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1 ied that encode a palmitoyltransferase for a Ras GTPase.
2 1 also activates the functionally distinct R-Ras GTPase.
3 have in common the ability to interact with ras GTPase.
4 ble to elicit the activation of both Ral and Ras GTPases.
5 ction and intermediate G proteins, including Ras GTPases.
6 y region retained activation by both Rho and Ras GTPases.
7 imited the ability of ExoS to ADP-ribosylate Ras GTPases.
8 ls, or the ability of ExoS to ADP-ribosylate Ras GTPases.
9 ucleotide exchange factors that activate the Ras GTPases.
10 ntain Rab, Rho, Arf, and Ran GTPases, but no Ras GTPases.
11 -promoting phorbol esters with activation of Ras GTPases.
12 fficiently than the oncogenic Ha-, K-, and N-Ras GTPases.
13 fically on Rho and not on the Rac, Cdc42, or Ras GTPases.
14 by binding p120RasGAP, a GAP protein for the Ras GTPases.
15 ponsible for the ubiquitination of classical RAS GTPases.
16 s catalytic activity or its interaction with RAS GTPases.
17 GTPases are directly activated by oncogenic Ras GTPases.
18 rovided a wealth of mechanistic insight into Ras GTPases.
19 ic MAP kinase activation by constitutive p21(ras) GTPases.
21 discovery of a new downstream target for the Ras GTPases - a Nore1-Mst1 protein complex - reveals a m
23 analysis reveals that Ubp3 interacts with a Ras GTPase-accelerating protein, Ira2, and regulates its
26 sential for signaling and contains a R-Ras/M-Ras GTPase activating protein (GAP) domain that is divid
28 la mutation on the interaction of H-Ras with Ras GTPase activating protein (GAP), neurofibromin 1 (NF
29 ells while the phosphorylation/activation of Ras GTPase activating protein (Ras GAP) and mitogen acti
31 effect found in our previous studies of the Ras GTPase activating protein (RasGAP) and the elongatio
33 n (G125V) in the scat Rasa3 gene, encoding a Ras GTPase activating protein (RasGAP), and elucidate th
34 One key regulator of this cascade is the Nf1 Ras GTPase activating protein (RasGAP), which attenuates
36 rat homolog, but not its mutant defective in Ras GTPase activating protein activity, reverses miR-431
42 precisely controlled by mechanisms involving Ras GTPase activating proteins (RasGAPs) responsible for
43 n of the effect of Ca2+ on Ras activity, and Ras GTPase activating-like protein (RASAL), which functi
45 ere we report that sphingosine can stimulate Ras-GTPase activating protein (GAP) activity in vitro, a
46 coded protein, neurofibromin, functions as a Ras-GTPase activating protein (GAP), nothing is known ab
48 ongly reduced by silencing expression of the Ras-GTPase activating protein (Ras-GAP) neurofibromin, a
50 emonstrates that the loss of DAB2IP, a novel Ras-GTPase activating protein frequently found in many c
53 completely rescued by expression of the GAP (RAS-GTPase activating protein) domain of neurofibromin.
54 992 receptors were associated with more SOS, Ras-GTPase activating protein, phosphatidylinositol 3-ki
55 Here, we describe the isolation of a novel Ras-GTPase activating protein, SynGAP, that interacts wi
56 that members of the Ras network of proteins, Ras-GTPase activating protein-SH3-domain-binding protein
58 in the cleavage of the SG-nucleating protein Ras-GTPase activating SH3 domain-binding protein (G3BP1)
61 GAP from the Rsu-1 transfectants showed less Ras GTPase-activating activity than GAP from control cel
64 The NF1-encoded protein neurofibromin is a Ras GTPase-activating protein (GAP) and can directly lim
65 t their effects via an intracellular R-Ras/M-Ras GTPase-activating protein (GAP) domain or by activat
68 DAB2 interacting protein) is a member of the Ras GTPase-activating protein (GAP) family that has been
69 at Ras, through an effector-like function of Ras GTPase-activating protein (GAP) in neonatal cardiac
72 romoted Ras inactivator), a Ca(2+)-dependent Ras GTPase-activating protein (GAP) that switches off th
73 To distinguish between inhibition of Ras by Ras GTPase-activating protein (GAP) versus a potential e
77 In the present study, we identified a novel Ras GTPase-activating protein (Ras-GAP) as an ASK1-inter
79 l abolished the association of PDGFalphar to Ras GTPase-activating protein (Ras-GAP), but it did not
82 acted with the SH3 domain and phosphorylated Ras GTPase-activating protein (RasGAP) and upregulated R
83 aptor Grb2-associated binder-1 (GAB1) on its RAS GTPase-activating protein (RASGAP) binding sites and
84 orylation of Dok-1, augmented recruitment of Ras GTPase-activating protein (RasGAP) by Dok-1, and inh
85 AP1 as a human protein related to a putative Ras GTPase-activating protein (RasGAP) from the fission
89 of activated Ras by blocking recruitment of Ras GTPase-activating protein (RasGAP) to the plasma mem
90 otifs in the C terminus and does not bind to Ras GTPase-activating protein (RasGAP) upon phosphorylat
91 y, including Nck adaptor protein (Nck), p120-Ras GTPase-activating protein (RasGAP), and the alpha- a
93 predicted, growth-related targets, including Ras GTPase-activating protein (RasGAP), cyclin-dependent
94 peptide derived from the N2 fragment of p120 Ras GTPase-activating protein (RasGAP), sensitizes tumor
99 otein (CREB) phosphorylation via RASA1 (p120 Ras GTPase-activating protein 1) down-regulation, wherea
100 al known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase
103 (AIP1), a recently identified member of the Ras GTPase-activating protein family, is highly expresse
105 novel GTPase-activating protein containing a Ras GTPase-activating protein homology domain (N terminu
110 tors (HERs), induced expression of G3BP, the Ras GTPase-activating protein SH3 domain-binding protein
111 We further show that nsp1 interacts with Ras GTPase-activating protein SH3 domain-binding protein
113 to citron, p135 SynGAP, an abundant synaptic Ras GTPase-activating protein that can bind to all three
116 e we report the characterisation of RASAL, a Ras GTPase-activating protein that senses the frequency
119 HB4 (ephrin receptor B4) and the RASA1 (p120 Ras GTPase-activating protein) are necessary for the dev
121 ating protein (SynGAP) is a neuronal RasGAP (Ras GTPase-activating protein) that is selectively expre
122 gene product, neurofibromin, functions as a Ras GTPase-activating protein, and has been proposed to
123 F receptors including phospholipase C gamma, Ras GTPase-activating protein, and phosphotyrosine phosp
124 The NF1 gene encodes for neurofibromin, a RAS GTPase-activating protein, and thus negatively regul
125 calcium-promoted Ras inactivator (CAPRI), a Ras GTPase-activating protein, functions as an adaptor f
126 ity of, Bruton's tyrosine kinase (Btk) and a Ras GTPase-activating protein, Gap1m, in vitro and in vi
127 ith PLCgamma, phosphatidylinositol 3-kinase, Ras GTPase-activating protein, or protein tyrosine phosp
128 -back' mutants in which association with the Ras GTPase-activating protein, phosphatidylinositol 3-ki
129 as, suggesting that it may also compete with Ras GTPase-activating protein, thus contributing to the
130 ing protein homologous to mammalian synaptic Ras GTPase-activating protein, which modify daf-7 expres
131 rategy and demonstrate its implementation on Ras GTPase-activating protein-binding protein 1 (G3BP1)
132 Stress granule (SG) formation mediated by Ras GTPase-activating protein-binding protein 1 (G3BP1)
133 ss granules are formed through the switch of Ras GTPase-activating protein-binding protein 1 (G3BP1)
134 s were enriched, including the SG-nucleating Ras GTPase-activating protein-binding protein 1 (G3BP1).
146 he tyrosine phosphorylation of two important Ras GTPase-activating proteins (GAPs), p120 Ras-GAP and
147 ced wild-type TC21 activity in vivo and that Ras GTPase-activating proteins (GAPs; p120-GAP and NF1-G
150 Rasal, belonging to the GAP1 subfamily of Ras GTPase-activating proteins (RasGAPs) with dual RasGA
151 an include functional alteration of GTPases, Ras GTPase-activating proteins, Ras guanine exchange fac
153 s of FliI immunoprecipitates showed abundant Ras GTPase-activating-like protein (IQGAP1), which in im
154 has a high affinity for the adaptor protein Ras GTPase-activating-like protein 1 (Iqgap1), which fac
157 iaD binds to the host cell protein IQGAP1 (a Ras GTPase-activating-like protein), thus displacing Rac
158 we have isolated a novel human gene, RASAL (Ras GTPase-activating-like) and its murine ortholog, MRA
160 we demonstrate that RASAL2, which encodes a RAS-GTPase-activating protein (RAS-GAP), is a functional
164 Ras-GRF mutant containing the PH domain from Ras-GTPase-activating protein in place of its own N-term
165 resis and identified by mass spectrometry as Ras-GTPase-activating protein SH3 domain-binding protein
166 teins (p85 (phosphoinositide 3-kinase), Vav, Ras-GTPase-activating protein SH3 domain-binding protein
168 alyzed GTP hydrolysis in water, Ras, and Ras.Ras-GTPase-activating protein using quantum mechanics/mo
169 n as DAB2IP), a novel member of the Ras-GAP (Ras-GTPase-activating protein) protein family, opens its
170 Nf1, a tumor suppressor gene that encodes a Ras-GTPase-activating protein, results in hyperactivity
172 xtracellular chemical gradients and position Ras GTPase activation and phosphatidylinositol (3,4,5)-t
173 NA maturation, and reveal a link between Rab/Ras GTPase activation and the process of pre-mRNA splici
174 stically, miR-132 regulated the mRNA for the Ras GTPase activator Rasa1, a novel target in neuronal f
177 ino acid substitutions that reduce intrinsic Ras GTPase activity and confer resistance to GTPase-acti
178 t keystone regulatory residue that modulates Ras GTPase activity and ensures unidirectionality to the
179 -GAP (RRFFLDIA) block NF1-GAP stimulation of Ras GTPase activity and Ras-mediated activation of mitog
180 romin is a tumor suppressor protein that has Ras GTPase activity, thus attenuating the MAPK (mitogen-
181 pe I transmembrane receptor with intrinsic R-Ras GTPase activity, which regulates cytoskeletal remode
188 t frequently display activating mutations in Ras GTPases and activation of signal transducer and acti
189 a unique function of RIT1 compared to other Ras GTPases and elucidate a direct link between a signal
190 e Raf protein kinases are major effectors of Ras GTPases and key components of the transcriptional re
191 n-3 RING E3 ubiquitin ligase, binds specific RAS GTPases and promotes their ubiquitination and protea
196 ng nontransformed fibroblasts, we found that Ras GTPases are dispensable for growth-factor-stimulated
207 essential for tracking: inactivation of the Ras GTPase Bud1 and positioning of actin-independent ves
218 fferentiation, and transformation, including Ras GTPase family members, require the covalent attachme
224 e shown that homozygous deletion of Nf1, the Ras GTPase gene underlying human neurofibromatosis type
226 Activities of Ras GTPases are triggered by Ras GTPase guanine nucleotide exchange factors (RasGEFs)
227 Self-assembly of plasma membrane-associated Ras GTPases has major implications to the regulation of
229 4-targeted tumors revealed inhibition of the RAS-GTPase, Hedgehog, and Notch pathways, along with evi
234 wo non-tagged endogenous proteins, actin and RAS GTPase, involved in complex functional networks sens
235 Regulated activation of the highly conserved Ras GTPase is a central event in the stimulation of cell
239 Here, we show that low expression of kappaB-Ras GTPases is frequently detected in PDAC and correlate
244 of downstream effector pathways such as the RAS GTPase/MAP kinase (MAPK) signaling cascade is though
246 endothelial cell apoptosis by attenuation of Ras GTPase methylation and activation and its downstream
247 Apart from the classic (H-, K-, and N-) Ras GTPases, only the R-Ras subfamily (R-Ras, R-Ras2/TC2
250 ystander tyrosine residue present in Ral and Ras GTPases provide a strategy that could lead to therap
256 tantly activated by both RhoA and individual Ras GTPases resulting in diverse upstream control of sig
263 n fusion and analyzed for protein stability, Ras GTPase stimulating activity, affinity for Ras-GTP, a
264 over, p120 N-terminal sequences enhanced the Ras GTPase-stimulating activity of the neurofibromin GAP
266 it is one of the original members of a novel Ras GTPase subfamily that uses distinct effector pathway
268 erence at Snowmass Village, Colorado, on the Ras GTPase superfamily provided testimony to the broad i
271 or synaptic plasticity, most notably in the Ras/GTPase superfamily, and in pathways that regulate cy
272 rminal hypervariable region (HVR) of Rho and Ras GTPases target these proteins to specific membrane c
273 y involved in the control of Ral, Rap, and R-Ras GTPases that may participate in the progression of b
274 colon cancers have a mutation in K-RAS or N-RAS, GTPases that operate as central hubs for multiple k
275 -state mechanisms, such as activation of the Ras GTPase, the diffusion-limited activation rate consta
276 re, we describe a novel mechanism connecting RAS GTPase to nutrient availability in fission yeast.
278 connect the membrane targeting sequences in Ras GTPases to talin, thereby recruiting talin to the pl
280 ne nucleotide exchange factors that activate Ras GTPases, ultimately leading to MAPK activation and m
282 n the major signaling cascade, activation of Ras GTPase, we constructed fusions of Grb2, Shc, H-Ras,
283 K) As this disease mutation is also found in RAS GTPases, we assessed GAP-stimulated GTP hydrolysis f
284 nto the regulation of integrin activation by Ras GTPases, we created a series of H-Ras/R-Ras chimeras
285 e discovery that activating mutations of the Ras GTPase were associated with 30% or more of human can
290 M/lamellipodin (MRL) proteins link activated Ras-GTPases with actin regulatory Ena/VASP proteins to i