(Q53437948)

14 May 2018

title

Reversal of methylation tolerance by transfer of human chromosome 2. (English)

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14 May 2018

author

Andrea Zijno

3

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14 May 2018

author name string

Aquilina G

1

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14 May 2018

Fiumicino S

2

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14 May 2018

Martinelli S

4

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14 May 2018

Overkamp WJ

5

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14 May 2018

Zdzienicka MZ

6

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14 May 2018

Oshimura M

7

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14 May 2018

Wild CP

8

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14 May 2018

Bignami M

9

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14 May 2018

language of work or name

English

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publication date

1 November 1997

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14 May 2018

published in

Mutation Research

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14 May 2018

volume

385

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14 May 2018

issue

2

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14 May 2018

page(s)

115-126

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14 May 2018

Processing of O6-methylguanine by mismatch correction in human cell extracts

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A mismatch recognition defect in colon carcinoma confers DNA microsatellite instability and a mutator phenotype

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An alkylation-tolerant, mutator human cell line is deficient in strand-specific mismatch repair.

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Analysis of mismatch repair genes in hereditary non–polyposis colorectal cancer patients

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A hPMS2 mutant cell line is defective in strand-specific mismatch repair

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3-aminobenzamide and/or O6-benzylguanine evaluated as an adjuvant to temozolomide or BCNU treatment in cell lines of variable mismatch repair status and O6-alkylguanine-DNA alkyltransferase activity

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Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

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Genomic instability in repeated sequences is an early somatic event in colorectal tumorigenesis that persists after transformation

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GTBP, a 160-kilodalton protein essential for mismatch-binding activity in human cells

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Isolation of an hMSH2-p160 heterodimer that restores DNA mismatch repair to tumor cells

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hMutSbeta, a heterodimer of hMSH2 and hMSH3, binds to insertion/deletion loops in DNA

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Identifiers

DOI

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14 May 2018

PubMed ID

9447233

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14 May 2018