Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-11-2
pubmed:abstractText
Preexposure of HL-60 cells to a DNA-damaging agent, cytosine arabinoside (Ara-C), dramatically induced the levels of H1 kinase activities associated with cyclin E (CycE-H1K) but not cyclin A. This induction was cell cycle-independent and accompanied by loss of cell viability, a late event in apoptosis. When an Ara-C-resistant variant of HL-60 cells were treated with Ara-C at a low concentration, neither CycE-H1K nor apoptosis were observed. Both events were induced in the resistant cells but only after treatment with Ara-C at a much higher concentration for a longer period. The DNA-damage-induced CycE-H1K is proposed to be involved in a late apoptosis checkpoint.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
214
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
771-80
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Activation of cyclin E-dependent kinase by DNA-damage signals during apoptosis.
pubmed:affiliation
Department of Pharmacology, University of Pittsburgh School of Medicine, PA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't