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Article

RECQL4 and p53 potentiate the activity of polymerase γ and maintain the integrity of the human mitochondrial genome.

Carcinogenesis - 1 Jan 2014

Gupta Shruti, De Siddharth, Srivastava Vivek, Hussain Mansoor, Kumari Jyoti, Muniyappa K, Sengupta Sagar

Abstract excerpt

UNLABELLED: Germline mutations in RECQL4 and p53 lead to cancer predisposition syndromes, Rothmund-Thomson syndrome (RTS) and Li-Fraumeni syndrome (LFS), respectively. RECQL4 is essential for the transport of p53 to the mitochondria under unstressed conditions. Here, we show that both RECQL4 and p53 interact with mitochondrial polymerase (PolγA/B2) and regulate its binding to the mitochondrial DNA (mtDNA) control...

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Share to DNA-Directed DNA Polymerase
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 24067899
DOI: 10.1093/carcin/bgt315

Genes

RECQL4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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RECQL4 and p53 potentiate the activity of polymerase γ and maintain the integrity of the human mitochondrial genome.PMID 24067899Read ↗

RECQL4 is essential for the transport of p53 to mitochondria in normal human cells in the absence of exogenous stressSemantic proximity Read ↗

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Human RecQL4 helicase plays multifaceted roles in the genomic stability of normal and cancer cells.Semantic proximity Read ↗

Minute amounts of helicase-deficient truncated RECQL4 are sufficient for DNA replicationSemantic proximity Read ↗

Novel mutations in the RECQL4 gene affect its helicase functions, interactions with the BLM helicase and chemotherapeutics-induced cell deathSemantic proximity Read ↗

The involvement of human RECQL4 in DNA double‐strand break repairSemantic proximity Read ↗

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Functional characterisation of a RECQL4 mutation in Rothmund-Thomson syndromeSemantic proximity Read ↗

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