Circulating human B lymphocytes are deficient in nucleotide excision repair and accumulate mutations upon proliferation.

doi:10.1182/blood-2010-12-326637

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Article

Circulating human B lymphocytes are deficient in nucleotide excision repair and accumulate mutations upon proliferation.

Blood - 9 Jun 2011

Hyka-Nouspikel Nevila, Lemonidis Kimon, Lu Wei-Ting, Nouspikel Thierry

Abstract excerpt

Faithful repair of DNA lesions is a crucial task that dividing cells must actively perform to maintain genome integrity. Strikingly, nucleotide excision repair (NER), the most versatile DNA repair system, is specifically down-regulated in terminally differentiated cells. This prompted us to examine whether NER attenuation might be a common feature of all G₀-arrested cells, and in particular of those that retain...

Topics

B-Lymphocytes
Cyclin D2
DNA Damage
DNA Repair
DNA-Binding Proteins
Down-Regulation
Genome, Human
Genomic Instability
Humans
Mutagenesis
Mutation
Proto-Oncogene Proteins c-bcl-6
Resting Phase, Cell Cycle
Ubiquitin-Activating Enzymes

Source

Open in PubMed

Identifiers

PMID: 21478426
DOI: 10.1182/blood-2010-12-326637

Genes

BCL6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026.

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