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Mfng is an oncogene (show RAB1A Proteins) acting through Notch (show NOTCH1 Proteins)-mediated induction of Pik3cg (show PIK3CG Proteins).
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.
the presence of Gal (show GAL Proteins) on O-fucose glycans differentially affects DLL1 (show DLL1 Proteins)-induced NOTCH (show NOTCH1 Proteins) signaling modulated by LFNG (show LFNG Proteins) versus MFNG
Myt1 (show MYT1 Proteins), Myt3, and Ngn3 (show NEUROG3 Proteins) are induced by Mfng and have roles in Mfng-mediated repression of Notch (show NOTCH1 Proteins) signaling which could serve as a trigger for endocrine islet differentiation
Jag1 (show JAG1 Proteins)/fringe genes (Lfng (show LFNG Proteins), Rfng, and Mfng) may regulate postnatal bile duct growth and remodeling, and serve as candidate modifiers of the hepatic phenotype in Alagille syndrome.
Lunatic Fringe (Lfng (show LFNG Proteins)) and Manic Fringe (Mfng) cooperatively enhanced the DL1-Notch2 (show NOTCH2 Proteins) interaction to promote marginal zone B cell development
MFng colocalized with the proendocrine transcription factor Ngn3 (show NEUROG3 Proteins) in the developing mouse pancreas between embryonic days 9 and 14
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.
, beta-1,3-N-acetylglucosaminyltransferase manic fringe
, manic fringe homolog