ArticleOncogene1999
Progressive impairment of kidneys and reproductive organs in mice lacking Rho GDIalpha.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
What it found
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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.
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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
80 citing papers in PubMed, 204 citations in OpenAlex.
- A preliminary study of the miRNA restitution effect on CNV-induced miRNA downregulation in CAKUT.BMC genomics · 2024Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- RhoGDIα regulates spermatogenesis through Rac1/cofilin/F-actin signaling.Communications biology · 2023Article
- The Dual Function of RhoGDI2 in Immunity and Cancer.International journal of molecular sciences · 2023Review
- Correlation scan: identifying genomic regions that affect genetic correlations applied to fertility traits.BMC genomics · 2022Article
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Testicular aging, male fertility and beyond.Frontiers in endocrinology · 2022Review
- Synaptopodin Is Dispensable for Normal Podocyte Homeostasis but Is Protective in the Context of Acute Podocyte Injury.Journal of the American Society of Nephrology : JASN · 2020Article
- Changes in salivary analytes in canine parvovirus: A high-resolution quantitative proteomic study.Comparative immunology, microbiology and infectious diseases · 2018Article
- Actin dynamics at focal adhesions: a common endpoint and putative therapeutic target for proteinuric kidney diseases.Kidney international · 2018Review
- Rac1 in podocytes promotes glomerular repair and limits the formation of sclerosis.Scientific reports · 2018Article
- Kindlin-2 Association with Rho GDP-Dissociation InhibitorJournal of the American Society of Nephrology : JASN · 2017Article
- Mineralocorticoid receptor as a therapeutic target in chronic kidney disease and hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Review
- Disease-causing mutations of RhoGDIα induce Rac1 hyperactivation in podocytes.Small GTPases · 2016Article
- Human genetics of nephrotic syndrome and the quest for precision medicine.Current opinion in nephrology and hypertension · 2016Review
- Podocytes.F1000Research · 2016Review
- Article
- Glypican-5 Increases Susceptibility to Nephrotic Damage in Diabetic Kidney.The American journal of pathology · 2015Article
- De novo deletions and duplications of 17q25.3 cause susceptibility to cardiovascular malformations.Orphanet journal of rare diseases · 2015Article
- Review series: The cell biology of renal filtration.The Journal of cell biology · 2015Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Rho small G protein family members regulate various actin cytoskeleton-dependent cell functions. The Rho GDI (GDP dissociation inhibitor) family, consisting of Rho GDIalpha, -beta, and -gamma, is a regulator that keeps the Rho family members in the cytosol as the GDP-bound inactive form and translocates the GDP-bound form from the membranes to the cytosol after the GTP-bound form accomplishes their functions. Rho GDIalpha is ubiquitously expressed in mouse tissues and shows GDI activity on all the Rho family members in vitro. We have generated mice lacking Rho GDIalpha by homologous recombination to clarify its in vivo function. Rho GDIalpha -/- mice showed several abnormal phenotypes. Firstly, Rho GDIalpha -/- mice were initially viable but developed massive proteinuria mimicking nephrotic syndrome, leading to death due to renal failure within a year. Histologically, degeneration of tubular epithelial cells and dilatation of distal and collecting tubules were readily detected in the kidneys. Secondly, Rho GDIalpha -/- male mice were infertile and showed impaired spermatogenesis with vacuolar degeneration of seminiferous tubules in their testes. Thirdly, Rho GDIalpha -/- embryos derived from Rho GDIalpha -/- female mice were defective in the postimplantation development. In addition, these morphological and functional abnormalities showed age-dependent progression. These results suggest that the signaling pathways of the Rho family members regulated by Rho GDIalpha play important roles in maintaining the structure and physiological function of at least kidneys and reproductive systems in adult mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.