Linked Life Data

11765062

Source:http://linkedlifedata.com/resource/pubmed/id/11765062

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-12-17
pubmed:abstractText
Growth arrest induced by DNA damage in mammalian cells requires the function of the retinoblastoma tumor suppressor protein (RB). RB-deficient cells cannot undergo G1, mid-S or G2 arrest following DNA damage, although they can activate the G2 checkpoint, which is reversible. RB-deficient cells are also hypersensitive to DNA damage-induced apoptosis. Induction of apoptosis in RB wild-type cells is associated with the loss of RB protein through cleavage by caspase. Two substitution mutations in exon 25 of the Rb gene have been created in the mouse germline to generate the Rb-MI allele that codes for a caspase-resistant RB protein. The RB-MI protein desensitizes cells to apoptosis. Taken together, these results suggest that RB plays a critical role in determining the cell fate following DNA damage. Growth arrest is dependent on RB and apoptosis is activated following RB degradation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0284-186X
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
689-95
pubmed:dateRevised
2009-5-12
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Role of retinoblastoma tumor suppressor protein in DNA damage response.
pubmed:affiliation
Division of Biology and the Cancer Center, University of California, San Diego, La Jolla, USA. jywang@ucsd.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't