ライフサイエンスコーパス: kinase activity

1 in ATPase, Rho kinase, or myosin light-chain kinase activity).

2 actions requires AR phosphorylation and CHK2 kinase activity.

3 ially dependent on TARGET OF RAPAMYCIN (TOR) kinase activity.

4 lop a genetically encoded reporter for SnRK2 kinase activity.

5 G2019S is hypothesized to increase LRRK2 kinase activity.

6 a highly specific inhibitor of LRRK2 protein kinase activity.

7 ck the Ku-DNA interaction and inhibit DNA-PK kinase activity.

8 tic effect that was rescued by blocking PERK kinase activity.

9 models, due in part to inhibition of MEK1/2 kinase activity.

10 s in dimerization; however, a subset retains kinase activity.

11 id kinase activity, or Gbetagamma-stimulated kinase activity.

12 0delta of the PI3K significantly reduced its kinase activity.

13 ic progression requires cyclin B3-associated kinase activity.

14 uced concomitant with increased HDAC1 and S6 kinase activity.

15 e substrates, either enhancing or inhibiting kinase activity.

16 known about how ligand binding triggers DDR1 kinase activity.

17 of variants in these genes and found reduced kinase activity.

18 sensing can be decoupled from activation of kinase activity.

19 enriched in brain (Rheb) stimulates mTORC1's kinase activity.

20 easuring the effects of reaction products on kinase activity.

21 e impact of caspase-3-mediated activation of kinase activity.

22 , at least in part, to a decrease in IKKbeta kinase activity.

23 However, SidJ fails to demonstrate kinase activity.

24 ucidate its high potency in inhibiting c-KIT kinase activity.

25 NKP and DNA and efficiently activates PNKP's kinase activity.

26 8) kinase activity or inhibition of Aurora B kinase activity.

27 d the interaction is needed for optimal PLK1 kinase activity.

28 tive to mTOR (mammalian target of rapamycin) kinase activity.

29 te content, consistent with the PKDs lacking kinase activity.

30 lation in cells, but only Cdr1 inhibits Wee1 kinase activity.

31 gy regulation by LATS1 is independent of its kinase activity.

32 eversed by pharmacologic inhibition of RIPK1 kinase activity.

33 vidual subunits of MRX and DNA regulate Tel1 kinase activity.

34 eraction partners and thereby regulate ATM's kinase activity.

35 ataxia-telangiectasia based on retained ATM kinase activity.

36 ylates and destabilizes BIN2 to inhibit BIN2 kinase activity.

37 92, Rabin8, and DVL3 are substrates of TTBK2 kinase activity.

38 transmembrane mutations but did not require kinase activity.

39 retained ataxia telangiectasia-mutated (ATM) kinase activity.

40 interacts with lamin A/C, independent of its kinase activity.

41 /cyclin B rather than through canonical mTOR kinase activity.

42 mune receptors in a manner dependent on BIK1 kinase activity.

43 is an auto-inhibitory domain that suppresses kinase activity.

44 e show that Rif2 inhibits MRX-dependent Tel1 kinase activity.

45 ysosome maturation is not dependent on LRRK2 kinase activity.

46 bserved in the absence of zeaxanthin or STT7 kinase activity.

47 ficiency can therefore serve as a readout of kinase activity.

48 es vascular integrity through focal adhesion kinase activity.

49 n be achieved in vitro by inhibiting CDK8/19 kinase activity.

50 nion binding sites that dynamically regulate kinase activity.

51 d BRI1 internalization without affecting its kinase activity.

52 lds, opening a new avenue to study localized kinase activity.

53 c toxicity caused by full inhibition of PERK kinase activity.

54 l segment, JM4, is an important regulator of kinase activity.

55 on of Chk1 expression in cells that have ATR kinase activity.

56 , marmoset LRRK2 G2019S resulted in elevated kinase activity.

57 ed, though these activities did require FGFR kinase activity.

58 xakisphosphate (IP6) is required for Lpg2603 kinase activity.

59 s directly and indirectly by inhibiting BRD4 kinase activity.

60 functions as an allosteric activator of its kinase activity.

61 e stress, along with reduced JNK and p38 MAP kinase activity.

62 ity and can selectively interfere with their kinase activities.

63 KD) and, therefore, exhibits both GTPase and kinase activities.

64 tion and mutant expression, we show that FAK kinase activity, along with its proximity to and potenti

65 Loss of RIPK1 kinase activity also prevented Ripk1(D325A/D325A) embryo

66 landscape of Abl in complex ways: increased kinase activity, altered affinity, and cooperativity for

67 synthesis, accompanied by a decrease in mTOR kinase activity, an increase in the phosphorylation of e

68 Here, we demonstrate that ABL1/2 kinase activities and/or expression are potentiated in c

69 to AKT activation include enhanced p110alpha kinase activity and a decrease in PTEN level.

70 We found increased pyruvate kinase activity and a decreased ratio of reduced/oxidize

71 e inhibitor, verteporfin, that inhibited GLK kinase activity and AhR-ROR-gammat interaction.

72 SINE activation is linked to ORF36 kinase activity and can also be induced by inhibition of

73 lting in a massive increase in inhibition of kinase activity and cell viability by irreversible inhib

74 RBD (E125K) stabilized state B and enhanced kinase activity and cellular MAPK signaling.

75 t of mtDNA damage is a "surrogate" for LRRK2 kinase activity and consequently of kinase inhibitor act

76 prospectively identify residues that mediate kinase activity and drug resistance across the kinome.

77 , confirming PstP as a negative regulator of kinase activity and global serine and threonine phosphor

78 uctose metabolism through its glyceraldehyde kinase activity and in the generation of riboflavin cycl

79 , Atg13 is dephosphorylated, triggering Atg1 kinase activity and macroautophagy induction.

80 These data suggest that the kinase activity and nuclear localization of HIPK2 are es

81 nt modification, can allosterically regulate kinase activity and oligomerization state.

82 tributions to the large increase in VPS34CII kinase activity and PI3P production triggered by membran

83 as a key mechanism directly inhibiting RIPK1 kinase activity and preventing TNF-mediated RIPK1-depend

84 s in 25 missense TBK1 mutations, focusing on kinase activity and protein-protein interactions.

85 ular events underpinning ligand-induced DDR1 kinase activity and provide an explanation for the unusu

86 levels may be a sensitive measure of altered kinase activity and provide an extended profile of LRRK2

87 system that combines genetic engineering of kinase activity and quantitative proteomics to rapidly s

88 n-deficient BRAF mutant displays compromised kinase activity and reduced tumorigenicity.

89 signaling mediated by AKT2 and elevated FAK-kinase activity and ROCK-RhoA levels but low levels of p

90 fyve autophosphorylation represses its lipid kinase activity and stimulates Fig4 lipid phosphatase ac

91 ed Raf1 isoform alters DNA-dependent protein kinase activity and the DNA damage response.

92 FYN expression, kinase activity and the phosphorylation of its target Ta

93 and further defined it by demonstrating that kinase activity and Tyr-1022 and Tyr-1162 of ERBB4, as w

94 QR) and DNA-PKcs(SD/SD) mice retained normal kinase activity and underwent efficient V(D)J recombinat

95 autophagy and are sufficient to enhance ULK1 kinase activity and, in turn, autophagic flux.

96 ERBB3 had little, if any, intrinsic tyrosine kinase activity and, thus, was unlikely to be an importa

97 a protein LHCB6, which was dependent on STN8 kinase activity, and found specific phosphorylations on

98 nsistent with this, free Lck also had higher kinase activity, and free Lck mediated higher T cell act

99 The semidominant Lgn-R mutation lacks kinase activity, and phenotypic severity is dependent on

100 ing that localization to the cell periphery, kinase activity, and phosphorylation by PRRs are critica

101 This phenotype switch is driven by FAK kinase activity, and signaling through the p130Cas>c-Jun

102 um ion signals and mitogen-activated protein kinase activity, and that its activity extends to other

103 tromeric pool of SET on Sgo2 depends on Bub1 kinase activity, and the centromeric localization of SET

104 ) for diverse processes such as translation, kinase activity, and transcription in mammals, yeast, an

105 ly kinase biosensors showed that the nuclear kinase activities are much suppressed compared to those

106 f possible phosphorylation states on protein kinase activity are difficult to study experimentally be

107 Large-scale data on cellular kinase activity are limited, because existing assays are

108 damage, and found that DYRK1A expression and kinase activity are required for maintenance of 53BP1 ex

109 n between AR and SLIRP was disrupted by Ack1 kinase activity as well as androgen or heregulin treatme

110 inhibitor necrosulfonomide but requires the kinase activity, as well as RHIM signaling of RIPK1.

111 By employing a Xenopus laevis oocyte kinase activity assay, we demonstrate how these chimeric

112 mutagenesis showed markedly elevated protein kinase activities associated with the activation of mTOR

113 his method, we also were able to measure the kinase activities at the single cell level.

114 Early in mitosis, kinase activity at kinetochores is high to promote attac

115 ponents, mTOR and MAPKAP1, to promote mTORC2 kinase activity at the plasma membrane.

116 we first review common design strategies for kinase activity biosensors, including signaling targets,

117 te-directed mutant lacking histidine protein kinase activity but retaining nucleoside diphosphate kin

118 ible, reversible disruption of BDNF receptor kinase activity by administration of 1NMPP1, a PP1 deriv

119 Assessment of full-length LRRK2 kinase activity by measuring phosphorylation of Rab10, a

120 se substrates of LRRK2, shows enhancement of kinase activity by several dimerization-defective mutant

121 Here we introduce an approach to controlling kinase activity by using monobodies that bind to the hig

122 ction of ataxia telangiectasia-mutated (ATM) kinase activity can ameliorate mutant huntingtin (mHTT)

123 Paradoxically, increasing DAG kinase activity can enhance the robustness of DAG/active

124 esults indicate that targeting HIPK2 and its kinase activity can have neuroprotective effects by elev

125 Inhibition of rho kinase activity can reduce these activities, but may als

126 utation-specific, and drug-driven changes of kinase activity conformations.

127 urodevelopmental dysfunction and reduced DNA kinase activity correlating with neurodegeneration.

128 tion in BER-depleted cells requires ATR/Chk1 kinase activities, demonstrating that PD-L1 upregulation

129 demonstrate that NLK lowers mHTT levels in a kinase activity-dependent manner, while having no signif

130 3 at T598 and can be regulated by LRRK2 in a kinase activity-dependent way.

131 itochondrial DNA (mtDNA) damage and is LRRK2 kinase activity-dependent.

132 The receptors inhibit or stimulate CheA kinase activity depending on the presence of attractants

133 to the expected phosphatidic acid-producing kinase activity, DGK4 recombinant protein also revealed

134 trast to our hypothesis, MLK3 activated PAK1 kinase activity directly, as well as in the cells.

135 long-standing model, we show Pkn8 and Pkn14 kinase activities do not play obvious roles in controlli

136 n domain (SDD) of TBK1 can cause the loss of kinase activity due to structural disruption, despite an

137 ut not TOPBP1, results in decreased Aurora B kinase activity during mitosis.

138 and demonstrate that the attenuation of its kinase activity during the initial steps of the repair p

139 charomyces cerevisiae, Cln3-cyclin-dependent kinase activity enables Start, the irreversible commitme

140 mature Sox2 expression was sensitive to LATS kinase activity, even though LATS proteins normally do n

141 ase acting on PIKfyve to stimulate its lipid kinase activity, explaining why catalytically active Fig

142 F4 in vitro, and a mutant SPA1 affecting the kinase activity fails to rescue the PIF4 level in additi

143 We propose that high Polo-kinase activity following mitotic entry directs the RZZ

144 In vivo, CEK1, CEK2, and CEK3 exhibited kinase activity for Cho but not Etn, although the latter

145 propose that the CaM/Ca(2+)-dependent NAD(+) kinase activity found in photosynthetic organisms is car

146 echanisms of resistance to inhibition of MET kinase activity from a single clonally derived cancer ce

147 ntiation, demonstrated by increased creatine kinase activity, fusion index and myotube diameter; like

148 RIPK1 kinase activity has been shown to be essential to drivin

149 scriptional changes, whereas inhibiting CDK8 kinase activity has minimal effects.

150 elective CSF1R inhibitors devoid of type III kinase activity has proven to be challenging.

151 ciliogenesis is critically dependent on its kinase activity; however, the precise mechanism of TTBK2

152 We conclude that loss of TBK1 kinase activity impacts ALS disease progression through

153 are inconsistent reports of hypoxia-induced kinase activities in different cancer cell-lines, where

154 c kinase signaling in living cells and image kinase activities in tumors or to decipher the mechanism

155 O-EE-07, that could block both RSK1 and MSK2 kinase activity in a dose-dependent manner.

156 phosphorylation is required for maximal Akt2 kinase activity in adipocytes.

157 contrast, point mutations that decrease TBK1 kinase activity in all cells also accelerate disease ons

158 owed rather minor contributions to total Cho kinase activity in both shoots and roots.

159 on between Hippo and Salvador enhances Hippo kinase activity in cells, whereas complex formation with

160 ion might be responsible for higher pyruvate kinase activity in db/db mouse retina.

161 Rho kinase activity in hepatic stellate cells (HSCs) is asso

162 demonstrate that precise regulation of CDK2 kinase activity in male germ cell development is crucial

163 d lipid-phosphatase activity and reduced Akt kinase activity in most of the cell lines examined.

164 is in part due to the role of HIPK2 and its kinase activity in promoting Parkin degradation via the

165 nation in hRIPK1 in regulating its pro-death kinase activity in response to TNFalpha and pro-survival

166 regulation of cyclin D1, which limits CDK4/6 kinase activity in SCCOHT cells and leads to in vitro an

167 divergent, responses to inhibition of FGFR2 kinase activity in the canonical RAF/MAPK/ERK/RSK and PI

168 nism whereby the RQ mutation increases basal kinase activity in the human PKG1alpha and PKG1beta isof

169 ral walls, and enhanced growth and metabolic kinase activity in the late-contracting lateral wall.

170 However, the role of CDK2 kinase activity in the process of CO formation remains u

171 u and p.Glu239Lys) showed markedly decreased kinase activity in vitro comparable to a known pathogeni

172 ating Plk4 (the master centriole duplication kinase) activity in Drosophila asymmetrically dividing n

173 ise (preexisting cell-to-cell differences in kinase activity) in PI3K and mTORC1.

174 n macrophage metabolism, a reduction in mTOR kinase activity, increased LC3-associated host defense a

175 Periostin interacted with FAM20C in a kinase-activity independent manner and the binding was d

176 ruitment of NLRP3 and ASC into a novel RIPK1 kinase activity-independent cell death complex to drive

177 hts a previously unknown mechanism for RIPK1 kinase activity-independent inflammasome activation and

178 Furthermore, we found fully functional RIPK1 kinase activity-independent necroptosis driven by the RI

179 However, here we show a kinase activity-independent role for RIPK1 in these proc

180 Kinase activity inhibition using a specific drug validat

181 Specifically, DNA-PKcs kinase activity initiates phosphorylation of the chromat

182 Beyond kinase activity, IRAKs and TAK1 act as molecular scaffol

183 by which Sec14-like PITPs potentiate PtdIns kinase activities is a heterotypic lipid-exchange cycle

184 se(3,4), suggesting that inhibition of LRRK2 kinase activity is a promising therapeutic strategy.

185 kinase substrate in vitro This dual Thr-Tyr kinase activity is also observed for a eukaryotic dual-s

186 The higher G328V mutant intrinsic kinase activity is consistent with the statistically sig

187 d to spinocerebellar ataxia type 11, and its kinase activity is crucial for ciliogenesis.

188 rovide evidence for a mechanism whereby DDR1 kinase activity is determined by its molecular density.

189 es a molecular logic OR, by which the output kinase activity is modulated by a phosphorylation signal

190 phenotype of spaQ, suggesting that the SPA1 kinase activity is necessary for thermomorphogenesis.

191 Using inhibitors, we found that Cdk8 kinase activity is not required for CKM movement or repr

192 R-1 protein is not essential, and that PAR-1 kinase activity is regulated spatially.

193 We further demonstrated that FAK's kinase activity is required for FAK/CAT-induced tumorige

194 Furthermore, CDK11(p58) kinase activity is required for formation of endosomal s

195 PDXK kinase activity is required for PLP production and AML c

196 s is inactivated, we show here that DNA-PKcs kinase activity is required for the cellular response to

197 nd CRY2 recruit TLK2 to SCF(FBXL3), and TLK2 kinase activity is required for this interaction.

198 Consistently, we show that Tao kinase activity is required in developing and as well as

199 alization signal to demonstrate that the Fyn kinase activity is significantly lower in the nucleus th

200 s a potent competitive inhibitor of CK1alpha kinase activity (K(i) = 8 nM).

201 rturbed DNA replication, indicating that ATR kinase activity limits replication initiation in the abs

202 have led to new approaches for manipulating kinase activity, localization, and in some instances spe

203 of-function allele that increases basal EGFR kinase activity, males had progressive glomerulopathy, a

204 Our kinase activity-mapping system is a versatile strategy t

205 ing, and clarifies how compartmentalized Src-kinase activity may drive cell fate.

206 f autoreactive antibodies, inhibitors of BTK kinase activity may provide therapeutic value to patient

207 Inhibitor studies indicated that ATM kinase activity might not grossly impact on mitotic prog

208 bind with high affinity to PKA and block its kinase activity, modulating the extent, and duration of

209 However, inhibition of focal-adhesion-kinase activity not only attenuates Fyn activity, but ab

210 ed for eNAD(P)(+) signaling and SAR, and the kinase activities of LecR-VI.2 and BAK1 are indispensabl

211 cetyllysine binding function of BRD4 and the kinase activities of PI3K and CDK4/6 by the TP inhibitor

212 s a negative regulator of plant PTI, and the kinase activities of StMKK1 are required for its suppres

213 n MAP3K1 disrupt the balance between the pro-kinase activities of the RHOA and MAP3K4 binding partner

214 Here we report that Cdh1 suppresses the kinase activity of c-Src in an APC-independent manner.

215 The transcriptional kinase activity of CDK7 is regulated by HER2, and by the

216 D28 upon T cell activation, and the in vitro kinase activity of CSK is enhanced in the presence of ph

217 during ribosome biogenesis that require the kinase activity of DNA-PKcs and its phosphorylation at t

218 minate a new connection between the tyrosine kinase activity of EGFR and innate immune functions of S

219 teracts with HRI and activates the eIF2alpha kinase activity of HRI.

220 Although the kinase activity of IRAK1 was not required for signal pro

221 and in mice was positively regulated by the kinase activity of IRAK4.

222 The kinase activity of MUS is dispensable for its function i

223 d V15, can specifically inhibit the in vitro kinase activity of mutant c-KIT(D816V) with an IC(50) va

224 Interestingly, kinase activity of OsWAKL21.2 is necessary to activate r

225 sm by which Tyr1 phosphorylation directs the kinase activity of P-TEFb and alters its specificity fro

226 amplification, overexpression, and elevated kinase activity of P21 (RAC1) activated kinase 4 (PAK4)

227 ings highlight the importance of the protein kinase activity of PCK1 in the activation of SREBPs, lip

228 n of these two residues results in increased kinase activity of PLK1, leading to accelerated mitosis

229 ly, and its recruitment is controlled by the kinase activity of Plk4, but how this works remains poor

230 ) complex 1 (PI3KC3-C1), increases the lipid kinase activity of purified PI3KC3-C1, and is required f

231 s to trigger cell death mediated by TNF, the kinase activity of RIPK1 and FADD-caspase-8.

232 pression effect does not rely on the protein kinase activity of SERK1 and that activation of signalin

233 Using an extract system, we found that local kinase activity of the Aurora B kinase (AURKB) subunit o

234 insulin resistance through reduced tyrosine kinase activity of the insulin receptor; however, its im

235 sponse to environmental cues by exerting its kinase activity on multiple substrates(1-3).

236 at the centromere/kinetochore regulate both kinase activities one another in an inter-kinetochore di

237 Combined, these data suggest that CDK11(p58) kinase activity opposes Aurora B activity to enable absc

238 ype PI4KIIalpha, but not of variants lacking kinase activity or AP-3 binding.

239 ed kinase domain (KD) mutations that abolish kinase activity or display substrate-specific defects in

240 rescue of this phenotype requires CDK11(p58) kinase activity or inhibition of Aurora B kinase activit

241 without affecting Rac1 binding, basal lipid kinase activity, or Gbetagamma-stimulated kinase activit

242 nt displays a 1.8-fold increase in intrinsic kinase activity over wild-type, whereas the R206H mutant

243 This resulted not from pyruvate kinase activity per se but rather from the formation of

244 catalytic activity, protein phosphorylation, kinase activity, pollination, and transport.

245 he interaction of HY5 with BIN2 enhances its kinase activity possibly by the promotion of BIN2 Tyr(20

246 Here we establish that Pom1's kinase activity prevents septation at cell tips even if

247 1) and Aurora A (AurA) inhibitors attenuates kinase activity, produces spindle defects, and prolongs

248 interacting protein kinase 2 (HIPK2) and its kinase activity promote Parkin degradation via the prote

249 n-on sequencing (PRO-seq), we show that CDK8 kinase activity promotes RNA polymerase II pause release

250 Here, we showed that loss of SIK1 kinase activity protected against adverse cardiac remode

251 ing, microRNA splicing, translation, protein kinase activity, protein degradation, heme degradation,

252 PCa associated CHK2 mutants with impaired kinase activity reduced IR-induced AR-CHK2 interactions.

253 We show that Tao kinase activity regulates cytoskeletal dynamics and sens

254 ss granules in part via its PrLD, and Sky1's kinase activity regulates timely stress granule disassem

255 cessful mitosis requires that cyclin B1:CDK1 kinase activity remains high until chromosomes are corre

256 d reporter that we designed, aPKC-specific C kinase activity reporter (aCKAR), we found that the lipi

257 Inhibition of Pef1 kinase activity rescued cohesin loader deficiencies.

258 Furthermore, loss of DNA-PKcs kinase activity results in a marked decrease in the recr

259 Inhibition of LRRK2 kinase activity results in increased GCase activity in D

260 Measurement of kinase activity showed that PDK1 is the principal isozym

261 ulation is abrogated by inhibition of TGFBR2 kinase activity, small interfering RNA silencing of Tgfb

262 In the absence of Aurora kinase activity, SPICE1 remains at centrioles but does n

263 for live-cell measurements of autoinhibitory kinase activity states.

264 ed agonist-mediated contraction and RhoA/Rho kinase activity, suggesting RhoBTB1 selectively controls

265 dly, this function is not dependent on Rad53 kinase activity, suggesting steric inhibition of DDK by

266 alian utricles, whereas constitutive LATS1/2 kinase activity suppresses YAP-TEAD signaling in mammali

267 Kinase activity testing of takinib analogs against IRAK-

268 Fls3 had greater in vitro kinase activity than Fls2 and could transphosphorylate a

269 it is unclear whether it is involved in non-kinase activities that contribute to the generation of t

270 A20(ZF7) cells exhibited prolonged IkappaB kinase activity that drove exaggerated transcription of

271 NAD(+) Cell lysates possess an ATP-dependent kinase activity that efficiently converts NRH to the com

272 icing defects and proved that it is the CKR9 kinase activity that is required for pre-mRNA processing

273 e of RIPK4 in mouse development requires its kinase activity; that RIPK4 and IRF6 expressed in the ep

274 Independent of its kinase activity, the TGFbeta-activated kinase 1 (TAK1) m

275 Thus, ATR and CHK1 signaling suppresses CDK1 kinase activity throughout the S phase and stabilizes an

276 WEE1 suppresses CDK1 and CDK2 kinase activities to regulate the G1/S transition after

277 dynamics of EGFR dimerization and found EGFR kinase activity to be essential for dimerization.

278 normal immune receptor control of Tec-family kinase activity to enhance the viral life cycle.

279 transition in a manner that relies upon Nek2 kinase activity to ensure low DA levels at mitotic centr

280 trate that ERK MAPK signal fluctuations link kinase activity to stem cell dynamics.

281 Such coupling of kinase activity to that of the transporter ensures the c

282 with actin remodeling pathways, notably SRC kinase activity, to establish and maintain long-lasting

283 We also demonstrate that ArlS has kinase activity toward ArlR in vitro, although it has sl

284 why are there widely contrasting results in kinase activity under hypoxia in different cancer cell-l

285 a scaffold to maintain mTORC2 integrity and kinase activity, unveiling a new avenue for development

286 meric SET/TAF1 on Sgo2 up-regulates Aurora B kinase activity via PP2A inhibition in prometaphase.

287 Importantly, MASTL kinase activity was not required for regulation of cell

288 The mutant LRRK2 increased kinase activity was reduced by pharmacological inhibitio

289 Instead, we found that Mps1 kinase activity was sufficient to promote its release fr

290 Also, cAMP and PKA (cAMP dependent protein kinase) activity were monitored by Forster resonance ene

291 CDK8-dependent regulation required its kinase activity, whereas CDK19 governed IFN-gamma respon

292 F-mediated necroptosis was mediated by RIPK1 kinase activity, whereas TLR3- or TLR4-mediated death wa

293 y selective small-molecule inhibitors of its kinase activity, which have demonstrated safety in precl

294 y regulator of abscission timing is Aurora B kinase activity, which inhibits abscission and forms the

295 the hub domain as an allosteric regulator of kinase activity, which may provide a pharmacological tar

296 s a gain-of-function allele causing elevated kinase activity, which underlies these differentiation d

297 the mechanism by which Rab5A activates lipid kinase activity will have broad impacts in both signalin

298 contains RNA endonuclease and polynucleotide kinase activities with known roles in ribosomal RNA proc

299 enetic approach to specifically inhibit TrkA kinase activity with 1-NM-PP1 in TrkA(F592A)-knock-in (T

300 Indeed, we found that inhibition of PLK4 kinase activity with a small-molecule inhibitor, CFI-400