ArticlePloS one2011
RhoE deficiency produces postnatal lethality, profound motor deficits and neurodevelopmental delay in mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Rnd3 deletion affects neuroblast behavior through the RhoA/ROCK pathway but not neural stem cells in postnatal mice subventricular zone.Frontiers in cell and developmental biology · 2025Article
- RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages.Journal of immunology research · 2024Article
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- Rnd3 is necessary for the correct oligodendrocyte differentiation and myelination in the central nervous system.Brain structure & function · 2022Article
- Rnd3 Expression is Necessary to Maintain Mitochondrial Homeostasis but Dispensable for Autophagy.Frontiers in cell and developmental biology · 2022Article
- Plexin-B2 controls the timing of differentiation and the motility of cerebellar granule neurons.eLife · 2021Article
- Review
- Genetic deletion ofOncotarget · 2017Article
- Transient cerebellar alterations during development prior to obvious motor phenotype in a mouse model of spinocerebellar ataxia type 6.The Journal of physiology · 2017Article
- RND3 promotes Snail 1 protein degradation and inhibits glioblastoma cell migration and invasion.Oncotarget · 2016Article
- Rnd3-induced cell rounding requires interaction with Plexin-B2.Journal of cell science · 2016Article
- Rnd3 as a Novel Target to Ameliorate Microvascular Leakage.Journal of the American Heart Association · 2016Article
- Pathophysiological Functions of Rnd3/RhoE.Comprehensive Physiology · 2015Review
- A central role for TOR signalling in a yeast model for juvenile CLN3 disease.Microbial cell (Graz, Austria) · 2015Article
- Downregulation of RND3/RhoE in glioblastoma patients promotes tumorigenesis through augmentation of notch transcriptional complex activity.Cancer medicine · 2015Article
- RhoE is required for contact inhibition and negatively regulates tumor initiation and progression.Oncotarget · 2015Article
- Genetic deletion of Rnd3/RhoE results in mouse heart calcium leakage through upregulation of protein kinase A signaling.Circulation research · 2015Article
- Analysis of RhoE expression in the testis, epididymis and ductus deferens, and the effects of its deficiency in mice.Journal of anatomy · 2014Article
- Expression analysis of mouse Rhobtb3 using a LacZ reporter and preliminary characterization of a knockout strain.Histochemistry and cell biology · 2014Article
- Rnd3 haploinsufficient mice are predisposed to hemodynamic stress and develop apoptotic cardiomyopathy with heart failure.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rnd proteins are a subfamily of Rho GTPases involved in the control of actin cytoskeleton dynamics and other cell functions such as motility, proliferation and survival. Unlike other members of the Rho family, Rnd proteins lack GTPase activity and therefore remain constitutively active. We have recently described that RhoE/Rnd3 is expressed in the Central Nervous System and that it has a role in promoting neurite formation. Despite their possible relevance during development, the role of Rnd proteins in vivo is not known. To get insight into the in vivo function of RhoE we have generated mice lacking RhoE expression by an exon trapping cassette. RhoE null mice (RhoE gt/gt) are smaller at birth, display growth retardation and early postnatal death since only half of RhoE gt/gt mice survive beyond postnatal day (PD) 15 and 100% are dead by PD 29. RhoE gt/gt mice show an abnormal body position with profound motor impairment and impaired performance in most neurobehavioral tests. Null mutant mice are hypoactive, show an immature locomotor pattern and display a significant delay in the appearance of the hindlimb mature responses. Moreover, they perform worse than the control littermates in the wire suspension, vertical climbing and clinging, righting reflex and negative geotaxis tests. Also, RhoE ablation results in a delay of neuromuscular maturation and in a reduction in the number of spinal motor neurons. Finally, RhoE gt/gt mice lack the common peroneal nerve and, consequently, show a complete atrophy of the target muscles. This is the first model to study the in vivo functions of a member of the Rnd subfamily of proteins, revealing the important role of Rnd3/RhoE in the normal development and suggesting the possible involvement of this protein in neurological disorders.
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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.