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Literature DB >> 468239

Further analysis of the replication bypass model for sister chromatid exchange.

Abstract

The replication bypass model for sister chromatid exchange (SCE) proposed by Shafer is examined in detail. When applied through two cell cycles, the model predicts that potentially observable SCEs induced during one S phase will then be cancelled and rendered undetectable during the subsequent S phase. This aspect of replication bypass is inconsistent with the observation of twin SCEs in tetraploid cells. Furthermore, the model cannot account for the efficient induction of SCEs by non-cross-linking chemical agents.

Mesh：

Substances：
Bromodeoxyuridine

Year: 1979 PMID： 468239 DOI： 10.1007/bf00277687

Source DB: PubMed Journal: Hum Genet ISSN： 0340-6717 Impact factor: 4.132

12 in total

5. Sister chromatid exchange as an assay for genetic damage induced by mutagen-carcinogens. I. In vivo test for compounds requiring metabolic activation.

Authors: D G Stetka; S Wolff
Journal: Mutat Res Date: 1976-12 Impact factor: 2.433

6. Insights on chromosome structure from sister chromatid exchange ratios and the lack of both isolabelling and heterolabelling as determined by the FPG technique.

Authors: S H Wolff; P Perry
Journal: Exp Cell Res Date: 1975-06 Impact factor: 3.905

1. Segregation of DNA polynucleotide strands into sister chromatids and the use of endoreduplicated cells to track sister chromatid exchanges induced by crosslinks, alkylations, or x-ray damage.

Authors: S Wolff; V Afzal
Journal: Proc Natl Acad Sci U S A Date: 1996-06-11 Impact factor: 11.205

Review 5. Sister chromatid exchange analysis.

Authors: S A Latt; R R Schreck
Journal: Am J Hum Genet Date: 1980-05 Impact factor: 11.025

6. Higher inductions of twin and single sister chromatid exchanges by cross-linking agents in Fanconi's anemia cells.

Authors: Y Kano; Y Fujiwara
Journal: Hum Genet Date: 1982 Impact factor: 4.132

6 in total

Further analysis of the replication bypass model for sister chromatid exchange.

1. Induction by alkylating agents of sister chromatid exchanges and chromatid breaks in Fanconi's anemia.

2. Sister Chromatid Exchanges in Tritium-Labeled Chromosomes.

3. Cross-link repair in human cells and its possible defect in Fanconi's anemia cells.

4. Bloom's syndrome. IV. Sister-chromatid exchanges in lymphocytes.

5. Sister chromatid exchange as an assay for genetic damage induced by mutagen-carcinogens. I. In vivo test for compounds requiring metabolic activation.

6. Insights on chromosome structure from sister chromatid exchange ratios and the lack of both isolabelling and heterolabelling as determined by the FPG technique.

7. Differential Giemsa staining of sister chromatids and the study of chromatid exchanges without autoradiography.

8. Direct evidence for the role of incorporated BUdR in the induction of sister chromatid exchanges.

9. Cytological detection of mutagen-carcinogen exposure by sister chromatid exchange.

10. Replication bypass model of sister chromatid exchanges and implications for Bloom's syndrome and Fanconi's anemia.

1. Segregation of DNA polynucleotide strands into sister chromatids and the use of endoreduplicated cells to track sister chromatid exchanges induced by crosslinks, alkylations, or x-ray damage.

2. Persistence of DNA lesions and the cytological cancellation of sister chromatid exchanges.

3. Effect of tissue culture variables on sister chromatid exchange in a nontransformed rat cell line.

Review 4. Sister chromatid exchange (SCE) and structural chromosome aberration in mutagenicity testing.

Review 5. Sister chromatid exchange analysis.

6. Higher inductions of twin and single sister chromatid exchanges by cross-linking agents in Fanconi's anemia cells.