Sister chromatid exchange induction and cell cycle inhibition by aniline and its metabolites in human fibroblasts

1981 ◽  
Vol 3 (6) ◽  
pp. 627-638 ◽  
Author(s):  
James L. Wilmer ◽  
Andrew D. Kligerman ◽  
Gregory L. Erexson
Keyword(s):  
Cell Cycle ◽  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Fibroblasts ◽  
Cell Cycle Inhibition

DNA-mediated transfer of a human DNA repair gene that controls sister chromatid exchange

1985 ◽  
Vol 5 (4) ◽  
pp. 881-884
Author(s):  
L H Thompson ◽  
K W Brookman ◽  
J L Minkler ◽  
J C Fuscoe ◽  
K A Henning ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Chinese Hamster Cell Line ◽  
Dna Strand ◽  
Repair Defect

The Chinese hamster cell line mutant EM9, which has a reduced ability to repair DNA strand breaks, is noted for its highly elevated frequency of sister chromatid exchange, a property shared with cells from individuals with Bloom's syndrome. The defect in EM9 cells was corrected by fusion hybridization with normal human fibroblasts and by transfection with DNA from hybrid cells. The transformants showed normalization of sister chromatid exchange frequency but incomplete correction of the repair defect in terms of chromosomal aberrations produced by 5-bromo-2'-deoxyuridine.

scholarly journals DNA-mediated transfer of a human DNA repair gene that controls sister chromatid exchange.

1985 ◽  
Vol 5 (4) ◽  
pp. 881-884 ◽  
Author(s):  
L H Thompson ◽  
K W Brookman ◽  
J L Minkler ◽  
J C Fuscoe ◽  
K A Henning ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Chinese Hamster Cell Line ◽  
Dna Strand ◽  
Repair Defect

The Chinese hamster cell line mutant EM9, which has a reduced ability to repair DNA strand breaks, is noted for its highly elevated frequency of sister chromatid exchange, a property shared with cells from individuals with Bloom's syndrome. The defect in EM9 cells was corrected by fusion hybridization with normal human fibroblasts and by transfection with DNA from hybrid cells. The transformants showed normalization of sister chromatid exchange frequency but incomplete correction of the repair defect in terms of chromosomal aberrations produced by 5-bromo-2'-deoxyuridine.

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