コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 her revealed that DOK3 was phosphorylated by Bruton's tyrosine kinase.
2 ectors phospholipase C (PLC)gamma2, Akt, and Bruton's tyrosine kinase.
3 on factor and a target of phosphorylation by Bruton's tyrosine kinase.
4 ction of TEC family tyrosine kinases such as Bruton's tyrosine kinase.
5 r II-I), which encodes BAP-135, a target for 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
28 h as the epidermal growth factor receptor or Bruton's tyrosine kinase, and we recently described thei
29 olipase Cgamma2 in mediating PKC activation, Bruton's tyrosine kinase- and phospholipase Cgamma2-defi
32 s of the anti-apoptotic tyrosine kinase BTK (Bruton's tyrosine kinase) as anti-leukemic agents with a
33 eficient (xid) mice possess mutations in the Bruton's tyrosine kinase (Btk kinase) gene and display d
36 directly to, and stimulates the activity of, Bruton's tyrosine kinase (Btk) and a Ras GTPase-activati
38 is an FDA-approved irreversible inhibitor of Bruton's tyrosine kinase (BTK) and IL-2 inducible T cell
39 have immunomodulatory effects by inhibiting Bruton's tyrosine kinase (BTK) and IL-2-inducible T cell
41 Ibrutinib is an irreversible inhibitor of Bruton's tyrosine kinase (BTK) and is effective in chron
42 B-cell-restricted factor that complexes with Bruton's tyrosine kinase (Btk) and its substrate, transc
46 trated that Bright coimmunoprecipitates with Bruton's tyrosine kinase (Btk) and that these proteins a
47 his study, we show that both the stimulatory Bruton's tyrosine kinase (Btk) and the inhibitory SHIP-1
55 acologic inhibition and genetic knockdown of Bruton's tyrosine kinase (BTK) blocks AML blast prolifer
61 gnaling supports Notch2(+/-)/NOD MZ B cells, Bruton's tyrosine kinase (Btk) deficiency was introduced
64 tionally, wild type or constitutively active Bruton's tyrosine kinase (Btk) enhanced, whereas the xid
66 egulating B cell development and activation, Bruton's tyrosine kinase (Btk) functions downstream of m
68 ime PCR revealed a higher mRNA expression of Bruton's tyrosine kinase (BTK) gene in DRG after CaP inj
69 the pleckstrin homology domain of the mouse Bruton's tyrosine kinase (btk) gene results in an X-link
73 (lo)) expressing 25% of endogenous levels of Bruton's tyrosine kinase (Btk) have B cell functional re
75 ncovered a previously unappreciated role for Bruton's tyrosine kinase (Btk) in actin tail formation i
77 rs have implicated a role for the Tec kinase Bruton's tyrosine kinase (Btk) in inflammatory cytokine
78 lly applied to the measurement of the RO for Bruton's tyrosine kinase (BTK) in the blood lysate of mo
81 BDHI electrophile was further exploited in Bruton's tyrosine kinase (BTK) inhibitor design using a
82 olecule inhibitors of BCR signaling kinases, Bruton's tyrosine kinase (Btk) inhibitor ibrutinib and t
83 We show that an analogue of the covalent Bruton's tyrosine kinase (BTK) inhibitor Ibrutinib beari
87 a single agent, and in combination with the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib or th
88 e progression during or after the receipt of Bruton's tyrosine kinase (BTK) inhibitor therapy have a
115 ating both B cell and Fc receptor signaling, Bruton's tyrosine kinase (BTK) is a promising target for
123 ed that functional, but not kinase-inactive, Bruton's tyrosine kinase (Btk) is critical for Bright ac
157 in Gqalpha binds directly to the nonreceptor Bruton's tyrosine kinase (Btk) to a region composed of a
159 y, we showed that dual targeting of TLR9 and Bruton's tyrosine kinase (BTK) was strongly synergistic
160 Previously, defects in the gene coding for Bruton's tyrosine kinase (Btk) were shown to result in d
161 uld directly increase the kinase activity of Bruton's tyrosine kinase (Btk) whose defects are respons
167 an interact physically and functionally with Bruton's tyrosine kinase (Btk), a hematopoietic non-rece
169 ated cells is mediated by stimulation of the Bruton's tyrosine kinase (BTK), a member of the Src-rela
181 promoters and requires Bright dimerization, Bruton's tyrosine kinase (Btk), and the Btk substrate, T
186 an orally administered covalent inhibitor of Bruton's tyrosine kinase (BTK), is an effective treatmen
189 hree protein tyrosine kinases, Lyn, Syk, and Bruton's tyrosine kinase (Btk), leading to the secretion
190 inhibitors targeting BCR-associated kinases [Bruton's tyrosine kinase (BTK), phosphoinositide 3-kinas
191 been delineated based on the involvements of Bruton's tyrosine kinase (Btk), protein kinase C (PKC),
192 ymphocytic leukemia (CLL) with inhibitors of Bruton's tyrosine kinase (BTK), such as ibrutinib, is li
193 e now report that Bright coprecipitates with Bruton's tyrosine kinase (Btk), the defective enzyme in
194 inical phenotype of patients with defects in Bruton's tyrosine kinase (Btk), the gene that is abnorma
196 ing ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase (BTK), to bendamustine plus rit
197 llular dsDNA sensor that, upon activation by Bruton's tyrosine kinase (BTK), triggers type I IFN prod
198 erleukin-2-inducible T-cell kinase (Itk) and Bruton's tyrosine kinase (Btk), two Tec-family kinases e
199 nt (IRC) binders, affects the degradation of Bruton's Tyrosine Kinase (BTK), we serendipitously disco
200 activity of a purified non-receptor kinase, Bruton's tyrosine kinase (Btk), whereas purified alpha-s
203 peration between the protein tyrosine kinase Bruton's tyrosine kinase (Btk), which regulates the acti
206 posure of wild-type DT40 lymphoma B cells or Bruton's tyrosine kinase (BTK)-deficient DT40 cells reco
209 1 (MAV-1) infection of B-cell-deficient and Bruton's tyrosine kinase (Btk)-deficient mice resulted i
210 ther define the nature of the protective Ab, Bruton's tyrosine kinase (Btk)-deficient mice were chara
221 which is caused by mutations in the gene for Bruton's tyrosine kinase (Btk); however, there are femal
223 cute myeloid leukaemia have high activity of Bruton's tyrosine-kinase (BTK) in their blast cells comp
224 ty of kinases (spleen tyrosine kinase [Syk], Bruton's tyrosine kinase [Btk], phosphatidylinositol 3-k
227 ndent differences in Lyn phosphorylation and Bruton's tyrosine kinase distribution were observed betw
228 osine kinase R544 on the activation loop and Bruton's tyrosine kinase E445 on the C-helix also aids i
229 PUVA caused poor membrane binding of Akt and Bruton's tyrosine kinase effectors following activation
230 Suppressed expression of c-Src or downstream Bruton's tyrosine kinase, Ets1, Ets2, USF1, or USF2 bloc
231 hich express Bmx and Src as their major Btk (Bruton's tyrosine kinase) family and Src family tyrosine
232 T-cell kinase (Itk) is a member of the Btk (Bruton's tyrosine kinase) family of tyrosine kinases.
233 truct of the pleckstrin homology domain from Bruton's tyrosine kinase (GFP-BTK-PH) localized in intra
234 dentified a novel signaling pathway (c-Src-->Bruton's tyrosine kinase-->transcription factors Ets1, E
236 to homeostatic B cell proliferation require Bruton's tyrosine kinase; however, c-Rel, a Bruton's tyr
237 entify the alpha isoform of the inhibitor of Bruton's tyrosine kinase (IBTKalpha) as a member of the
238 identified the alpha isoform of inhibitor of Bruton's tyrosine kinase (IBTKalpha) as being subject to
240 miR-185 is a microRNA (miR) that targets Bruton's tyrosine kinase in B cells, with reductions in
244 ngagement bypasses or mitigates the need for Bruton's tyrosine kinase in subsequent BCR signaling for
245 -gamma2 (PLCgamma2), Vav, B cell linker, and Bruton's tyrosine kinase in the formation of highly coor
246 ficacy of ibrutinib, a covalent inhibitor of Bruton's tyrosine kinase, in patients at risk for a poor
247 of ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase, in relapsed or refractory pati
248 Bruton's tyrosine kinase; however, c-Rel, a Bruton's tyrosine kinase-induced NF-kappaB/Rel transcrip
249 The activation of N-WASP is suppressed by Bruton's tyrosine kinase-induced WASP activation, and is
250 ying mechanism associated with resistance to Bruton's tyrosine kinase inhibition by ibrutinib in both
252 integrated safety profile of evobrutinib, a Bruton's tyrosine kinase inhibitor (BTKi), using pooled
253 le blocking both BCRs and TLR-MyD88 by using Bruton's tyrosine kinase inhibitor and histone deacetyla
257 synergy, additivity, and antagonism with the Bruton's tyrosine kinase inhibitor ibrutinib, which targ
265 mantle cell lymphoma following prior failed Bruton's tyrosine kinase inhibitor therapy, with an over
270 cell lymphoma (DLBCL) subtypes vulnerable to Bruton's tyrosine kinase inhibitors (BTKis), but is chal
271 ammalian target of rapamycin inhibitors, and Bruton's tyrosine kinase inhibitors are promising and ma
274 (e.g. spleen tyrosine kinase inhibitors and Bruton's tyrosine kinase inhibitors) or the downstream p
277 Ibrutinib, an oral covalent inhibitor of Bruton's tyrosine kinase, is an effective therapy for pa
278 en revealed that a BCR signalling component, Bruton's tyrosine kinase, is essential for the survival
280 etermined the x-ray crystal structure of the Bruton's tyrosine kinase kinase domain in its unphosphor
282 inase inhibitors and flavopiridol to inhibit Bruton's tyrosine kinase localization at the membrane an
283 was observed in mutated WM cells exposed to Bruton's tyrosine kinase, mammalian target of rapamycin,
285 production in a manner that is dependent on Bruton's tyrosine kinase, p38 MAPK, and TANK-binding kin
286 1), as demonstrated by the individual use of Bruton's tyrosine kinase, p38 MAPK, and TBK1 inhibitors.
287 judged by increased levels of phosphorylated Bruton's tyrosine kinase (pBtk), phosphorylated Spleen t
289 rmation, which resulted in the activation of Bruton's tyrosine kinase, phospholipase and phosphoinosi
290 uces an alternate signaling pathway in which Bruton's tyrosine kinase, PI3K, phospholipase Cgamma2, a
291 , and fostamatinib (respective inhibitors of Bruton's tyrosine kinase, PI3Kdelta, and spleen tyrosine
292 cks chemokine-induced triggering of JAK2 and Bruton's tyrosine kinase protein tyrosine kinases and of
293 conserved electrostatic interaction between Bruton's tyrosine kinase R544 on the activation loop and
294 ity of a gain-of-function variant (S180A) of Bruton's tyrosine kinase that evokes B cell malignancy p
295 and phosphorylated tyrosine kinases Lyn and Bruton's tyrosine kinase to membrane rafts after Fc alph
299 s are dependent on the BCR signal transducer Bruton's tyrosine kinase, which is dispensable for the T
300 burden in the spleens of B1a cell-deficient Bruton's tyrosine kinase x-linked immunity-deficient (BT