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1 romote eNOS denitrosylation concomitant with enzyme activation.
2 scussed with respect to the implications for enzyme activation.
3 nd reveal that Glu493 is critical for low pH enzyme activation.
4 T followed by its GSH-mediated reduction and enzyme activation.
5 r-783 phosphorylation was not sufficient for enzyme activation.
6  proposed to be necessary and sufficient for enzyme activation.
7 calcineurin, whereas U-73343 failed to block enzyme activation.
8 omain amino acids are responsible for low-pH enzyme activation.
9 ent of Pgamma from the PDE6 active site, and enzyme activation.
10 nformational dynamics that may be related to enzyme activation.
11 ulting in a 50-60% reduction in the level of enzyme activation.
12 hox)) that undergo structural changes during enzyme activation.
13 NOS dephosphorylation at serine 116 leads to enzyme activation.
14 hereby facilitating eNOS phosphorylation and enzyme activation.
15 nterdomain interactions that are critical to enzyme activation.
16 l outside the protease domain also influence enzyme activation.
17 ch stabilizes a disordered loop and leads to enzyme activation.
18 sabled by Ser(1179) phosphorylation-elicited enzyme activation.
19 )-) resulting in propeptide dissociation and enzyme activation.
20 el incorporation matched the time course for enzyme activation.
21 -induced structural changes in PLA2, and the enzyme activation.
22  amino half of calcineurin-B is critical for enzyme activation.
23  GSTP1-1-JNK interaction and concomitant JNK enzyme activation.
24 -Ca-ATPase that are normally associated with enzyme activation.
25 liver Ni(II) to the urease apoprotein during enzyme activation.
26 protein kinase C-mediated, and extracellular enzyme activation.
27 eractions with the PM Ca-ATPase that induces enzyme activation.
28 important to high-affinity binding and rapid enzyme activation.
29 n of the amino-terminal domain necessary for enzyme activation.
30 ic state of GPI-PLC during latency and after enzyme activation.
31 ylglycerol binding, which eventually lead to enzyme activation.
32 her than impairment of (13S)-HPODE-dependent enzyme activation.
33 te on the PM-Ca-ATPase are not necessary for enzyme activation.
34 and/or for the subsequent steps that lead to enzyme activation.
35 uired for both the conformational change and enzyme activation.
36 nity for substrate and consequently leads to enzyme activation.
37 andem C1a and C1b domains in PKC, leading to enzyme activation.
38  Kd (0.1 microM) corresponds to the EC50 for enzyme activation.
39 Galphaq, is suggested as a mechanism for the enzyme activation.
40 eavage is necessary, but not sufficient, for enzyme activation.
41 nding of Ca2+-calmodulin to eNOS, leading to enzyme activation.
42 effect of PAF on PLA2-II gene expression and enzyme activation.
43 oteins, which, in normal controls, parallels enzyme activation.
44  Swiss 3T3 cells, palytoxin causes prolonged enzyme activation.
45 to play a role in membrane translocation and enzyme activation.
46 n; and (4) mTOR-membrane engagement and full enzyme activation.
47 al light-absorbing rhodopsin responsible for enzyme activation.
48 ctivation, with a K(D) of 29 muM and 387% of enzyme activation.
49 dynamics of USP7 in solution and its role in enzyme activation.
50 gnition as a putative mechanism of cGAS-like enzyme activation.
51 -protein interaction specificity that alters enzyme activation.
52  reveals key details of the mechanism of TIR enzyme activation.
53 utilize substrate dianion binding energy for enzyme activation.
54 , thereby imposing a novel checkpoint during enzyme activation.
55 x that leads to acidification and hydrolytic enzyme activation.
56 x into the heterodimer interface, leading to enzyme activation.
57 effector binding plays an additional role in enzyme activation.
58 e dimer-to-tetramer transition necessary for enzyme activation.
59 poglycemia reveal two distinct mechanisms of enzyme activation.
60 jor regulating element for self-assembly and enzyme activation.
61 ion site for Nox1-NOXA1 binding required for enzyme activation.
62 ant cellular processes such as signaling and enzyme activation.
63 of class C sortase substrate recognition and enzyme activation.
64 clases have a common molecular mechanism for enzyme activation.
65 where it can lead to intracellular digestive enzyme activation.
66 cular insight into the mechanism of PKCalpha enzyme activation.
67 (2+) dependencies for calmodulin binding and enzyme activation.
68 at oxidation disrupts calmodulin binding and enzyme activation.
69  more compact structure that is required for enzyme activation.
70 o differentiate between specific and general enzyme activation.
71 eneration of superoxide anion (O(2)(*)) upon enzyme activation.
72 tion is coupled to phosphorylation-dependent enzyme activation.
73 rdomain contacts important for DNA-dependent enzyme activation.
74 ut significant effect on the Zn2+ K(1/2) for enzyme activation.
75 ion of PLCgamma1 Y783, which is critical for enzyme activation.
76 ardiolipin (CL) is the best phospholipid for enzyme activation.
77 r 5-LO expression in splenocytes, indicating enzyme activation after GVHD.
78  specific residues involved in PIP2-mediated enzyme activation, amino acids with functional side chai
79 he close correspondence between caspase-like enzyme activation and an associated increase in immunore
80 functions as a regulator of membrane binding/enzyme activation and as an inhibitor of catalysis in th
81 ues involved in Tyr(P) binding abrogated the enzyme activation and association of PKCtheta with Tyr-p
82 e H activity where one metal is required for enzyme activation and binding of a second metal is inhib
83 sduction is controlled both by regulation of enzyme activation and by organization of enzymatic compl
84 evation in intracellular calcium, leading to enzyme activation and cell death.
85                               The reciprocal enzyme activation and competitive inhibition exhibited b
86 ull-length cGAS and thus reduces the rate of enzyme activation and cyclic GMP-AMP synthesis.
87 ed cysteine residues were also necessary for enzyme activation and H(2)O(2) generation.
88                   Owing to the decoupling of enzyme activation and imaging tag immobilization, TCO-C-
89 eptide and protein/protein interactions, and enzyme activation and inactivation, in response to Ca2+
90           To unravel the molecular basis for enzyme activation and localization, we determined the cr
91  of caspase 1 processing, thereby inhibiting enzyme activation and maturation of IL1beta/18 in a LUBA
92 mplications of the structural change for the enzyme activation and mechanism are discussed.
93 as a basis for identifying the mechanism for enzyme activation and substrate specificity.
94 omains cover the active site to control both enzyme activation and substrate specificity.
95 subtype localization and its relationship to enzyme activation and target phosphorylation have not, h
96  discuss the recent uses of ionic liquids in enzyme activation and their combination with nanosized m
97 genin is very low, and the mechanisms of the enzyme activation and tRNA specificity have remained a p
98 timulatory eNOS phosphorylation (Ser(1177)), enzyme activation, and NO synthesis.
99 sors that can measure analyte concentration, enzyme activation, and protein-protein interactions in l
100  IP(3)-3KB structure suggests a mechanism of enzyme activation, and raises the possibility that an in
101 , which enhance catechin production, terpene enzyme activation, and stress tolerance, important featu
102 rcolemmal receptor activation, intracellular enzyme activation, and ultimately mitochondrial stabilis
103  RAPTOR-membrane engagement and intermediate enzyme activation; and (4) mTOR-membrane engagement and
104 ing the affinity for substrates, whereas the enzyme activation appeared to be specifically controlled
105 ed with using only trypsin and CID, the dual-enzyme/activation approach enabled the identification of
106 man SIRT2), only SIRT1 exhibited significant enzyme activation ( approximately 8-fold) using the comm
107  in the protein tryptophan fluorescence) and enzyme activation are both cooperative with Hill coeffic
108 er, details of YC-1 interaction with sGC and enzyme activation are incomplete.
109 mma1 phosphorylation to dramatically enhance enzyme activation as observed, we found that high intram
110 gainst SOD1 misfolding does not require SOD1 enzyme activation as the same effect was obtained with t
111 or of Gbetagamma attenuated S1P-induced eNOS enzyme activation, as well as S1P-induced phosphorylatio
112 ed out, including multiplexed assays and pro-enzyme activation assays.
113 rminated reporters, followed by the assay of enzyme activation at a later time and place.
114 rylation of Nox5 at key residues facilitates enzyme activation at lower levels of intracellular calci
115 the differential requirement of Ca2+/CaM for enzyme activation between eNOS and iNOS by either deleti
116 spase-3 by 24 hours and a clear induction of enzyme activation by 48 hours, which was identified by t
117 ion of MT1-MMP (Ser466Pro) resulted in lower enzyme activation by bicelles.
118          In contrast, both mutations reduced enzyme activation by blocking the ability of ATP to decr
119               Kinetic modeling which invokes enzyme activation by both dimerization and excess substr
120 and Asp(818) to Asn interferes strongly with enzyme activation by Ca(2+) binding and formation of pho
121       SERCA E-P formation is rate-limited by enzyme activation by Ca(2+), demonstrated by the additio
122                                              Enzyme activation by cardiolipin (n=2.8), CDP-diacylglyc
123 thelial plasma membranes, and Ptox prevented enzyme activation by E(2) in COS-7 cells expressing ERal
124                                  The mode of enzyme activation by effector binding is unknown.
125 scoclaurine alkaloid known to inhibit PLA(2) enzyme activation by heterotrimeric G-proteins, effectiv
126 c ion, as well as a prodomain that regulates enzyme activation by modulation of a cysteine residue wi
127                                              Enzyme activation by monovalent cations is widely docume
128  rich repertoire of molecular mechanisms for enzyme activation by Na(+) and K(+) Strategies range fro
129 alytic residues, and determine the origin of enzyme activation by the hydrophobic leaving group.
130 W indicates that Ca(2+)/CaM binding promotes enzyme activation by transferring F293 from an internal
131 ulated active conformations, indicating that enzyme activation can occur spontaneously, even in the a
132 ear channel binding affinity and potency for enzyme activation, confirming the mechanism of allosteri
133 D brain, it is hypothesized that the lack of enzyme activation contributes to the accumulation of ins
134                                              Enzyme activation could be prevented by pretreating the
135 that the role of tyrosine phosphorylation in enzyme activation differs between vertebrates and invert
136 gion in a manner similar to the mechanism of enzyme activation elicited by the R794G mutation.
137                                   In type II enzymes, activation entails two steps: binding of the mo
138                               In contrast to enzyme activation, EPR signal formation did not require
139 s polyP may differentially modulate specific enzyme activation events within the contact pathway.
140 nase that requires charged phospholipids for enzyme activation, for regulation by Gbetagamma subunits
141 0)(Ca(2+)) values for calmodulin binding and enzyme activation from the control values of 182 +/- 2 a
142 0(Ca (2+)) values for calmodulin binding and enzyme activation from the wild-type values of 180 +/- 2
143 egulated genes in the mouse uterus, and eNOS enzyme activation further indicated that EDC specificall
144                                           If enzyme activation happens exclusively or predominantly i
145        During apoptosis, executioner caspase enzyme activation has been considered a point of no retu
146 ation of the MgATP-binding pocket leading to enzyme activation has been demonstrated for ribokinases.
147 on of cytosolic NADPH oxidase components and enzyme activation has been identified but is not well un
148 novel models to study the role of pathologic enzyme activation has led to advances in our understandi
149 r Ca(2+) homeostasis and premature digestive enzyme activation; however, the molecular mechanisms by
150 llular calcium and may provide an avenue for enzyme activation in response to a greater variety of ex
151 or CCS in the SOD1 pathway, namely mediating enzyme activation in response to increases in oxygen ten
152 ction (CE-F) is a powerful method to measure enzyme activation in single cells.
153 d for at least 30min and was able to trigger enzyme activation in vitro at heparin level of 0.4U/mL.
154 ubcellular distribution of PKC (a measure of enzyme activation) in a growth factor-dependent pluripot
155 the signature of somatic hypermutation (SHM) enzyme, Activation Induced Deaminase (AID), which overla
156 ction of DNA damage into the Ig genes by the enzyme activation-induced cytidine deaminase (AID) and t
157                          The B cell-specific enzyme activation-induced cytidine deaminase (AID) has b
158                                The mutagenic enzyme activation-induced cytidine deaminase (AID) is re
159                    Aberrant targeting of the enzyme activation-induced cytidine deaminase (AID) resul
160 ) is characterized by elevated levels of the enzyme activation-induced cytidine deaminase (AID), an e
161 n of the oncogenic LMP1 and the DNA-mutating enzyme activation-induced cytidine deaminase (AID), in t
162 ition, including one lacking the DNA-editing enzyme activation-induced cytidine deaminase (AID), whic
163 alongside mRNA for the transiently-expressed enzyme Activation-induced cytidine Deaminase (AID).
164 es of high affinity Abs are dependent on the enzyme activation-induced cytosine deaminase (AID).
165 ed immunoglobulin gene and expression of the enzyme activation-induced deaminase (AID) are essential
166  proliferating centroblasts that express the enzyme activation-induced deaminase (AID) to undergo som
167 is a critical immune process governed by the enzyme activation-induced deaminase (AID), a member of t
168 e created transgenic mice overexpressing the enzyme activation-induced deaminase (AID), which has a n
169 expression of FOXP1 and the B-cell mutagenic enzyme activation-induced deaminase, and immune evasion
170 pendent on the action of the B cell specific enzyme, activation-induced cytidine deaminase (AID), and
171  been difficult to uncouple because a single enzyme, activation-induced cytidine deaminase (encoded b
172 ressing B cells up-regulate the CSR-inducing enzyme, activation-induced cytidine deaminase, and under
173  linked with both processes dependent on the enzyme, activation-induced deaminase, and occurring prin
174 current view of the structural basis for CaM enzyme activation is based on biophysical studies of CaM
175                                              Enzyme activation is detectable within 30 seconds and su
176 vior is consistent with the observation that enzyme activation is detected at low short-chain anionic
177 ivation of myo-inositol monophosphatase, and enzyme activation is enhanced under conditions in which
178            The PR is active only as a dimer; enzyme activation is initiated when the PR domains in tw
179 h an eNOS-caveolin regulatory cycle, wherein enzyme activation is modulated by reversible protein-pro
180 common probe design approach based on single-enzyme activation is not applicable.
181                              We propose that enzyme-activation is a possible, and perhaps probable, c
182 pid-containing membranes, a crucial step for enzyme activation, is not fully understood.
183  SH3 domains in promoting substrate binding, enzyme activation likely reorients the relative spatial
184  including the regulation of blood pressure, enzyme activation, maintenance of muscular strength, reg
185 high affinity and suggest that inhibition of enzyme activation may be an unrecognized mechanism of in
186 vity of PDE5 suggests that this mechanism of enzyme activation may be common among other GAF domain-c
187  of eNOS has been studied as a surrogate for enzyme activation may need to be reassessed.
188          No analogous small molecule-induced enzyme activation mechanism involving dissociation and r
189 i-associated furin is analogous to a similar enzyme activation mechanism observed with stromelysin-3.
190 ata from these structures in terms of target enzyme activation mechanisms is that the larger enzyme s
191 omeostasis, regulation of protein synthesis, enzyme activation, membrane potential adjustment and ele
192                                      Maximum enzyme activation occurred at an MT-2:apo-CA molar ratio
193                  In this complex reversal of enzyme activation occurs when Ca(2+) dissociates from th
194 th PAF and LPS induce gene transcription and enzyme activation of PLA2-II in the small intestine; 2)
195                                              Enzyme activation of prodrugs to improve the therapeutic
196                                        Thus, enzyme activation of the Ca-ATPase may occur through dif
197            Array use involves two steps: (1) enzyme activation of the test chemical and metabolite re
198                                              Enzyme activation, on the other hand, is prevented under
199 bove antisense oligodeoxynucleotides inhibit enzyme activation, our results exemplify an unusual mode
200 +/ATPase activation occurred and binding and enzyme activation persisted long after the Ca transient
201 for affinity column binding, suggesting that enzyme activation precedes carbohydrate maturation and t
202                  Thus, cytochrome P450 (CYP) enzyme activation presents as a potential drug-drug inte
203                                          The enzyme activation rates by two most active compounds at
204 ism that relates calmodulin (CaM) binding to enzyme activation remains to be established within the c
205 click" method utilizing an alkyne-terminated enzyme activation reporter, aldehyde-based fixation, and
206 of the molecular mechanism for CaM-dependent enzyme activation requires additional structural informa
207                                              Enzyme activation requires calcium-induced dimerisation
208 As is the case for all retroviral proteases, enzyme activation requires the formation of protease hom
209                                              Enzyme activation requires translocation of p67(phox), p
210 2a inhibition by decreasing K(Ca) values for enzyme activation, respectively.
211                           Here, we show that enzyme activation screens can also uncover compounds tha
212                    We develop strategies for enzyme activation, shell self-assembly, and cargo encaps
213 in the K0.5 values for calcium dependence of enzyme activation (shifted from 1.1 microM to 9.1 microM
214 hen added to the enzyme as a peptide, causes enzyme activation similar to that with Gbetagamma subuni
215            To further describe changes after enzyme activation, site-directed spin labeling at amino
216 nes thought to be associated with pathologic enzyme activation (such as serine protease inhibitor 1)
217 gely responsible for the decreased extent of enzyme activation, suggesting that this site is critical
218 sphodianion-driven conformational changes to enzyme activation suggests that this catalytic motif has
219 erent mechanisms of action involved in these enzyme activation techniques.
220 gements in three sites implicated earlier in enzyme activation-the VSD-PD linker, gating loop and R l
221 anding of pancreatic intracellular digestive enzyme activation; the pancreatic inflammatory response;
222  lack of SAMe by bypassing the deficiency in enzyme activation; this is done by providing the product
223 ng to AKAPs and consequent modulation of the enzyme activation threshold rather than on overall chang
224 new molecular mechanisms in proximity-driven enzyme activation, threshold behavior, signal amplificat
225        We elucidated a structural pathway of enzyme activation through cryo-electron microscopy analy
226                For some UbiD family members, enzyme activation through prFMNH(2) binding and subseque
227  calmodulin binding and calmodulin-dependent enzyme activation to 65 +/- 4 and 118 +/- 4 nM, respecti
228 0)(Ca(2+)) values for calmodulin binding and enzyme activation to 77 +/- 2 and 130 +/- 5 nm.
229                                              Enzyme activation translated directly to elevation of NA
230                               Conditions for enzyme activation upon removal of the pro-sequence have
231 properties of the tissue and ligand for both enzyme activation via collision coupling and the generat
232 onents was required for enzyme activity, and enzyme activation was associated with membrane transloca
233 steines as evidenced by the observation that enzyme activation was attenuated by thiol-containing nuc
234  In adherent multicellular isolate cultures, enzyme activation was followed by precipitation of arago
235 ds the C2 domain of PKCdelta tightly, but no enzyme activation was observed with PKCdelta.
236 phinyl-oxy-TEMPO, respectively, suggest that enzyme activation was only weakly affected by changes in
237                               LPA-stimulated enzyme activation was significantly attenuated in an eNO
238 to the lipid bilayer-a usual requirement for enzyme activation-was determined by using a sucrose-load
239 ntify structural changes that correlate with enzyme activation, we have used frequency-domain phospho
240      To probe the molecular mechanism of the enzyme activation, we performed a detailed account of th
241  NO coordination state, NO dissociation, and enzyme activation were significantly affected by the pre
242 These results are consistent with a model of enzyme activation where phosphorylation of the MAP kinas
243  of grade, had the highest overall degree of enzyme activation, whereas oligodendrogliomas had the le
244 euronal calpain nitrosylation and results in enzyme activation, which, in turn, leads to tau phosphor
245 ensus HEXXH zinc-binding region required for enzyme activation, while their cysteine-rich domains app
246  new concept in combination therapy, that of enzyme activation with two compounds that hit the same b

 
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