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anti-Human Manic Fringe Antikörper:
anti-Mouse (Murine) Manic Fringe Antikörper:
anti-Rat (Rattus) Manic Fringe Antikörper:
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MFNG imposes a negative correlation between Jag1 and Notch, being high Jag1 in the absence of MFNG predictive of poor prognosis.
Mfng is an oncogene acting through Notch-mediated induction of Pik3cg.
down regulated in Papillomavirus-mediated cervical neoplasia.
These results show that Notch signaling is finely calibrated in the cochlea via Lfng and Mfng 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.
each Fringe contributes to T and B cell development, and Fringe is required for optimal in vitro stimulation of T and B cells.
the presence of Gal on O-fucose glycans differentially affects DLL1-induced NOTCH signaling modulated by LFNG versus MFNG
The catalytic domain of murine Manic Fringe was expressed in the baculovirus/insect-cell system as a secreted protein
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
The structure of Manic Fringe reveals amino acid residues involved in recognition of donor substrates and catalysis, and a putative binding pocket for acceptor substrates. Mutations of several residues in this pocket impair Fringe activity in vivo.
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.
Lunatic Fringe (Lfng) and Manic Fringe (Mfng) cooperatively enhanced the DL1-Notch2 interaction to promote marginal zone B cell development
MFng colocalized with the proendocrine transcription factor Ngn3 in the developing mouse pancreas between embryonic days 9 and 14
Manic fringe is not required for embryonic development.
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