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