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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1990-3-22
pubmed:abstractText
Herbimycin A, an inhibitor of pp60src tyrosin kinase, caused src oncogene-expressed cells to become sensitive to contact inhibition, but did not affect ras oncogene-expressed cells. The cell lines tested were temperature sensitive v-src- and temperature sensitive v-ras-integrated nontransformed rat kidney cell line (NRK) (srctsNRK and rastsNRK, respectively) and a wild-type v-src-integrated NIH3T3 (src3T3). srctsNRK cells in densely populated cultures (plated at 1.25 x 10(4) cells/cm2), grown at 33 degrees C in the presence of 0.45 micrograms/ml of herbimycin A, ceased the cell cycle at the G0-G1 stage within 2 days, and the cells showed normal morphology. Upon removal of herbimycin A, the quiescent cells resumed the cell cycle in concert with morphological alteration from 'normal' to 'transformed', and proceeded through the S and M stages successively in a synchronized manner. Cells in the late S stage, compared with those in other stages of the cell cycle, were more sensitive to the killing effect of 5-fluorodeoxyuridine. Such synchronism of the cell cycle was not observed with sparsely populated cultures (2.5 x 10(3) cells/cm2); the cells resumed their asynchronous growth after removal of herbimycin A, although their morphology returned to 'transformed' as in the experiment with the densely populated cultures. The induction by herbimycin A of contact inhibition in densely populated cultures was also observed with src3T3 (grown at 37 degrees C) but not with rastsNRK (grown at 33 degrees C).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-8820
pubmed:author
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1831-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Induction by herbimycin A of contact inhibition in v-src-expressed cells.
pubmed:affiliation
Showa College of Pharmaceutical Sciences, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't