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Literature summary for 2.4.1.222 extracted from

  • Kato, T.M.; Kawaguchi, A.; Kosodo, Y.; Niwa, H.; Matsuzaki, F.
    Lunatic fringe potentiates Notch signaling in the developing brain (2010), Mol. Cell. Neurosci., 45, 12-25.
    View publication on PubMed
Search for more literature for 2.4.1.222

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
[Notch]-fucose + UDP-alpha-D-N-acetylglucosamine Mus musculus Fringe genes encode beta-1,3-N-acetyl-glucosaminyltransferases, which elongate O-fucose on the EGF repeat of Notch and its ligands [Notch]-(3-O-beta-D-N-acetylglucosaminyl)fucose + UDP
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Organism

Organism UniProt Comment Textmining
Mus musculus
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 gene lfng
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Source Tissue

Source Tissue Comment Organism Textmining
brain in the developing brain, Lfng is expressed in self-renewing progenitors Mus musculus
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
[Notch]-fucose + UDP-alpha-D-N-acetylglucosamine
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 Mus musculus [Notch]-(3-O-beta-D-N-acetylglucosaminyl)fucose + UDP
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 ?
[Notch]-fucose + UDP-alpha-D-N-acetylglucosamine Fringe genes encode beta-1,3-N-acetyl-glucosaminyltransferases, which elongate O-fucose on the EGF repeat of Notch and its ligands Mus musculus [Notch]-(3-O-beta-D-N-acetylglucosaminyl)fucose + UDP
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 ?

Synonyms

Synonyms Comment Organism
beta-1,3-N-acetyl-glucosaminyltransferase
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 Mus musculus
LFNG
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 Mus musculus
Lunatic Fringe
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 Mus musculus

General Information

General Information Comment Organism
malfunction Lfng depletion does not affect the balance between neuronally committed cells and selfrenewing progenitors, irrespective of the cell density of Lfng-depleted cells, and causes no obvious defects in brain development, but in vivo overexpression of Lfng shows that it strongly augments Notch signaling mediated by Delta-like 1 but not Jagged 1, phenotypes, overview Mus musculus
physiological function Notch signaling is essential for the self-renewal of mammalian neural progenitor cells. A variety of mechanisms modulate Notch signaling to balance the self-renewal and differentiation of progenitor cells. Fringe is a major Notch regulator and promotes or suppresses Notch signaling, depending on the Notch ligands. Lfng potentiates Notch signaling cell autonomously in neural progenitor cells of developinmg brain. Lfng and Notch intracellular domain affect embryonic self-renewing progenitor cell identity and cell proliferation in a similar way Mus musculus