{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["22(8)"],"submitter":["Fernandez-Medarde A"],"pubmed_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 mi"],"journal":["Molecular and cellular biology"],"pagination":["2498-504"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC133706"],"repository":["biostudies-literature"],"pubmed_title":["Targeted disruption of Ras-Grf2 shows its dispensability for mouse growth and development."],"pmcid":["PMC133706"],"pubmed_authors":["Santos E","Nunez A","Tessarollo L","Esteban LM","Fernandez-Medarde A","Porteros A"],"additional_accession":[]},"is_claimable":false,"name":"Targeted disruption of Ras-Grf2 shows its dispensability for mouse growth and development.","description":"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 mi","dates":{"release":"2002-01-01T00:00:00Z","publication":"2002 Apr","modification":"2025-04-04T12:41:30.965Z","creation":"2019-03-27T00:17:21Z"},"accession":"S-EPMC133706","cross_references":{"pubmed":["11909944"],"doi":["10.1128/mcb.22.8.2498-2504.2002","10.1128/MCB.22.8.2498-2504.2002"]}}