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1                                              Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2) constitute a family
2                                              Ras-GRF1 and Ras-GRF2 constitute a family of calmodulin-
3                                              Ras-GRF1 plus H-Ras induced a novel, expanded morphology
4                                              Ras-GRF1 required coexpression of H-Ras to induce morpho
5   Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1) and Ras-GRF2 are highly similar calcium-stimul
6 f Ras-guanine nucleotide-releasing factor 1 (Ras-GRF1), a neuronal activator of Ras proteins, causes
7 of Ras guanine nucleotide exchange factor 1, Ras-GRF1, by microarray analysis as a c-Jun/AP-1 regulat
8 tion of the Ras/ERK pathway partly through a Ras-GRF1 mechanism to modulate the production of MMP-9.
9 ted CaMKI, the Ca2+-stimulated Ras activator Ras-GRF1 (Ras-guanyl-nucleotide releasing factor), and E
10 directly represses expression of the Akt and Ras-GRF1 oncogenes.
11                       Although both Sos1 and Ras-GRF1 activate the Ras proteins Ha-Ras, N-Ras, and Ki
12 vidual amino acid exchanges between Sos1 and Ras-GRF1 revealed that the critical amino acids reside w
13                                    Tiam1 and Ras-GRF1 are guanine nucleotide exchange factors (GEFs)
14          These findings imply that Tiam1 and Ras-GRF1 can contribute to Rac signaling specificity by
15 Ras was significantly inhibited by antisense Ras-GRF1 oligomers.
16                 Analysis of chimeras between Ras-GRF1 and Ras-GRF2 demonstrated that a 30-amino acid
17 ncorporation of (32)P into Ser(898) of brain Ras-GRF1 following activation of protein kinase A.
18  coordinated activation of H-Ras and Rac1 by Ras-GRF1 may be a significant controller of neuronal cel
19  chronic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway-independent, apparently stochastic
20                                 In contrast, Ras-GRF1 mediates signaling from ifenprodil-sensitive (N
21 ersions of the Ras-specific exchange factors Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2), which are expressed
22  acids (aa) 828-838 in Sos1 and 1057-1067 in Ras-GRF1) of Ras guanine nucleotide exchange factors.
23                                 Increases in Ras-GRF1 activity toward Ras that are stimulated by rece
24                                    Increased Ras-GRF1 expression, in response to inducible c-Jun expr
25                                  Full-length Ras-GRF1 that contains an alanine 916 mutation was only
26 s a catalytically inactive dominant negative Ras-GRF1, which prevented ERK activation, reduced MMP-9
27 ation of the Ras exchange factor activity of Ras-GRF1 by muscarinic receptors.
28                              The activity of Ras-GRF1 is regulated by increases in intracellular calc
29 t did not, however, increase the activity of Ras-GRF1, indicating that it is not sufficient for activ
30                    We defined the effects of Ras-GRF1 and truncation mutants that include only one of
31                        Ectopic expression of Ras-GRF1 was accompanied by ERK activation and elevated
32                             Co-expression of Ras-GRF1 with subtype 1 human muscarinic receptors in CO
33 and thus could contribute to the function of Ras-GRF1 in neuronal signal transduction pathways that u
34                       A truncation mutant of Ras-GRF1 that included the Rac GEF domains, GRFdeltaC, p
35                       A truncation mutant of Ras-GRF1 that included the Ras GEF domain, GRFdeltaN, pl
36 ulates an increase in the phosphorylation of Ras-GRF1 at certain serine residues.
37  widespread and selective phosphorylation of Ras-GRF1 at Ser(898).
38                           Phosphorylation of Ras-GRF1 at Ser(916) is also required for maximal induct
39 ) confirmed the regulated phosphorylation of Ras-GRF1 by Western blotting in both model systems of tr
40 s a major site of in vivo phosphorylation of Ras-GRF1 in both COS-7 cells and NIH-3T3 fibroblasts.
41 ortex, there was striking phosphorylation of Ras-GRF1 in the dendritic tree, supporting a role for Ra
42  associated with enhanced phosphorylation of Ras-GRF1 on one or more serine residues.
43 d with destabilization and ubiquitylation of Ras-GRF1, a guanine nucleotide exchange factor that acti
44 Ras proteins Ha-Ras, N-Ras, and Ki-Ras, only Ras-GRF1 also activates the functionally distinct R-Ras
45                        In addition, Tiam1 or Ras-GRF1 binding to IB2/JIP2 increases the association o
46 in cells potentiates the ability of Tiam1 or Ras-GRF1 to activate the p38 MAP kinase cascade but not
47 heir similar functional domain organization, Ras-GRF1 and Ras-GRF2 mediate opposing forms of synaptic
48                                         p140 Ras-GRF1 and p130 Ras-GRF2 constitute a family of calciu
49 ese exchange factors revealed that both p140 Ras-GRF1 and p130 Ras-GRF2 couple NMDA glutamate recepto
50                                          p75-Ras-GRF1 expression occurred with a concomitant increase
51 5A, demonstrating an interaction between p75-Ras-GRF1 and Ras.
52 ude that c-Jun/AP-1 regulates endogenous p75-Ras-GRF1 expression and that c-Jun/AP-1-regulated anchor
53                                Moreover, p75-Ras-GRF1 could be coprecipitated with a Ras dominant-neg
54   A 75-kDa c-Jun/AP-1-inducible protein, p75-Ras-GRF1, was detected, and the inhibition of its expres
55 dy (termed 2152) that selectively recognizes Ras-GRF1 when it is phosphorylated at Ser(916/898) confi
56 urs through the calcium/calmodulin regulated Ras-GRF1 and Ras-GRF2 exchange factors, which form AMPA-
57                     We demonstrate here that Ras-GRF1 is highly expressed in rat brain compared with
58                                          The Ras-GRF1 exchange factor has regulated guanine nucleotid
59                                          The Ras-GRF1 exchange factor is strongly implicated in the c
60                                          The Ras-GRF1 exchange factor, which is regulated by increase
61 ow that c-Jun/AP-1 can bind and activate the Ras-GRF1 promoter in vivo.
62 he induction of NMDAR-dependent LTP, whereas Ras-GRF1 contributes predominantly to the induction of N
63                    Here we show that whereas Ras-GRF1 activated both Ha-Ras and R-Ras in cells, Ras-G
64 ed reactivity only under conditions in which Ras-GRF1 was phosphorylated at Ser(916/898).

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