ArticleProceedings of the National Academy of Sciences of the United States of America2003
Heterogeneous nuclear ribonucleoprotein (hnRNP) binding to hormone response elements: a cause of vitamin D resistance.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Vitamin D-Dependent Rickets Type 3: A Case Report and Systematic Review.Calcified tissue international · 2023Pooled it
- CYP3A4 Mutation Causes Vitamin D-Dependent Rickets Type 3: A Case Report in Saudi Arabia.Cureus · 2023Article
- Refractory Rickets.Indian journal of pediatrics · 2023Review
- Review
- Review
- hnRNP A/B Proteins: An Encyclopedic Assessment of Their Roles in Homeostasis and Disease.Biology · 2021Review
- The Causes of Hypo- and Hyperphosphatemia in Humans.Calcified tissue international · 2021Review
- A Comprehensive Analysis of the Role of hnRNP A1 Function and Dysfunction in the Pathogenesis of Neurodegenerative Disease.Frontiers in molecular biosciences · 2021Review
- Idiosyncrasies of hnRNP A1-RNA recognition: Can binding mode influence function.Seminars in cell & developmental biology · 2019Review
- Acidosis enhances the self-renewal and mitochondrial respiration of stem cell-like glioma cells through CYP24A1-mediated reduction of vitamin D.Cell death & disease · 2019Article
- CYP3A4 mutation causes vitamin D-dependent rickets type 3.The Journal of clinical investigation · 2018Article
- Functions of vitamin D in bone.Histochemistry and cell biology · 2018Review
- Genetic Causes of Rickets.Journal of clinical research in pediatric endocrinology · 2017Review
- Extraovarian gonadotropin negative feedback revealed by aromatase inhibition in female marmoset monkeys.American journal of physiology. Endocrinology and metabolism · 2017Article
- microRNA-451-modulated hnRNP A1 takes a part in granulocytic differentiation regulation and acute myeloid leukemia.Oncotarget · 2017Article
- Concerted effects of heterogeneous nuclear ribonucleoprotein C1/C2 to control vitamin D-directed gene transcription and RNA splicing in human bone cells.Nucleic acids research · 2017Article
- CYP2R1 Mutations Impair Generation of 25-hydroxyvitamin D and Cause an Atypical Form of Vitamin D Deficiency.The Journal of clinical endocrinology and metabolism · 2015Article
- Vitamin D and alternative splicing of RNA.The Journal of steroid biochemistry and molecular biology · 2015Review
- Article
- Mutations in the vitamin D receptor and hereditary vitamin D-resistant rickets.BoneKEy reports · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
In previous studies, we have shown that steroid hormone resistance in New World primates occurs in the absence of abnormal expression of cognate nuclear receptors. Rather, these animals have elevated levels of heterogeneous nuclear ribonucleoproteins (hnRNPs) that act as hormone response element-binding proteins and attenuate target gene transactivation. Here we present evidence for a similar mechanism in humans via a patient with resistance to the active form of vitamin D [1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3))] who presented with normal vitamin D receptor (VDR) expression. Initial cotransfection studies showed that the cells of the patient suppressed basal and hormone-induced transactivation by wild-type VDR. Electrophoretic mobility-shift assays and Western/Southwestern blot analyses indicated that this suppressive effect was due to overexpression of a nuclear protein that specifically interacts with a DNA response element known to bind retinoid X receptor-VDR heterodimers. Ab blocking in electrophoretic mobility-shift assays indicated that this dominant-negative acting protein was in the hnRNPA family of nucleic acid-binding proteins. Further studies have shown that several members of this family, most notably hnRNPA1, were able to suppress basal and 1,25(OH)(2)D(3)-induced luciferase activity. We therefore propose that this case of vitamin D resistance in a human subject is similar to that previously described for New World primates in which abnormal expression of a hormone response element-binding protein can cause target cell resistance to 1,25(OH)(2)D(3). That this protein is a member of the hnRNP family capable of interacting with double-stranded DNA highlights a potentially important new component of the complex machinery required for steroid hormone signal transduction.
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Registered trials
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