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- W1644335823 abstract "Mik1 was characterized via a genetic screen designed to identify mitotic inhibitors in the fission yeast, Schizosaccharomyce pombe(S. pombe). The mik1 gene complements the mitotic catastrophe defect in the double mutant strain, cdc2-3w wee1–50. It was sequenced and shown to be most homologous to the SpWee1 protein kinase that also complements cdc2-3w wee1–50. The mik1 gene disruption strain shows no apparent phenotype, but, the mik1::ura4 wee1–50 double mutant is inviable, suggesting that the two kinases have a redundant function in S. pombe: phosphorylation of the SpCdc2 protein kinase on Tyr15. The ATP-binding site is not completely conserved in Mik1. Instead of the GXGXXG motif, Mik1 has HXSXXS. However, mutation of the highly conserved lysine (K320A) results in a Mik1 that is unable to complement the mik1::ura wee1–50 double mutant. The wild-type mik1 and wee1 genes are able to complement the double mutant. Genetic analysis predicts that the substrate for Mik1 (and Wee1) is the Tyr15 residue of SpCdc2." @default.
- W1644335823 created "2016-06-24" @default.
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- W1644335823 date "1995-01-01" @default.
- W1644335823 modified "2023-09-27" @default.
- W1644335823 title "Mik1" @default.
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- W1644335823 doi "https://doi.org/10.1016/b978-012324719-3/50101-1" @default.
- W1644335823 hasPublicationYear "1995" @default.
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