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1 ectors phospholipase C (PLC)gamma2, Akt, and Bruton's tyrosine kinase.
2 on factor and a target of phosphorylation by Bruton's tyrosine kinase.
3 ction of TEC family tyrosine kinases such as Bruton's tyrosine kinase.
4 r II-I), which encodes BAP-135, a target for Bruton's tyrosine kinase.
5 her revealed that DOK3 was phosphorylated by Bruton's tyrosine kinase.
7 mast cell proliferation was not dependent on Bruton's tyrosine kinase, a downstream effector of PI3K,
10 pamycin, histone deacetylase, bcl-2, and the Bruton's tyrosine kinase, a pivotal enzyme in the BCR pa
12 aRIIb1 with BCR inhibits PIP3-dependent Btk (Bruton's tyrosine kinase) activation and the Btk-depende
13 19, as demonstrated by reduced activation of Bruton's tyrosine kinase and extracellular signal-regula
14 significant and dose-dependent inhibition of Bruton's tyrosine kinase and indirectly its downstream s
15 rreversible small-molecule inhibitor of both Bruton's tyrosine kinase and interleukin-2 inducible kin
16 right function is dependent upon both active Bruton's tyrosine kinase and its substrate, the transcri
17 CR-mediated DAG production is dependent upon Bruton's tyrosine kinase and phospholipase C-gamma2, enz
21 ant leukaemic cells expressed high levels of Bruton's tyrosine kinase and two ATP synthetases (ATP5A1
22 e proteins identified by MALDI-TOF including Bruton's tyrosine kinase and X-linked inhibitor of apopt
23 In osteoclasts, loss of CypA activates BtK (Bruton's tyrosine kinase) and subsequently integrates wi
24 n Fyn kinase, independent of Syk, PI3K, Akt, Bruton's tyrosine kinase, and JAK2, and enhanced in the
25 tor tyrosine kinases spleen tyrosine kinase, Bruton's tyrosine kinase, and phosphatidylinositol 3-kin
27 olipase Cgamma2 in mediating PKC activation, Bruton's tyrosine kinase- and phospholipase Cgamma2-defi
30 s of the anti-apoptotic tyrosine kinase BTK (Bruton's tyrosine kinase) as anti-leukemic agents with a
31 eficient (xid) mice possess mutations in the Bruton's tyrosine kinase (Btk kinase) gene and display d
33 directly to, and stimulates the activity of, Bruton's tyrosine kinase (Btk) and a Ras GTPase-activati
35 is an FDA-approved irreversible inhibitor of Bruton's tyrosine kinase (BTK) and IL-2 inducible T cell
36 have immunomodulatory effects by inhibiting Bruton's tyrosine kinase (BTK) and IL-2-inducible T cell
38 Ibrutinib is an irreversible inhibitor of Bruton's tyrosine kinase (BTK) and is effective in chron
39 B-cell-restricted factor that complexes with Bruton's tyrosine kinase (Btk) and its substrate, transc
41 trated that Bright coimmunoprecipitates with Bruton's tyrosine kinase (Btk) and that these proteins a
42 his study, we show that both the stimulatory Bruton's tyrosine kinase (Btk) and the inhibitory SHIP-1
49 acologic inhibition and genetic knockdown of Bruton's tyrosine kinase (BTK) blocks AML blast prolifer
55 gnaling supports Notch2(+/-)/NOD MZ B cells, Bruton's tyrosine kinase (Btk) deficiency was introduced
57 tionally, wild type or constitutively active Bruton's tyrosine kinase (Btk) enhanced, whereas the xid
59 egulating B cell development and activation, Bruton's tyrosine kinase (Btk) functions downstream of m
61 the pleckstrin homology domain of the mouse Bruton's tyrosine kinase (btk) gene results in an X-link
64 (lo)) expressing 25% of endogenous levels of Bruton's tyrosine kinase (Btk) have B cell functional re
66 ncovered a previously unappreciated role for Bruton's tyrosine kinase (Btk) in actin tail formation i
68 rs have implicated a role for the Tec kinase Bruton's tyrosine kinase (Btk) in inflammatory cytokine
70 olecule inhibitors of BCR signaling kinases, Bruton's tyrosine kinase (Btk) inhibitor ibrutinib and t
71 We show that an analogue of the covalent Bruton's tyrosine kinase (BTK) inhibitor Ibrutinib beari
74 a single agent, and in combination with the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib or th
91 ed that functional, but not kinase-inactive, Bruton's tyrosine kinase (Btk) is critical for Bright ac
117 in Gqalpha binds directly to the nonreceptor Bruton's tyrosine kinase (Btk) to a region composed of a
119 Previously, defects in the gene coding for Bruton's tyrosine kinase (Btk) were shown to result in d
120 uld directly increase the kinase activity of Bruton's tyrosine kinase (Btk) whose defects are respons
125 an interact physically and functionally with Bruton's tyrosine kinase (Btk), a hematopoietic non-rece
126 ated cells is mediated by stimulation of the Bruton's tyrosine kinase (BTK), a member of the Src-rela
132 promoters and requires Bright dimerization, Bruton's tyrosine kinase (Btk), and the Btk substrate, T
136 an orally administered covalent inhibitor of Bruton's tyrosine kinase (BTK), is an effective treatmen
139 hree protein tyrosine kinases, Lyn, Syk, and Bruton's tyrosine kinase (Btk), leading to the secretion
140 inhibitors targeting BCR-associated kinases [Bruton's tyrosine kinase (BTK), phosphoinositide 3-kinas
141 been delineated based on the involvements of Bruton's tyrosine kinase (Btk), protein kinase C (PKC),
142 e now report that Bright coprecipitates with Bruton's tyrosine kinase (Btk), the defective enzyme in
143 inical phenotype of patients with defects in Bruton's tyrosine kinase (Btk), the gene that is abnorma
145 ing ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase (BTK), to bendamustine plus rit
146 activity of a purified non-receptor kinase, Bruton's tyrosine kinase (Btk), whereas purified alpha-s
148 peration between the protein tyrosine kinase Bruton's tyrosine kinase (Btk), which regulates the acti
151 posure of wild-type DT40 lymphoma B cells or Bruton's tyrosine kinase (BTK)-deficient DT40 cells reco
154 1 (MAV-1) infection of B-cell-deficient and Bruton's tyrosine kinase (Btk)-deficient mice resulted i
155 ther define the nature of the protective Ab, Bruton's tyrosine kinase (Btk)-deficient mice were chara
164 which is caused by mutations in the gene for Bruton's tyrosine kinase (Btk); however, there are femal
166 cute myeloid leukaemia have high activity of Bruton's tyrosine-kinase (BTK) in their blast cells comp
167 ty of kinases (spleen tyrosine kinase [Syk], Bruton's tyrosine kinase [Btk], phosphatidylinositol 3-k
170 ndent differences in Lyn phosphorylation and Bruton's tyrosine kinase distribution were observed betw
171 osine kinase R544 on the activation loop and Bruton's tyrosine kinase E445 on the C-helix also aids i
172 PUVA caused poor membrane binding of Akt and Bruton's tyrosine kinase effectors following activation
173 Suppressed expression of c-Src or downstream Bruton's tyrosine kinase, Ets1, Ets2, USF1, or USF2 bloc
174 hich express Bmx and Src as their major Btk (Bruton's tyrosine kinase) family and Src family tyrosine
175 T-cell kinase (Itk) is a member of the Btk (Bruton's tyrosine kinase) family of tyrosine kinases.
176 truct of the pleckstrin homology domain from Bruton's tyrosine kinase (GFP-BTK-PH) localized in intra
177 dentified a novel signaling pathway (c-Src-->Bruton's tyrosine kinase-->transcription factors Ets1, E
179 to homeostatic B cell proliferation require Bruton's tyrosine kinase; however, c-Rel, a Bruton's tyr
180 entify the alpha isoform of the inhibitor of Bruton's tyrosine kinase (IBTKalpha) as a member of the
181 identified the alpha isoform of inhibitor of Bruton's tyrosine kinase (IBTKalpha) as being subject to
183 miR-185 is a microRNA (miR) that targets Bruton's tyrosine kinase in B cells, with reductions in
186 ngagement bypasses or mitigates the need for Bruton's tyrosine kinase in subsequent BCR signaling for
187 -gamma2 (PLCgamma2), Vav, B cell linker, and Bruton's tyrosine kinase in the formation of highly coor
188 ficacy of ibrutinib, a covalent inhibitor of Bruton's tyrosine kinase, in patients at risk for a poor
189 of ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase, in relapsed or refractory pati
190 Bruton's tyrosine kinase; however, c-Rel, a Bruton's tyrosine kinase-induced NF-kappaB/Rel transcrip
191 The activation of N-WASP is suppressed by Bruton's tyrosine kinase-induced WASP activation, and is
195 synergy, additivity, and antagonism with the Bruton's tyrosine kinase inhibitor ibrutinib, which targ
206 ammalian target of rapamycin inhibitors, and Bruton's tyrosine kinase inhibitors are promising and ma
209 (e.g. spleen tyrosine kinase inhibitors and Bruton's tyrosine kinase inhibitors) or the downstream p
211 en revealed that a BCR signalling component, Bruton's tyrosine kinase, is essential for the survival
213 etermined the x-ray crystal structure of the Bruton's tyrosine kinase kinase domain in its unphosphor
215 inase inhibitors and flavopiridol to inhibit Bruton's tyrosine kinase localization at the membrane an
216 was observed in mutated WM cells exposed to Bruton's tyrosine kinase, mammalian target of rapamycin,
218 production in a manner that is dependent on Bruton's tyrosine kinase, p38 MAPK, and TANK-binding kin
219 1), as demonstrated by the individual use of Bruton's tyrosine kinase, p38 MAPK, and TBK1 inhibitors.
220 judged by increased levels of phosphorylated Bruton's tyrosine kinase (pBtk), phosphorylated Spleen t
222 uces an alternate signaling pathway in which Bruton's tyrosine kinase, PI3K, phospholipase Cgamma2, a
223 , and fostamatinib (respective inhibitors of Bruton's tyrosine kinase, PI3Kdelta, and spleen tyrosine
224 conserved electrostatic interaction between Bruton's tyrosine kinase R544 on the activation loop and
225 and phosphorylated tyrosine kinases Lyn and Bruton's tyrosine kinase to membrane rafts after Fc alph
229 s are dependent on the BCR signal transducer Bruton's tyrosine kinase, which is dispensable for the T
230 burden in the spleens of B1a cell-deficient Bruton's tyrosine kinase x-linked immunity-deficient (BT
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