ArticleNucleic acids research2002
Deficiency of a novel mismatch repair activity in a bladder tumor cell line.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- The hMSH2(M688R) Lynch syndrome mutation may function as a dominant negative.Carcinogenesis · 2012Article
- Identification of regulatory factor X as a novel mismatch repair stimulatory factor.The Journal of biological chemistry · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We demonstrate here that a cell line derived from a bladder cancer is defective in strand-specific mismatch repair. The mismatch repair deficiency in this cell line is associated with microsatellite instability and blocks an early step in the repair pathway. Since the addition of a known mismatch repair component hMutSalpha, hMutSbeta, hMutLalpha, replication protein A or proliferating cellular nuclear antigen could not restore mismatch repair to the mutant extract, the bladder tumor cell line is likely to be defective in an uncharacterized repair component. However, the repair in the mutant extract could be complemented by a partially purified activity derived from HeLa nuclear extracts. Therefore, in addition to revealing that a loss of mismatch repair function is associated with bladder cancer, this study provides information implicating a new mismatch repair activity.
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Registered trials
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