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Mfng is an oncogene (show RAB1A ELISA Kits) acting through Notch (show NOTCH1 ELISA Kits)-mediated induction of Pik3cg (show PIK3CG ELISA Kits).
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 ELISA Kits) on O-fucose glycans differentially affects DLL1 (show DLL1 ELISA Kits)-induced NOTCH (show NOTCH1 ELISA Kits) signaling modulated by LFNG (show LFNG ELISA Kits) versus MFNG
Myt1 (show MYT1 ELISA Kits), Myt3, and Ngn3 (show NEUROG3 ELISA Kits) are induced by Mfng and have roles in Mfng-mediated repression of Notch (show NOTCH1 ELISA Kits) signaling which could serve as a trigger for endocrine islet differentiation
Jag1 (show JAG1 ELISA Kits)/fringe genes (Lfng (show LFNG ELISA Kits), Rfng (show RFNG ELISA Kits), 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 ELISA Kits)) and Manic Fringe (Mfng) cooperatively enhanced the DL1-Notch2 (show NOTCH2 ELISA Kits) interaction to promote marginal zone B cell development
MFng colocalized with the proendocrine transcription factor Ngn3 (show NEUROG3 ELISA Kits) 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