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Article

A polymorphic miR-155 binding site in AGTR1 is associated with cardiac hypertrophy in Friedreich ataxia.

Journal of molecular and cellular cardiology - 1 Nov 2011

Kelly Matthew, Bagnall Richard D, Peverill Roger E, Donelan Lesley, Corben Louise, Delatycki Martin B, Semsarian Christopher

Abstract excerpt

Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative condition with a heterogeneous cardiac phenotype caused primarily by an expanded GAA trinucleotide repeat in the frataxin gene (FXN). FXN is important in mitochondrial iron efflux, sensitivity to oxidative stress, and cell death...

Read the complete abstract on PubMed

Topics

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Share to Angiotensin-Converting Enzyme 2
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Heart Ventricles

Share to Hypertrophy, Left Ventricular

Share to Iron-Binding Proteins

Share to Receptor, Angiotensin, Type 1

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Source

Identifiers

PMID: 21771600
DOI: 10.1016/j.yjmcc.2011.07.001

Genes

AGTR1
FXN
GAA
ACE
ACE2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-21771600-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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