Linked Life Data

9036857

Source:http://linkedlifedata.com/resource/pubmed/id/9036857

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5304
pubmed:dateCreated
1997-3-18
pubmed:abstractText
The molecular mechanisms that link cell-cycle controls to the mitotic apparatus are poorly understood. A component of the Saccharomyces cerevisiae spindle, Ase1, was observed to undergo cell cycle-specific degradation mediated by the cyclosome, or anaphase promoting complex (APC). Ase1 was degraded when cells exited from mitosis and entered G1. Inappropriate expression of stable Ase1 during G1 produced a spindle defect that is sensed by the spindle assembly checkpoint. In addition, loss of ASE1 function destabilized telophase spindles, and expression of a nondegradable Ase1 mutant delayed spindle disassembly. APC-mediated proteolysis therefore appears to regulate both spindle assembly and disassembly.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
275
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1311-4
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
APC-mediated proteolysis of Ase1 and the morphogenesis of the mitotic spindle.
pubmed:affiliation
Department of Pediatric Oncology, The Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't