashville, United States. In Dev Biol, 2006
Myt1, Myt3, and Ngn3 are induced by Mfng and have roles in Mfng-mediated repression of Notch signaling which could serve as a trigger for endocrine islet differentiation
EWS/FLI1-induced manic fringe renders NIH 3T3 cells tumorigenic.
Denny et al., Birmingham, United States. In Nat Genet, 1997
We have found that EWS/FLI1 and structurally related fusion proteins upregulate manic fringe (MFNG), a recently described member of the Fringe gene family instrumental in somatic development.
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