Literature DB >> 2267631

The Chinese hamster V79 cell mutant V-H4 is phenotypically like Fanconi anemia cells.

M Z Zdzienicka1, F Arwert, I Neuteboom, M Rooimans, J W Simons.   

Abstract

It has been shown by genetic complementation analysis that a mitomycin C-sensitive mutant (V-H4) of Chinese hamster V79 cells is the first rodent equivalent of Fanconi anemia (FA) group A. The V-H4 mutant shows many typical characteristics of cells derived from FA patients. V-H4 cells exhibit increased sensitivity towards cross-linking agents as MMC (approximately 30-fold), cis-DDP (approximately 10-fold), DEB (approximately 10-fold), and PUVA (approximately 1.6-fold), but an only slightly increased sensitivity to monofunctional alkylating agents (EMS and MMS) and actinomycin D. V-H4 cells are also moderately sensitive to adriamycin (1.6-fold), and not sensitive to H2O2. The levels of chromosomal aberrations induced by MMC and cis-DDP treatment are higher (4- to 6-fold) in V-H4 cells than in the wild-type V79 cells. Genetic complementation analysis with other Chinese hamster mutants hypersensitive to MMC (irs1, irs1SF, UV20 and UV41) indicates clearly that V-H4 belongs to a different, new complementation group. This unique mutant is very stable and can serve as a vehicle to isolate the complementing FA-A gene from normal human DNA.

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Year:  1990        PMID: 2267631     DOI: 10.1007/bf01233098

Source DB:  PubMed          Journal:  Somat Cell Mol Genet        ISSN: 0740-7750


  6 in total

1.  Distinct cellular phenotype linked to defective DNA interstrand crosslink repair and homologous recombination.

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Journal:  Mol Med Rep       Date:  2017-06-15       Impact factor: 2.952

2.  Mammalian Rad51C contributes to DNA cross-link resistance, sister chromatid cohesion and genomic stability.

Authors:  Barbara C Godthelp; Wouter W Wiegant; Annemarie van Duijn-Goedhart; Orlando D Schärer; Paul P W van Buul; Roland Kanaar; Massgorzata Z Zdzienicka
Journal:  Nucleic Acids Res       Date:  2002-05-15       Impact factor: 16.971

3.  Interstrand cross-links induce DNA synthesis in damaged and undamaged plasmids in mammalian cell extracts.

Authors:  L Li; C A Peterson; X Lu; P Wei; R J Legerski
Journal:  Mol Cell Biol       Date:  1999-08       Impact factor: 4.272

Review 4.  Fanconi anemia proteins, DNA interstrand crosslink repair pathways, and cancer therapy.

Authors:  Paul R Andreassen; Keqin Ren
Journal:  Curr Cancer Drug Targets       Date:  2009-02       Impact factor: 3.428

5.  A quantitative PCR-based assay reveals that nucleotide excision repair plays a predominant role in the removal of DNA-protein crosslinks from plasmids transfected into mammalian cells.

Authors:  Lisa N Chesner; Colin Campbell
Journal:  DNA Repair (Amst)       Date:  2018-01-09

6.  Cellular Repair of DNA-DNA Cross-Links Induced by 1,2,3,4-Diepoxybutane.

Authors:  Lisa N Chesner; Amanda Degner; Dewakar Sangaraju; Shira Yomtoubian; Susith Wickramaratne; Bhaskar Malayappan; Natalia Tretyakova; Colin Campbell
Journal:  Int J Mol Sci       Date:  2017-05-18       Impact factor: 5.923

  6 in total

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