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Cited by 310

The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.

Reduced androgen receptor gene expression with first exon CAG repeat expansion

Open access
Choong, C. S.·1996·Molecular Endocrinology

Abstract

The molecular basis for partial androgen insensitivity associated with adult onset spinal/bulbar muscular atrophy was investigated by transient transfection of human androgen receptor (AR) expression vectors containing increasing CAG repeat lengths in the first exon. An inverse relationship was observed between CAG repeat length and AR mRNA and protein levels. Trinucleotide repeat lengths of 43 and 65 associated with spinal/bulbar muscular atrophy decreased AR mRNA and protein levels but did not alter equilibrium binding affinity for [3H]R1881 or inherent transcriptional activity of AR, expressed as androgen-dependent fold induction of a mouse mammary tumor virus promoter-luciferase reporter vector. The findings indicate that glutamine expansion up to 66 residues in the NH2-terminal domain of AR does not alter AR functional activity. Rather, CAG repeat expansion in the region of the first exon reduces AR mRNA and protein expression. The study reveals a previously unrecognized effect of CAG repeat length on AR mRNA expression and a novel molecular mechanism for androgen resistance.

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Metadata

Authors
Choong, C. S.
Venue
Molecular Endocrinology
Published
1996-12-01
Volume
10
Issue
12
Pages
1527-1535
ISSN
0888-8809 (ISSN-L)
OpenAlex
W2064549949
Cited by
310
References
57
FWCI
4.04
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Reduced androgen receptor gene expression with first exon CAG repeat expansion. https://app.cochat.ai/papers/10.1210/me.10.12.1527
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Choong, C. S. (1996). Reduced androgen receptor gene expression with first exon CAG repeat expansion. Molecular Endocrinology. https://doi.org/10.1210/me.10.12.1527

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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