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Article

MTRR 66A>G polymorphism in relation to congenital heart defects.

Clinical chemistry and laboratory medicine - 1 Jan 2006

van Beynum Ingrid M, Kouwenberg Margreet, Kapusta Livia, den Heijer Martin, van der Linden Ivon J M, Daniels Otto, Blom Henk J

Abstract excerpt

BACKGROUND: Evidence is accumulating that periconceptional folic acid supplementation may prevent congenital heart defects (CHD). The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine. We studied the influence of the MTRR 66A>G polymorphism on...

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Source

Identifiers

PMID: 17087642
DOI: 10.1515/CCLM.2006.254

Genes

MTRR
MTR

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.

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