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1                                              GRF1 can also mediate high frequency stimulation-induced
2 pathways include GROWTH REGULATORY FACTOR 1 (GRF1), PHOSPHATIDYLINOSITOL 4-KINASE beta1 (PI-4Kbeta1),
3 ere examined in transgenic plants carrying a GRF1-GF14 chi promoter-beta-glucuronidase construct.
4 cle was sensitive to the Ras GEFs, Sos1, and GRF1 and to p120 Ras GAP.
5 t functions, WT and various chimeras between GRF1 and GRF2 proteins were tested for their abilities t
6                            Oligomers between GRF1 and GRF2 were detected in a rat brain extract, and
7  This led to a significant reduction in both GRF1-dependent ERK phosphorylation and AP1-dependent rep
8                            We show that both GRF1 and GRFbeta are expressed selectively in beta cell
9 tional inactivation of oligomer formation by GRF1 is associated with impaired biological and signalin
10 signaling activities, and that in 293T cells GRF1 mediates at least two pathways for Raf activation:
11 lated an Arabidopsis 14-3-3 gene, designated GRF1-GF14 chi (for general regulatory factor1-G-box fact
12 evidence suggesting that the exchange factor GRF1 is upstream of H-Ras activation by alcohol.
13  kb, and the maize general regulatory factor GRF1 gene occupies a domain of 100 kb in length.
14            In search of partner proteins for GRF1, we identified another gene family, GRF-interacting
15  phosphorylation, consistent with a role for GRF1 in calcium-dependent Ras signaling in these cells.
16 ge reaction mechanism by a Ras specific GEF, GRF1.
17                                    Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2) constitute a family of similar
18  the Ras-specific exchange factors Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2), which are expressed in brain
19 eptors in the CA1 region of the hippocampus, GRF1 promotes LTD, whereas GRF2 promotes theta-burst sti
20 s induction is correlated with a decrease in GRF1, GRF2, and GRF3 transcripts.
21        Introduction of the L263Q mutation in GRF1 led to a protein that was deficient in oligomer for
22                                      Indeed, GRF1, GRF6, GRF7, GRF12, GRF15, and GRF17 were significa
23           In the absence of free nucleotide, GRF1 could not efficiently stimulate GDP dissociation fr
24 eptides that associate with the DH domain of GRF1.
25 strin homology and/or coiled-coil domains of GRF1 are key to the induction of HFS-LTP by GRF proteins
26  rat brain extract, and forced expression of GRF1 and GRF2 in cultured mammalian cells formed homo- a
27 ated, at least in part, by the expression of GRF1 and possibly other transcription factors of the GRF
28                     Finally, the IQ motif of GRF1 determines whether a GRF protein can induce LTD.
29 ein whose N terminus is identical to that of GRF1, a calcium-dependent guanine nucleotide exchange fa
30 smid encoding a dominant negative variant of GRF1 led to 70% reduction in ERK phosphorylation, consis
31                                           Os-GRF1 (Oryza sativa-GROWTH-REGULATING FACTOR1) was identi
32                                           Os-GRF1 displays general features of transcription factors,
33        To study its role in plant growth, Os-GRF1 was expressed in Arabidopsis.
34                 Our results indicate that Os-GRF1 belongs to a novel class of plant proteins and may
35                                          Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2) constitute a family of s
36                                          Ras-GRF1 and Ras-GRF2 constitute a family of calmodulin-regu
37                                          RAS-GRF1 is a guanine nucleotide exchange factor with the ab
38                                          Ras-GRF1 plus H-Ras induced a novel, expanded morphology in
39                                          Ras-GRF1 required coexpression of H-Ras to induce morphologi
40 s-guanine nucleotide-releasing factor 1 (Ras-GRF1) and Ras-GRF2 are highly similar calcium-stimulated
41 s-guanine nucleotide-releasing factor 1 (Ras-GRF1), a neuronal activator of Ras proteins, causes a sp
42 as guanine nucleotide exchange factor 1, Ras-GRF1, by microarray analysis as a c-Jun/AP-1 regulated g
43  of the Ras/ERK pathway partly through a Ras-GRF1 mechanism to modulate the production of MMP-9.
44 CaMKI, the Ca2+-stimulated Ras activator Ras-GRF1 (Ras-guanyl-nucleotide releasing factor), and ERK.
45 showed that beginning at 1 month of age, RAS-GRF1 mediates NMDA-type glutamate receptor (NMDAR)-induc
46                   Although both Sos1 and Ras-GRF1 activate the Ras proteins Ha-Ras, N-Ras, and Ki-Ras
47                                Tiam1 and Ras-GRF1 are guanine nucleotide exchange factors (GEFs) that
48      These findings imply that Tiam1 and Ras-GRF1 can contribute to Rac signaling specificity by thei
49 ctly represses expression of the Akt and Ras-GRF1 oncogenes.
50 al amino acid exchanges between Sos1 and Ras-GRF1 revealed that the critical amino acids reside withi
51 was significantly inhibited by antisense Ras-GRF1 oligomers.
52             Analysis of chimeras between Ras-GRF1 and Ras-GRF2 demonstrated that a 30-amino acid segm
53 poration of (32)P into Ser(898) of brain Ras-GRF1 following activation of protein kinase A.
54 rdinated activation of H-Ras and Rac1 by Ras-GRF1 may be a significant controller of neuronal cell si
55 onic L-DOPA treatment reveals a complex, Ras-GRF1 and pathway-independent, apparently stochastic invo
56 minate between closely related contexts, RAS-GRF1 begins to contribute to the induction of long term
57                             In contrast, Ras-GRF1 mediates signaling from ifenprodil-sensitive (NR2B-
58 ons of the Ras-specific exchange factors Ras-GRF1 (GRF1) and Ras-GRF2 (GRF2), which are expressed in
59                             Increases in Ras-GRF1 activity toward Ras that are stimulated by receptor
60 ds (aa) 828-838 in Sos1 and 1057-1067 in Ras-GRF1) of Ras guanine nucleotide exchange factors.
61                                Increased Ras-GRF1 expression, in response to inducible c-Jun expressi
62                              Full-length Ras-GRF1 that contains an alanine 916 mutation was only part
63 catalytically inactive dominant negative Ras-GRF1, which prevented ERK activation, reduced MMP-9 expr
64                We defined the effects of Ras-GRF1 and truncation mutants that include only one of its
65 es an increase in the phosphorylation of Ras-GRF1 at certain serine residues.
66 espread and selective phosphorylation of Ras-GRF1 at Ser(898).
67                       Phosphorylation of Ras-GRF1 at Ser(916) is also required for maximal induction
68 n of the Ras exchange factor activity of Ras-GRF1 by muscarinic receptors.
69 nfirmed the regulated phosphorylation of Ras-GRF1 by Western blotting in both model systems of transf
70 major site of in vivo phosphorylation of Ras-GRF1 in both COS-7 cells and NIH-3T3 fibroblasts.
71 thus could contribute to the function of Ras-GRF1 in neuronal signal transduction pathways that under
72 x, there was striking phosphorylation of Ras-GRF1 in the dendritic tree, supporting a role for Ras ac
73                          The activity of Ras-GRF1 is regulated by increases in intracellular calcium
74 ociated with enhanced phosphorylation of Ras-GRF1 on one or more serine residues.
75                   A truncation mutant of Ras-GRF1 that included the Rac GEF domains, GRFdeltaC, produ
76                   A truncation mutant of Ras-GRF1 that included the Ras GEF domain, GRFdeltaN, plus H
77                    Ectopic expression of Ras-GRF1 was accompanied by ERK activation and elevated leve
78                         Co-expression of Ras-GRF1 with subtype 1 human muscarinic receptors in COS-7
79 th destabilization and ubiquitylation of Ras-GRF1, a guanine nucleotide exchange factor that activate
80 d not, however, increase the activity of Ras-GRF1, indicating that it is not sufficient for activatio
81 proteins Ha-Ras, N-Ras, and Ki-Ras, only Ras-GRF1 also activates the functionally distinct R-Ras GTPa
82                    In addition, Tiam1 or Ras-GRF1 binding to IB2/JIP2 increases the association of th
83 ells potentiates the ability of Tiam1 or Ras-GRF1 to activate the p38 MAP kinase cascade but not the
84  similar functional domain organization, Ras-GRF1 and Ras-GRF2 mediate opposing forms of synaptic pla
85                                     p140 Ras-GRF1 and p130 Ras-GRF2 constitute a family of calcium/ca
86 exchange factors revealed that both p140 Ras-GRF1 and p130 Ras-GRF2 couple NMDA glutamate receptors (
87 demonstrating an interaction between p75-Ras-GRF1 and Ras.
88                            Moreover, p75-Ras-GRF1 could be coprecipitated with a Ras dominant-negativ
89 that c-Jun/AP-1 regulates endogenous p75-Ras-GRF1 expression and that c-Jun/AP-1-regulated anchorage-
90                                      p75-Ras-GRF1 expression occurred with a concomitant increase in
91 75-kDa c-Jun/AP-1-inducible protein, p75-Ras-GRF1, was detected, and the inhibition of its expression
92 termed 2152) that selectively recognizes Ras-GRF1 when it is phosphorylated at Ser(916/898) confirmed
93 through the calcium/calmodulin regulated Ras-GRF1 and Ras-GRF2 exchange factors, which form AMPA-indu
94                 We demonstrate here that Ras-GRF1 is highly expressed in rat brain compared with the
95                                      The Ras-GRF1 exchange factor has regulated guanine nucleotide ex
96                                      The Ras-GRF1 exchange factor is strongly implicated in the contr
97                                      The Ras-GRF1 exchange factor, which is regulated by increases in
98 hat c-Jun/AP-1 can bind and activate the Ras-GRF1 promoter in vivo.
99 ngly, LTP induction by CP-AMPARs through RAS-GRF1 occurs via activation of p38 MAP kinase rather than
100                Here we show that whereas Ras-GRF1 activated both Ha-Ras and R-Ras in cells, Ras-GRF2
101 nduction of NMDAR-dependent LTP, whereas Ras-GRF1 contributes predominantly to the induction of NMDAR
102 eactivity only under conditions in which Ras-GRF1 was phosphorylated at Ser(916/898).
103 ze plants overexpressing miRNA396a-resistant GRF1 support a model proposing that distinct association
104                             We conclude that GRF1 and GRF2 can form homo- and hetero-oligomers via th
105                              We propose that GRF1 and GIF1 act as transcription activator and coactiv
106                     The results suggest that GRF1 plays a role in mediating calcium-dependent signal
107  in Erk activity induced by ionomycin in the GRF1-expressing cells also induced a concomitant increas
108 cus-forming activity on NIH 3T3 cells of the GRF1 DH cluster mutant was reduced, while the L263Q muta
109 -263 to Gln (L263Q) in the N terminus of the GRF1 DH domain abolished the two-hybrid interaction, whi
110                   Sequence comparison of the GRF1-GF14 chi genomic clone with other 14-3-3 proteins d
111 ither alone, synergistically potentiated the GRF1-stimulated GDP dissociation from Ras.
112 f ionomycin, 293T cells expressing wild-type GRF1 contained much higher levels of Ras-GTP than contro
113                        Compared to wild-type GRF1, the focus-forming activity on NIH 3T3 cells of the
114 t was deficient in oligomer formation, while GRF1 containing the DH cluster mutations formed homo-oli
115 protein was involved in the interaction with GRF1.

 
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