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1 cal face was critical for mediating receptor transphosphorylation.
2 a, and subsequent autophosphorylation and/or transphosphorylation.
3 omains pivot on conserved hinges to modulate transphosphorylation.
4 on but require a type II receptor capable of transphosphorylation.
5 th ADP and UDP were effective substrates for transphosphorylation.
6 tors and activating their kinase domains via transphosphorylation.
7 utophosphorylation nor phospholipase C-gamma transphosphorylation.
8 er complex and likely activate each other by transphosphorylation.
9  multimers that carry out effective receptor transphosphorylation.
10 ensuring effective BRI1-SERK interaction and transphosphorylation.
11 -rotation allows them to orient properly for transphosphorylation.
12  and in fact, UVB did not alter PKC-mediated transphosphorylation.
13  with the inhibition of both FGFR1 and FGFR2 transphosphorylation.
14 e active sites for efficient activation loop transphosphorylation.
15 ces signaling output through reciprocal BRI1 transphosphorylation.
16 3-3 mediated heterooligomerization and C-RAF transphosphorylation.
17 e difluoromethyluridine residue via internal transphosphorylation.
18 on activates their kinase activities through transphosphorylation.
19 ires PKC but not PKD activity, indicative of transphosphorylation.
20 valence of complex activation via reciprocal transphosphorylation across the plant RK family has not
21 nce their appended PTKs, antigens induce PTK transphosphorylation, activating them to phosphorylate t
22 ining the balance between the hydrolysis and transphosphorylation activities and plays an important r
23 vel kinase nrdD with autophosphorylation and transphosphorylation activities in the lysates.
24  Galpha13 stimulates autophosphorylation and transphosphorylation activities of Tec.
25 domain decrease both autophosphorylation and transphosphorylation activities.
26 ted auto-activation of PKR and inhibited PKR transphosphorylation activities.
27 that tyrosine 360 of Bcr is critical for the transphosphorylation activity of Bcr and that in Ph-posi
28                                          The transphosphorylation activity of the K328C enzyme was se
29 pendent RcCDPK1 autophosphorylation and BTPC transphosphorylation activity, it is not critical for in
30 activity and sugar phosphate-dependent sugar transphosphorylation activity.
31 surface G protein-coupled receptors leads to transphosphorylation and activation of a number of recep
32  homology 2 (SH2) domain is critical for the transphosphorylation and activation of Emt/Itk catalytic
33 nding to the type II receptor results in the transphosphorylation and activation of the type I recept
34 ecruited a second Lyn molecule, allowing for transphosphorylation and amplification of Lyn activation
35 correlated with increased phosphotyrosine on transphosphorylation and autophosphorylation sites.
36 trating that CheA[1-149] fragments have both transphosphorylation and phosphotransfer capability in v
37           We first assessed in vitro PKC-PKD transphosphorylation and PKD activation.
38 he clustering of the Eph receptor, fostering transphosphorylation and signal transduction into the ce
39 tor BAK1 is then activated by BRI1-dependent transphosphorylation and subsequently enhances signaling
40 nduced dimerization, which promotes receptor transphosphorylation and thereby increases the receptor'
41 the SQ/TQ-cluster domain (SCD) abolished Mnk transphosphorylations and autophosphorylations, indicati
42 -elimination, Seyferth-Gilbert homologation, transphosphorylation, and a 1,3-dipolar cycloaddition re
43 ATM, followed by Chk2 oligomerization, auto-/transphosphorylation, and activation.
44 tor phosphorylation experiments, NDF-induced transphosphorylation appears to be correlated with syner
45  the hairpin ribozyme to enhance the rate of transphosphorylation are presented, and the roles of A38
46 such that high-affinity binding and receptor transphosphorylation are reduced.
47                    Using an in vitro peptide transphosphorylation assay, sorbitol treatment activates
48 -induced PlexinD1-VEGFR2 association, VEGFR2 transphosphorylation at Y1214, and p38 MAPK activation,
49                               This occurs by transphosphorylation at Y551 in the Btk catalytic domain
50  following ligand perception, and reciprocal transphosphorylation between a receptor and its corecept
51                               Interestingly, transphosphorylation between HER1 and HER4 can be stimul
52                                  (vi) Mutual transphosphorylation between pUL97 and CDK7 is not detec
53                                 Heterologous transphosphorylation between TrkB and TrkC kinase domain
54 otetramer is capable of a low-level receptor transphosphorylation, but C-terminal phosphorylation and
55  can occur by phosphorylation of HDAC4 or by transphosphorylation by CaMKII bound to HDAC4.
56  this may reflect PIP(3) effects on PDK-1 or transphosphorylation by endogenous full-length PKC-zeta.
57 omain, CheA[1-149], was a poor substrate for transphosphorylation by full-length CheA molecules, impl
58         These lesions reduced the rate of P1 transphosphorylation by P4.
59 rabidopsis PDK1 interacts with PID, and that transphosphorylation by PDK1 increases PID autophosphory
60                                         This transphosphorylation by RAFs is essential for SnRK2 acti
61                        Catalysis of RNA 2'-O-transphosphorylation by ribonuclease A is proposed to in
62                                              Transphosphorylation by Src family kinases is required f
63  membrane localization, Btk kinase activity, transphosphorylation by Src family kinases, and an intac
64 nly modified through autophosphorylation and transphosphorylation by TRPM6.
65 omplex that is necessary for stable receptor transphosphorylation differs from the signaling complex
66               PIKfyve autophosphorylation or transphosphorylation engaged Ser but not Thr or Tyr resi
67 ously that Itk is regulated by an activating transphosphorylation event in which Tyr-511 in the kinas
68 nsitions would render Y416 available for the transphosphorylation event that ultimately locks down th
69 ies indicated that the rate of extracellular transphosphorylation exceeds that of nucleotide hydrolys
70                                              Transphosphorylation is mediated by specific asymmetric
71 P occurs from most cell types indicates that transphosphorylation is physiologically important in the
72 structural arrangement of the enzyme and its transphosphorylation mechanism.
73 ogenous C-RAF, possibly via an allosteric or transphosphorylation mechanism.
74 ion is controlled by autophosphorylation and transphosphorylation mechanisms, which includes phosphor
75 istent with the recently proposed sequential transphosphorylation model for BRI1/BAK1 interaction and
76                      We propose a sequential transphosphorylation model in which BRI1 controls signal
77                                 KSR acts via transphosphorylation, not by increasing c-Raf-1 autophos
78                                 Trk receptor transphosphorylation occurs in the two non-neuronal cell
79 nonphosphorylatable CheA(S) protein mediates transphosphorylation of a CheA(L) variant defective in b
80 s RTK to a less potent enzyme by disfavoring transphosphorylation of activation loop tyrosines.
81  fluorometric assay based upon the enzymatic transphosphorylation of adenosine diphosphate to adenosi
82 1 with Akt3 and as a consequence facilitated transphosphorylation of Akt molecules, which may contrib
83 DK1 and is not due to autophosphorylation or transphosphorylation of Akt.
84 phorylation activity of ArcB and enhance the transphosphorylation of ArcA, but have no effect on the
85 uced both autophosphorylation of Tyr-811 and transphosphorylation of Bcr, a recently identified Fes s
86 ion pathway in which autophosphorylation and transphosphorylation of BRI1 and BAK1, as well as phosph
87 dependent homo-oligomer, as evidenced by the transphosphorylation of BRI1 kinase in vitro, the domina
88 nd in vitro experiments where it blocked the transphosphorylation of Cps2D even in the presence of th
89              The Ca(2+)/CaM binding triggers transphosphorylation of critical threonine residues prox
90  DNA-PKcs protein, we show that ATM-mediated transphosphorylation of DNA-PKcs regulates end-processin
91 are active in autophosphorylation as well as transphosphorylation of each other and specific peptide
92 riants defective for either G1 or G2 mediate transphosphorylation of each other poorly, if at all.
93                                              Transphosphorylation of EMS1 by SERK1 enhances EMS1 kina
94 mutant and Epo-R was associated with reduced transphosphorylation of Epo-R and expression of c-Myc.
95 he molecular basis underlying the control of transphosphorylation of FGF receptors and other receptor
96 tivated FGFR1 kinase domains is required for transphosphorylation of FGFR1 in FGF-stimulated cells.
97 t differentially with G(s) proteins and that transphosphorylation of GDP to GTP is not involved in th
98 ly than to ArcA; and that D1 accelerates the transphosphorylation of H2.
99 of the kinase impaired HER-3 as reflected in transphosphorylation of HER-3 and heteromers between HER
100 ssess the efficacy of HER TKIs should be the transphosphorylation of HER3 rather than autophosphoryla
101 ferent extracellular regions, intermolecular transphosphorylation of homologous cytoplasmic domains o
102 tion between ITK and SLP-76, recruitment and transphosphorylation of ITK, actin polarization at the T
103         This association is required for the transphosphorylation of Itk.
104 tor proximal complex assembly and reciprocal transphosphorylation of Jak1 and Tyk2 as well as the pho
105 thought to involve receptor dimerization and transphosphorylation of juxtaposed catalytic domains.
106 t a requisite for signaling, indicating that transphosphorylation of K721M by ErbB2 was not an essent
107 is likely because palmitoylation facilitates transphosphorylation of key sites in JAK1's activation l
108 bited by RNAi showed a dramatic reduction in transphosphorylation of myelin basic protein substrate.
109                                              Transphosphorylation of nucleotide triphosphates is the
110 tance, the microscopic chemical mechanism of transphosphorylation of nucleotide triphosphates is, in
111 s nuclear Erk1/2 signaling: It emanates from transphosphorylation of p21-activated kinases in their e
112                                         Sole transphosphorylation of p21-activated kinases is not suf
113 mains of TAFII250 are required for efficient transphosphorylation of RAP74 on serine residues.
114         Lysophosphatidic acid (LPA)-elicited transphosphorylation of receptor tyrosine kinases has be
115                                  Thus, auto-/transphosphorylation of S379 is required for Chk2 ubiqui
116 artic acid in the activation loop favors the transphosphorylation of the activation loop tyrosines, a
117 erization of the PH-TH domain and subsequent transphosphorylation of the activation loop.
118  intrinsically inactive and dependent on the transphosphorylation of the activation loop.
119                   Such dimers are capable of transphosphorylation of the cytoplasmic domain of the re
120                                  LPA-induced transphosphorylation of the EGFR, ErbB2, or PDGF recepto
121 I-mediated activation of MEK and Ras but not transphosphorylation of the epidermal growth factor (EGF
122  Also, PII significantly reduced the rate of transphosphorylation of the isolated central domain by t
123  dimerization induced by IP6, which promotes transphosphorylation of the kinase domains.
124 /Akt pathway is driven predominantly through transphosphorylation of the kinase-inactive HER3.
125 er of a CheA dimer form a unit that mediates transphosphorylation of the other protomer within that d
126                                              Transphosphorylation of the PKD activation loop at serin
127 gest that eATP activation of P2K1 results in transphosphorylation of the Raf-like MAPKKK ILK5, which
128  their receptors and driving association and transphosphorylation of the receptor intracellular tyros
129                                              Transphosphorylation of the receptor subunits is followe
130 o probe the mechanism of base-catalyzed 2'-O-transphosphorylation of the RNA dinucleotide 5'-UpG-3'.
131 meric (type I-type II) complex formation and transphosphorylation of the type I receptor by the type
132 e II receptor results in the recruitment and transphosphorylation of the type I receptor.
133 he T cell antigen receptor (TCR) induces the transphosphorylation of the zeta chain-associated protei
134 or transcripts, yet LPA caused no detectable transphosphorylation of these receptor tyrosine kinases.
135  activation of ERK-1/2 additionally requires transphosphorylation of TPL-2 on serine 400 in its C ter
136 lation or activation of ERK, but it inhibits transphosphorylation of Tyr845 and activation of signal
137                            Btk* enhances the transphosphorylation of Y551 by endogenous Src family ty
138 esized to occur as a consequence of auto- or transphosphorylation on tyrosine residues associated wit
139  Trk receptor was explored by determining if transphosphorylation on tyrosine residues can occur betw
140 ves ligand-induced receptor dimerization and transphosphorylation on tyrosine residues.
141 to catalyze RNA strand cleavage through 2'-O-transphosphorylation, provoking the question of whether
142  breakpoint in the pH dependence of the 2'-O-transphosphorylation rate to a pH independent phase abov
143         Variation in the linkers could alter transphosphorylation rates within a holoenzyme and the b
144 of adenylate kinase (ADK) in the equilibrium transphosphorylation reaction (ATP + AMP <--> 2ADP).
145 cause the fructose-1-phosphate:[14C]fructose transphosphorylation reaction appeared normal, we conclu
146                          The kinetics of the transphosphorylation reaction catalyzed by the two IIGlc
147 ecific hydrolysis of phosphomonoesters and a transphosphorylation reaction in which phosphate is tran
148 nly arise from the specific enzyme catalyzed transphosphorylation reaction.
149 phoenzyme intermediates, ComB can catalyze a transphosphorylation reaction.
150          The failure of TrkA to take part in transphosphorylation reactions with TrkB and TrkC was co
151 n-off assays monitor the forward and reverse transphosphorylation reactions, respectively.
152 or facilitate asymmetric dimer formation and transphosphorylation, respectively.
153              We propose a model whereby Mps1 transphosphorylation results in its release from kinetoc
154  ErbB4 receptors and were able to modulate a transphosphorylation signal from ErbB3 to ErbB2 in MCF7
155  enzymes and an intact Btk PH domain and Src transphosphorylation site.
156 225 and Glu314) within 2.8 A of the proposed transphosphorylation site.
157 hich individual Btk molecules undergo serial transphosphorylation (site 1) then autophosphorylation (
158    Among 12 in vitro autophosphorylation and transphosphorylation sites identified by tandem mass spe
159 se domains of chimeric receptors or act as a transphosphorylation substrate for these two receptors.
160                                              Transphosphorylation targeted Ser(744), whereas autophos
161                                              Transphosphorylation thio effects in solution are studie
162                             The ratio of the transphosphorylation to the hydrolysis activities increa
163 in a chemically detailed description of 2'-O-transphosphorylation transition states provides an oppor
164 al BRI1-SERK receptor complex and subsequent transphosphorylation upon ligand binding.
165  IIA as well as IIBC (the PEP reaction), and transphosphorylation using a sugar phosphate (glucose-6-
166             Both the autophosphorylation and transphosphorylation were demonstrated with PIKfyve immu
167                   As RLK activation requires transphosphorylation with a second associated RLK, it re
168              OsSERK2 undergoes bidirectional transphosphorylation with XA21 in vitro and forms a cons
169 he activity of Btk is partially regulated by transphosphorylation within its kinase domain by Src fam
170 naling is mediated by GRK2 and could involve transphosphorylation within the heteromeric receptor com
171 c variant of the protein underwent efficient transphosphorylation, yet failed to activate appreciably

 
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