ArticleMolecular and cellular biology2002
Targeted disruption of Ras-Grf2 shows its dispensability for mouse growth and development.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- GRF2 Is Crucial for Cone Photoreceptor Viability and Ribbon Synapse Formation in the Mouse Retina.Cells · 2023Article
- Nicotine self-administration and ERK signaling are altered in RasGRF2 knockout mice.Frontiers in pharmacology · 2022Article
- Ras GEF Mouse Models for the Analysis of Ras Biology and Signaling.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Regulation of the Small GTPase Ras and Its Relevance to Human Disease.Methods in molecular biology (Clifton, N.J.) · 2021Review
- The Inhibition of RasGRF2, But Not RasGRF1, Alters Cocaine Reward in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Human Endogenous Retrovirus-K HML-2 integration withinProceedings of the National Academy of Sciences of the United States of America · 2018Article
- A translational systems biology approach in both animals and humans identifies a functionally related module of accumbal genes involved in the regulation of reward processing and binge drinking in males.Journal of psychiatry & neuroscience : JPN · 2016Article
- Transcriptional profiling reveals functional links between RasGrf1 and Pttg1 in pancreatic beta cells.BMC genomics · 2014Article
- Rasgrf2 controls noradrenergic involvement in the acute and subchronic effects of alcohol in the brain.Psychopharmacology · 2014Article
- Rho guanine nucleotide exchange factors: regulators of Rho GTPase activity in development and disease.Oncogene · 2014Review
- Neuronal Rho GEFs in synaptic physiology and behavior.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2013Review
- RASGRF2 regulates alcohol-induced reinforcement by influencing mesolimbic dopamine neuron activity and dopamine release.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Regulation of Neuronal Function by Ras-GRF Exchange Factors.Genes & cancer · 2011Article
- RasGRF2, a guanosine nucleotide exchange factor for Ras GTPases, participates in T-cell signaling responses.Molecular and cellular biology · 2007Article
- ERK1 and ERK2 mitogen-activated protein kinases affect Ras-dependent cell signaling differentially.Journal of biology · 2006Article
- Developmentally regulated role for Ras-GRFs in coupling NMDA glutamate receptors to Ras, Erk and CREB.The EMBO journal · 2004Article
- Activation of H-Ras in the endoplasmic reticulum by the RasGRF family guanine nucleotide exchange factors.Molecular and cellular biology · 2004Article
- Two ENU-induced mutations in Rasgrf1 and early mouse growth retardation.Mammalian genome : official journal of the International Mammalian Genome Society · 2003Article
- Ras-GRF1 signaling is required for normal beta-cell development and glucose homeostasis.The EMBO journal · 2003Article
- Activation of the Ras superfamily of small GTPases. Workshop on exchange factors.EMBO reports · 2003Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mammalian Grf1 and Grf2 proteins are Ras guanine nucleotide exchange factors (GEFs) sharing a high degree of structural homology, as well as an elevated expression level in central nervous system tissues. Such similarities raise questions concerning the specificity and/or redundancy at the functional level between the two Grf proteins. grf1-null mutant mice have been recently described which showed phenotypic growth reduction and long-term memory loss. To gain insight into the in vivo function of Grf2, we disrupted its catalytic CDC25-H domain by means of gene targeting. Breeding among grf2(+/-) animals gave rise to viable grf2(-/-) adult animals with a normal Mendelian pattern, suggesting that Grf2 is not essential for embryonic and adult mouse development. In contrast to Grf1-null mice, analysis of grf2(-/-) litters showed similar size and weight as their heterozygous or wild-type grf2 counterparts. Furthermore, adult grf2(-/-) animals reached sexual maturity at the same age as their wild-type littermates and showed similar fertility levels. No specific pathology was observed in adult Grf2-null animals, and histopathological studies showed no observable differences between null mutant and wild-type Grf2 mice. These results indicate that grf2 is dispensable for mouse growth, development, and fertility. Furthermore, analysis of double grf1/grf2 null animals did not show any observable phenotypic difference with single grf1(-/-) animals, further indicating a lack of functional overlapping between the two otherwise highly homologous Grf1 and Grf2 proteins.
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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.