Linked Life Data

16762323

Source:http://linkedlifedata.com/resource/pubmed/id/16762323

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-6-20
pubmed:abstractText
Survivin is associated with Aurora B, inner centromere protein (INCENP), and borealin to form a chromosomal passenger complex that plays multiple roles during cell division. We used mutational analysis to study interaction of Survivin with Aurora B and the effect of this interaction on cell division. A Survivin mutant with the terminal domain deleted (Survivin 1-107) bound Aurora B as efficiently as Survivin wild type. This indicated that the proximal BIR domain of Survivin was responsible for Survivin binding to Aurora B. Survivin mutants (Surv-R18A, Surv-D53A, and Sur-KK78, and 79AA) all bound to Aurora B efficiently, but mutation in the conserved amino acid residues of the acidic patch on Survivin (Surv-DD70, 71AA) abolished the direct interaction of Survivin and Aurora B. The Survivin mutant (Surv-DD70, 71AA) localized diffusely in metaphase and failed to successfully accumulate in the midbody during cytokinesis. Furthermore, over-expression of the Survivin mutant (Surv-DD70, 71AA) severely disturbed cytokinesis, resulting in multinucleation in HeLa cell. This indicated that the direct interaction of Survivin and Aurora B was critical for the correct location of Survivin and the function of the Survivin complex in cell division.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
346
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
400-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Survivin mutant (Surv-DD70, 71AA) disrupts the interaction of Survivin with Aurora B and causes multinucleation in HeLa cells.
pubmed:affiliation
State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't