Abstract:
:We have identified a novel mammalian protein, MIR1, with microtubule-binding activity. MIR1 is a relative of MID1/midin, the protein implicated in Opitz G/BBB syndrome. In tissue culture cells, MIR1 is enriched at the centrosome. MIR1 dissociates from centrosomes at the G2/M transition and is recruited back to spindle poles during anaphase. When overexpressed during interphase, MIR1 binds along microtubule filaments, which become stabilized, bundled and detached from the centrosome. In mitosis, overexpressed MIR1 dissociates from microtubules but still affects the normally focused localization of gamma-tubulin in spindle poles. Tight binding to microtubules in interphase appears to require an oligomeric state of MIR1, and phosphorylation in mitosis at predicted cyclin-dependent kinase (cdk) sites weakens the interaction.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Stein PA,Toret CP,Salic AN,Rolls MM,Rapoport TAkeywords:
subject
Has Abstractpub_date
2002-09-01 00:00:00pages
3389-402issue
Pt 17eissn
0021-9533issn
1477-9137journal_volume
115pub_type
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