| 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 |
|