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| DC Field | Value | Language |
|---|---|---|
| dc.creator | Esteban, Luis Miguel | - |
| dc.creator | Núñez, Alejandro | - |
| dc.creator | Santos de Dios, Eugenio | - |
| dc.creator | Fernández-Medarde, Alberto | - |
| dc.creator | Porteros, Ángel | - |
| dc.creator | Tessarollo, Lino | - |
| dc.date | 2008-06-17T11:39:29Z | - |
| dc.date | 2008-06-17T11:39:29Z | - |
| dc.date | 2002-04 | - |
| dc.date.accessioned | 2017-01-31T01:42:41Z | - |
| dc.date.available | 2017-01-31T01:42:41Z | - |
| dc.identifier | Molecular and Cellular Biology 22(8): 2498–2504 (2002) | - |
| dc.identifier | 0270-7306 | - |
| dc.identifier | http://hdl.handle.net/10261/5140 | - |
| dc.identifier | 10.1128/MCB.22.8.2498-2504.2002 | - |
| dc.identifier.uri | http://dspace.mediu.edu.my:8181/xmlui/handle/10261/5140 | - |
| dc.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 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. | - |
| dc.description | This work was supported by FEDER grants 1FD97-1735 and 1FD97-1678 and CICYT grant SAF00-0069 from MCYT (Spain). A.F.-M. and L.M.E. contributed equally to this work. | - |
| dc.description | Peer reviewed | - |
| dc.format | 25097 bytes | - |
| dc.format | application/pdf | - |
| dc.language | eng | - |
| dc.publisher | American Society for Microbiology | - |
| dc.relation | http://dx.doi.org/22.8.2498–2504.2002 | - |
| dc.rights | closedAccess | - |
| dc.title | Targeted Disruption of Ras-Grf2 Shows Its Dispensability for Mouse Growth and Development | - |
| dc.type | Artículo | - |
| Appears in Collections: | Digital Csic | |
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