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Article

Site-to-site interdomain communication may mediate different loss-of-function mechanisms in a cancer-associated NQO1 polymorphism.

Scientific reports - 14 Mar 2017

Medina-Carmona Encarnación, Neira Jose L, Salido Eduardo, Fuchs Julian E, Palomino-Morales Rogelio, Timson David J, Pey Angel L

Abstract excerpt

Disease associated genetic variations often cause intracellular enzyme inactivation, dysregulation and instability. However, allosteric communication of mutational effects to distant functional sites leading to loss-of-function remains poorly understood. We characterize here interdomain site-to-site communication by which a common cancer-associated single nucleotide polymorphism (c.C609T/p.P187S) reduces the...

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Share to Allosteric Regulation
Share to Flavin-Adenine Dinucleotide

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to NAD(P)H Dehydrogenase (Quinone)

Share to Proteasome Endopeptidase Complex

Share to Protein Domains

Share to Protein Interaction Domains and Motifs

Share to Tumor Protein p73

Share to Tumor Suppressor Protein p53

Source

Open in PubMed Open full text

Identifiers

PMID: 28291250
DOI: 10.1038/srep44532
PMCID: PMC5349528

Genes

NQO1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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