Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-2-13
pubmed:abstractText
The utilization of dCTP derived from de novo synthesis through ribonucleotide reductase in exponentially growing CCRF-CEM cells was compared with the metabolic fate of dCTP produced by the salvage pathway. Exogenous dCyd was not effectively incorporated into replicating DNA; instead, dCTP derived from ribonucleotide reductase (labeled by [5-3H]Cyd) was the main precursor for that purpose, apparently because of functional compartmentation of the dCTP pool in these cells. Studies of the metabolic route of incorporation of exogenous [5-3H]dCyd into DNA of growing CCRF-CEM cells demonstrated that it was mainly incorporated through the DNA repair pathway. Incorporation of [5-3H]dCyd into DNA of synchronized cell populations was maximal in G1 cells, whereas [3H]dThd incorporation occurred predominantly in S phase cells. When cellular DNA was density labeled by incubation with BrdUrd, repaired DNA, which was less dense than replicated DNA, was preferentially labeled by [5-3H]dCyd. In contrast, replicated DNA was labeled by both [3H]dThd and [5-3H]Cyd. The DNA-damaging agents methylmethanesulfonate, ultraviolet irradiation, and gamma-irradiation inhibited [3H]dThd incorporation, whereas they stimulated the accumulation of [5-3H]dCyd in DNA. Based on these results, we propose that the dCTP pool is functionally compartmentalized in growing CCRF-CEM cells. dCTP derived from the salvage pathway is utilized predominantly for DNA repair, whereas the de novo pathway supplies dCTP for DNA replication.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
270
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
631-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Functional compartmentation of dCTP pools. Preferential utilization of salvaged deoxycytidine for DNA repair in human lymphoblasts.
pubmed:affiliation
Department of Clinical Investigation, University of Texas M. D. Anderson Cancer Center, Houston 77030.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't