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Literature summary for 2.4.1.255 extracted from

  • Pekkurnaz, G.; Trinidad, J.C.; Wang, X.; Kong, D.; Schwarz, T.L.
    Glucose regulates mitochondrial motility via Milton modification by O-GlcNAc transferase (2014), Cell, 158, 54-68.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Rattus norvegicus
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-
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Source Tissue

Source Tissue Comment Organism Textmining
hippocampus
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Rattus norvegicus
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neuron
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Rattus norvegicus
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
mitochondrial motor-adaptor protein milton + UDP-GlcNAc
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Rattus norvegicus ? + UDP mitochondrial motor-adaptor protein Milton is a required substrate for OGT to arrest mitochondrial motility by mapping and mutating the key O-GlcNAcylated serine residues ?

General Information

General Information Comment Organism
physiological function increased extracellular glucose decreases mitochondrial motility in hippocampal axons, and OGT overexpression reduces axonal mitochondrial motility and density. The mitochondrial motor-adaptor protein Milton is a required substrate for OGT to arrest mitochondrial motility by mapping and mutating the key O-GlcNAcylated serine residues Rattus norvegicus