ArticleProceedings of the National Academy of Sciences of the United States of America1996
Alternative splicing of exon 3 of the human growth hormone receptor is the result of an unusual genetic polymorphism.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 68 citations in OpenAlex.
- The Exon 3-Deleted Growth Hormone Receptor (d3GHR) Polymorphism-A Favorable Backdoor Mechanism for the GHR Function.International journal of molecular sciences · 2023Review
- Alternative splicing isoform in succinate dehydrogenase complex, subunit C causes downregulation of succinate-coenzyme Q oxidoreductase activity in mitochondria.Oncology letters · 2015Article
- Origin and evolution of spliceosomal introns.Biology direct · 2012Review
- The growth hormone receptor gene deleted for exon three (GHRd3) polymorphism is associated with birth and placental weight.Clinical endocrinology · 2012Article
- The exon 3-deleted growth hormone receptor: molecular and functional characterization and impact on GH/IGF-I axis in physiological and pathological conditions.Journal of endocrinological investigation · 2011Review
- Alternative RNA splicing in expression of the glutathione synthetase gene in human cells.Molecular biology reports · 2010Article
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- Maternal-placental-fetal interactions in the endocrine regulation of fetal growth: role of somatotrophic axes.Endocrine · 2002Review
- Physiology and disorders of the growth hormone receptor (GHR) and GH-GHR signal transduction.Endocrine · 2000Review
- Article
- Expression profile of a gamma-deletion variant of the human telomerase reverse transcriptase gene.Neoplasia (New York, N.Y.)Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Two isoforms of the human growth hormone receptor (hGHR), which differ in the presence (hGHRwt) or absence (hGHRd3) of exon 3, are expressed in the placenta. Specifically, three expression patterns are observed: only hGHRwt, only hGHRd3, or an approximately 1:1 combination of both isoforms. We investigated several potential regulatory mechanisms which might account for the expression of the hGHR isoforms. The frequency of hGHRd3 expression did not change when placentas from differing stages of gestation were examined, suggesting splicing was not developmentally regulated. However, when hGHR isoform expression patterns were examined in each component of a given placenta, it was evident that alternative splicing of exon 3 is individual-specific. Surprisingly, the individual-specific regulation of hGHR isoforms appears to be the result of a polymorphism in the hGHR gene. We analyzed hGHRwt and hGHRd3 expression in Hutterite pedigrees, and our results are consistent with a simple Mendelian inheritance of two differing alleles in which exon 3 is spliced in an "all-or-none" fashion. We conclude the alternative splicing of exon 3 in hGHR transcripts is the result of an unusual polymorphism which significantly alters splicing of the hGHR transcript and that the relatively high frequency (approximately 10%) of homozygous hGHRd3 expression suggests the possibility it may play a role in polygenic determined events.
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