ライフサイエンスコーパス: kinase

1 n tyrosine kinase and phosphatidylinositol 3 kinase.

2 unctional characterization of this important kinase.

3 2A:B55 phosphatase inactivation by Greatwall kinase.

4 c expression of NPM-ALK, a chimeric tyrosine kinase.

5 hat beta1 subunits are phosphorylated by FYN kinase.

6 , through noncanonical interaction with polo kinase.

7 alphaC helix, which is conserved across all kinases.

8 reactivation of PP2C-dephosphorylated SnRK2 kinases.

9 nositol 3-kinase (PI3K) and cyclin-dependent kinases.

10 ofiled on near-kinome-wide panels of protein kinases.

11 ndered cells completely independent of these kinases.

12 ism of post-translational control of protein kinases.

13 inding of BMP-9 to the receptor activin-like kinase 1 (ALK-1) promotes endothelial cell quiescence.

14 ase brassinosteroid insensitive 1-associated kinase 1 (BAK1) conformational ensemble, we performed Ga

15 Calcium dependent protein kinase 1 (CDPK1) is an essential Ser/Thr kinase that con

16 APK1, encoding the mitogen-activated protein kinase 1 (i.e., extracellular signal-regulated protein k

17 the PD familial genes PTEN-induced putative kinase 1 (PINK1) and parkin (PRKN) in mediating mitochon

18 ORC2-specific serum/glucocorticoid-regulated kinase 1 (SGK1) are constitutively activated in MN with

19 K/GSK3) signaling, with serum-glucocorticoid kinase 1 (SGK1), an inhibitor of glycogen synthase kinas

20 DAC7 by the CaMK group member salt-inducible kinase 1 (SIK1) stabilized the deacetylase, leading to i

21 Abrocitinib, an oral selective Janus kinase 1 inhibitor, was effective and well tolerated in

22 n (ETX) or sFlt-1 (soluble fms-like tyrosine kinase 1), and in a postnatal model due to prolonged hyp

23 eceptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls w

24 IF2alpha, surprisingly mediated by eIF2alpha kinase 1, or heme-regulated kinase inhibitor (HRI).

25 encompassing extracellular signal-regulated kinase 1/2 (ERK1/2), p38 and Jun amino-terminal kinase (

26 ase (MEK) and extracellular signal-regulated kinase 1/2 signaling; however, the clinical efficacy of

27 by identifying interleukin 1 type I receptor kinase-1 (IRAK-1) as a Nck1-selective binding partner, d

28 nsion and elevated soluble Fms-Like Tyrosine Kinase-1 (sFlt-1).

29 etic ring components, GCK-1 (germinal center kinase-1) and CCM-3 (cerebral cavernous malformations-3)

30 Genetic depletion of cyclin-dependent kinase 12 (CDK12) or selective inhibition of an analog-s

31 Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of late-onset

32 leoside treatment in patients with thymidine kinase 2 (TK2) deficiency and compared it to FGF-21.

33 Tau tubulin kinase 2 (TTBK2) is a key player in the cilium assembly

34 porated in cells expressing uridine/cytidine kinase 2 and characterize selectivity mechanisms using m

35 i.e., extracellular signal-regulated protein kinase 2, ERK2), cause a neurodevelopmental disease with

36 We found that CBL-interacting protein kinase 23 (CIPK23) interacts with both phot1 and phot2.

37 phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling, with serum-glucocorticoi

38 ) by activating receptor-interacting Ser/Thr kinase 3 (RIPK3), caspase-8, and the NLRP3 inflammasome.

39 eceptor-interacting serine/threonine-protein kinase 3 (RIPK3)-mediated pathways of apoptosis and mixe

40 brotic compounds targeting glycogen synthase kinase 3, which has a consistent role as a key mediator

41 We found that glycogen synthase kinase-3 (GSK3) is overactivated in corticolimbic parval

42 hway, including receptor-interacting protein kinase-3 (RIPK3), mixed lineage kinase-like (MLKL) and N

43 ent evidence suggests that glycogen-synthase kinase 3beta (GSK3beta) plays a key role in memory forma

44 1 (SGK1), an inhibitor of glycogen synthase kinase 3beta, as part of this pathway.

45 i.e., 100- to 250-fold) by glycogen synthase kinase-3beta (GSK-3beta) inhibition using CHIR99021 and

46 ogram by activating cyclin-dependent protein kinase 4/6 (CDK4/6).

47 We show that Plasmodium berghei CDK-related kinase 5 (CRK5), is a critical regulator of atypical mit

48 chain of T cell receptor-associated protein kinase 70).

49 Dynamic subcellular regulation of protein kinase A (PKA) activity is important for the motile beha

50 adenosine monophosphate (cAMP), and Protein Kinase A (PKA) exist in an oscillatory circuit character

51 ) Inhibitors of adenylyl cyclase and protein kinase A (PKA) prevented the effects of Lgmn.

52 ted with cAMP-mediated activation of protein kinase A (PKA).

53 el mTORC1-interacting protein called protein kinase A anchoring protein 8L (AKAP8L).

54 Ryanodine receptor was protein kinase A-hyperphosphorylated, S-nitrosylated, oxidized,

55 a) is an important positive regulator of SRC kinase activation and a known promoter of cancer growth,

56 rations cause rapid telomere elongation, ATR kinase activation, telomere fragility, and accelerated t

57 s finding suggests a multi-step mechanism of kinase activation.

58 tive of uncharged tRNA accumulation and Gcn2 kinase activation.

59 revented the effect of leptin, whereas a Src kinase activator peptide mimicked it.

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

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

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

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

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

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

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

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

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

69 We next found that the AKT Ser/Thr kinase (AKT) inhibitor MK2206 blocks the starvation-depe

70 reased due to impaired AMP-activated protein kinase (AMPK) signaling.

71 vestigated the role of AMP-activated protein kinase (AMPK), a master regulator of energy metabolism,

72 Here we report the identification of A-Kinase Anchor Protein (AKAP8) as a splicing regulatory f

73 ial cells, and regulatory protein AKAP150 (A-kinase anchoring protein 150) enhances the activity of T

74 agonist NF546 is blocked by disruption of A-kinase anchoring protein 5 (AKAP5) function in arterial

75 onal and epigenetic regulator with intrinsic kinase and histone acetyltransferase (HAT) activities th

76 , we demonstrate efficient regulation of the kinase and identify temporally distinct signaling respon

77 ptor signaling pathway, like Bruton tyrosine kinase and phosphatidylinositol 3 kinase.

78 the ER lumen, IRE1 activates its cytoplasmic kinase and ribonuclease domains to transduce the signal.

79 This shows that both the ERK5 kinase and TAD must be considered when assessing the rol

80 m signaling through the ERK serine/threonine kinase and the Fos transcription factor, thereby enhanci

81 larity between the autophagy-initiating TBK1 kinase and the ULK1 kinase complex.

82 cological inhibition of phosphatidylinositol kinases and cholesterol homeostasis reduced replication

83 Activation of mitogen-activated protein kinases and NFkappaB signaling was unaffected by global

84 ols to modulate the activities of regulatory kinases and phosphatases.

85 aldehyde-3-phosphate dehydrogenase, pyruvate kinase, and glucose-6-phosphate isomerase showed IgE-bin

86 s structurally similar to eukaryotic protein kinases, and that MOB1A directly binds to the LegK7 kina

87 those in the cytosol, suggesting that these kinases are regulated differently in the nucleus and in

88 Kinases are the enzymes that catalyze the phosphorylatio

89 ase), JNK, and p38 mitogen-activated protein kinases as well as NFkappaB (nuclear factor kappa B).

90 were identified in the original panel of 260 kinases as well as surfaced other kinases that it potent

91 nisation of the activity of cyclin dependent kinases at distinct stages of the cell cycle, suppresses

92 t that inhibitors of the DNA damage response kinase ATR can significantly potentiate ionizing radiati

93 affects mRNA stability of receptor tyrosine kinase AXL in an m(6)A-dependent way.

94 s the protein level of the receptor tyrosine kinase AXL to induce oncogenic signaling in ovarian canc

95 have a mouse line with Tropomyosin receptor kinase B (TrkB) receptor deletion from D1-expressing cel

96 in kinase B pathway by injecting the protein kinase B activator SC79 in Lgr4(-/-) mice can effectivel

97 Importantly, the reactivation of the protein kinase B pathway by injecting the protein kinase B activ

98 Even though mTOR/protein kinase B signaling is important for adipogenesis, the ro

99 REDD1), a negative regulator of mTOR/protein kinase B, is poorly understood.

100 e (ACLY) in a TGF-beta receptor/PI3K/protein kinase B-dependent manner, to regulate hepatic acetyl-Co

101 Breakpoint Cluster Region-Abelson kinase (BCR-Abl) is a driver oncogene that causes chroni

102 Previous studies with various Src family kinase biosensors showed that the nuclear kinase activit

103 ltisite phosphorylation on the plant protein kinase brassinosteroid insensitive 1-associated kinase 1

104 Using Bruton's tyrosine kinase (BTK) as a clinically relevant model system, we s

105 Bruton's tyrosine kinase (BTK) is a non-receptor tyrosine kinase that sign

106 pathway, and specifically of Bruton tyrosine kinase (BTK), is a leading therapeutic strategy in B-cel

107 ls via JNK and p38 mitogen-activated protein kinase but not NF-kappaB.

108 nstrated to occur by their cognate histidine kinases but also by low molecular weight phosphodonors s

109 olarity, with expression of atypical protein kinase C (aPKC) at the contact-free domain, nuclear expr

110 Purkinje cell-specific inhibition of protein kinase C decreased and phase-shifted the translation com

111 osphorylation of the kinases Lyn and protein kinase C-beta and MAPKs MKK-3/6 and p38MAPK or to upregu

112 The receptor kinase c-MET has emerged as a target for glioblastoma th

113 The Ras-binding domain of the protein kinase c-Raf (c-Raf-RBD) is the tightest known binder of

114 regulatory input provided by the Hippo-Warts kinase cascade.

115 the pathway, but how each controls this core kinase cassette is not fully understood.

116 olocalization with the DNA-dependent protein kinase catalytic subunit (DNA-PKcs).

117 nses, whereas de novo translation in protein kinase Cdelta-expressing inhibitory neurons in the centr

118 (Kip1) ) inhibit cyclin and cyclin-dependent kinase (CDK) complex that promotes fibrosis and hypertro

119 pecific docking motifs help cyclin-dependent kinases (CDKs) phosphorylate different substrates at dif

120 ses the autophosphorylation of the histidine kinase CheA2, followed by CheY2-mediated dephosphorylati

121 ized that ATP transfer rate through creatine kinase (CK) (k(f)(CKrest)) would be increased, compensat

122 utophagy-initiating TBK1 kinase and the ULK1 kinase complex.

123 d to the RAC-binding domain of p21-activated kinase, consistent with our earlier findings.

124 ctional space of other eukaryotic cell-cycle kinases controlling DNA replication.

125 Multiple kinases converge on the transcription factor cAMP respon

126 idine substrate and docking domains with the kinase core, thus preventing catalytic activity.

127 at the Arabidopsis calcium-dependent protein kinase CPK3 is a key regulator of both pattern-triggered

128 ase (WAK), Catharanthus roseus receptor-like kinase (CrRLK1L) and others involved in abiotic stress r

129 To start, cells first activate the kinase cyclin D-CDK4/6, which leads to eventual inactiva

130 opathy-candidiasis-ectodermal dystrophy-like kinase-dead Ikkalpha knockin mice and patients with auto

131 Using U(S)3 deletion and U(S)3 kinase-dead recombinant MDV, we identified U(S)3-respons

132 cal inhibition of Src or overexpression of a kinase-dead Src mutant prevented the effect of leptin, w

133 er TTK knockdown; however, reintroduction of kinase-dead TTK did not.

134 drives multi-organ immune dysregulation via kinase dependent and independent mechanisms.

135 ayed increased p38 mitogen-activated protein kinase-dependent Ripk1-independent IL-1 and tumor necros

136 biologically important AMP-activated protein kinase deprived of any metal Pd contamination.

137 (3'UTR) of the dystrophia myotonica protein kinase (DMPK) gene.

138 DNA-dependent protein kinase (DNA-PK) plays a critical role in the non-homolog

139 However, the phosphorylation status of a kinase does not always reflect its activity state, becau

140 ated pathways of apoptosis and mixed lineage kinase domain-like pseudokinase (MLKL)-dependent necropt

141 , and that MOB1A directly binds to the LegK7 kinase domain.

142 protein modification and incorporation into kinase drug scaffolds.

143 ferentiation and cell-cycle progression, and kinase dysregulation is associated with numerous disease

144 engagement of alternative receptor tyrosine kinases either through upregulation of FGF3 or HBEGF or

145 resides in the ER and deploys a cytoplasmic kinase-endoribonuclease module to activate the transcrip

146 Eukaryotic protein kinases (EPKs) catalyze the transfer of a phosphate grou

147 kinase (MAPK)/extracellular-signal-regulated kinase (ERK) (MEK) 1/2, which has been approved for trea

148 targeting against multiple receptor tyrosine kinases, exerts potent antiangiogenesis.

149 nformin to enhance the efficacy of BRAF-MAPK kinase-extracellular signal-regulated kinase pathway inh

150 results establish NUAK2 as an indispensable kinase for brain development in humans and suggest that

151 elated with peptidoglycan-responsive Ser/Thr kinases for cell signaling, and the germination of rpf m

152 displacement of paxillin and focal adhesion kinase from the signaling layer of focal adhesions, wher

153 tional mechanistic insights into full-length kinase functions by reporting protein-protein interactio

154 psis (Arabidopsis thaliana) cyclin-dependent kinase G1 (CDKG1) is necessary for recombination and syn

155 With either kinase, gamma-H2AX spreads as far as ~50 kb on both side

156 ragine, activating the ISR via the eIF2alpha kinase GCN2.

157 at least two of the stress-activated protein kinases (GCN2 and PERK) that act on the translational ma

158 hed in pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling,

159 G protein-coupled receptor (GPCR) kinases (GRKs) play a key role in terminating signals in

160 Aurora B kinase has a critical role in regulating attachments bet

161 red SH4 and Unique domains of the Src family kinase Hck.

162 we report increased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilat

163 hrough a Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-mediated mechanism, and CaMKII inhibi

164 myocytes caused calcium/calmodulin-dependent kinase II activation and altered myocyte bioenergetics.

165 Deleting the canonical NF-kappaB kinase, IKKbeta, in Scx-lineage cells in mice increased

166 alytic domain of the ERBB2 receptor tyrosine kinase in a patient with schwannomatosis-associated N/S

167 Here, we explored the function of this kinase in macrophages with studies of its regulation of

168 a indicate functional roles for RhoA and Rho-kinase in mediating depression-like behaviors via dendri

169 DC1) was identified as the most up-regulated kinase in patients with AH.

170 tion of prokaryotic serine/threonine protein kinases in bacterial pathogens is emerging as an importa

171 itor of B-cell lymphoma-2, and inhibitors of kinases in the B-cell receptor signaling pathway, like B

172 15 has confirmed it as a potent inhibitor of kinases including BRSK1 and BRSK2 that were identified i

173 ole of PLK1 have relied on RNA knockdown and kinase inhibition approaches, as Plk1 null mutations are

174 ted by eIF2alpha kinase 1, or heme-regulated kinase inhibitor (HRI).

175 Consistent with this, the IkappaB kinase inhibitor BAY11-7085 and dominant-negative mutant

176 Ripretinib is a novel switch-control kinase inhibitor designed to inhibit a wide range of KIT

177 depletion of Pyk2 and treatment with a Pyk2 kinase inhibitor increased viral DNA content in keratino

178 ontrol the stability of the CYCLIN-DEPENDENT KINASE inhibitor KIP-RELATED PROTEIN (KRP), which may un

179 s to proliferate in the presence of the HER2 kinase inhibitor lapatinib.

180 t screen of PI5P4Kalpha against our in-house kinase inhibitor library.

181 The Published Kinase Inhibitor Set (PKIS) is a publicly-available chem

182 hibitors, such as the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome after HCT.

183 oma following prior failed Bruton's tyrosine kinase inhibitor therapy, with an overall response rate

184 nib is a selective, covalent Bruton tyrosine-kinase inhibitor with activity in chronic lymphocytic le

185 with regimens that do not contain a tyrosine-kinase inhibitor, despite the use of high-risk chemother

186 roxyisoflavone), a tyrosine-specific-protein kinase inhibitor, has been shown to exert an anti-inflam

187 n of TJ proteins, which was blocked by a Rho-kinase inhibitor.

188 le to the clinical efficacy of EGFR tyrosine kinase inhibitors (TKI).

189 nt a fundamental cellular response to Aurora kinase inhibitors and contributes to therapy resistance

190 This repurposing of existing kinase inhibitors could lay the foundation for alternati

191 er and inflammation, and small-molecule ERK5 kinase inhibitors have been developed.

192 Small-molecule kinase inhibitors have the potential for broad efficacy,

193 e models for predicting different classes of kinase inhibitors including types I, I(1)/(2), and II as

194 ble method that exploits the large number of kinase inhibitors that have been profiled on near-kinome

195 tion of the amidobenzimidazoles (AB) protein kinase inhibitors that show nanomolar potency against T.

196 The activity of MET tyrosine kinase inhibitors varies by MET alteration category.

197 the discovery of a series of JAK1-selective kinase inhibitors with high potency and excellent JAK fa

198 including G protein-coupled receptor (GPCR) kinase interactor 1 (GIT1), which we found to play an un

199 transcription factors and a nodal cytosolic kinase involved in insulin signaling.

200 ATM kinase is a tumor suppressor and a master regulator of t

201 The Mec1/ATR kinase is one of the primary sensor kinases responsible

202 the activation of oncogenic c-Jun N-terminal kinase (JNK) signaling, induced by the latent membrane p

203 ated protein kinase (MAPK), Jun NH2-terminal kinase (JNK), and nuclear factor kappa-light-chain-enhan

204 ase 1/2 (ERK1/2), p38 and Jun amino-terminal kinase (JNK), which consequently potentiates Pi triggere

205 ress- and immune-responsive c-Jun N-terminal kinase (JNK).

206 of TNFalpha and activation of JUN N-terminal kinase (JNK).

207 ation of ERK (extracellular signal-regulated kinase), JNK, and p38 mitogen-activated protein kinases

208 ) (ruxolitinib) or mitogen-activated protein kinase kinase (MEK) (trametinib) and with STAT3 knockdow

209 The calcium-calmodulin-dependent protein kinase kinase-2 (CaMKK2) is a key regulator of cellular

210 ation sites that can be used to infer >1,500 kinase-kinase interactions and devised algorithms that c

211 is known to cleave mitogen-activated protein kinase kinases (MEKs/MKKs) and some variants of the NLRP

212 silenced the expression of the Hippo pathway kinase LATS2, and this effect led to subsequent activati

213 Src family kinase Lck plays critical roles during T cell developmen

214 ting protein kinase-3 (RIPK3), mixed lineage kinase-like (MLKL) and NADPH oxidase.

215 inhibit CD40-induced phosphorylation of the kinases Lyn and protein kinase C-beta and MAPKs MKK-3/6

216 MADD, the mitogen-activated protein kinase (MAPK) activating death domain protein, regulates

217 ined activation of mitogen-activated protein kinase (MAPK) and AKT.

218 components of the mitogen activated protein kinase (MAPK) pathway enhancing GFP(rare) expression.

219 lied on downstream mitogen-activated protein kinase (MAPK) pathways.

220 regulated through mitogen-activated protein kinase (MAPK) signaling or genetic alteration across hum

221 vated Pi activates mitogen-activated protein kinase (MAPK) signaling, encompassing extracellular sign

222 ator 1 (Act1), p38 mitogen-activated protein kinase (MAPK), Jun NH2-terminal kinase (JNK), and nuclea

223 rs are released by mitogen-activated protein kinase (MAPK)-stimulated acetylation to promote increase

224 teric inhibitor of mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinase (ERK

225 erg and PMBL cells, we hypothesized that PIM kinases may be overexpressed in PMBL and involved in PMB

226 exchange factors (GEFs) or receptor tyrosine kinase-mediated and GEF-dependent RAS activation (such a

227 Kinase-mediated phosphorylation events within peripheral

228 NRAS mutations leading to activation of MAPK kinase (MEK) and extracellular signal-regulated kinase 1

229 proach, as we demonstrate by compiling a MAP kinase model.

230 whether the plant lysin-motif receptor-like kinase MtLYK10 intervenes in recognition of succinoglyca

231 Pathogenic muscle-specific tyrosine kinase (MuSK)-specific IgG4 autoantibodies in autoimmune

232 and devised algorithms that can reconstruct kinase network topologies from these phosphoproteomics d

233 The kinase-off state was especially stable, had relatively l

234 ing eukaryotic-like serine/threonine protein kinases (PASTA-eSTK) that sense PG fragments.

235 We show that the stress-activated protein kinase pathway (SAPK) and its effector, MAPK Sty1, downr

236 F-MAPK kinase-extracellular signal-regulated kinase pathway inhibition and to inhibit myeloid-derived

237 demonstrate that activation of pancreatic ER kinase (PERK) protects oligodendrocytes against inflamma

238 Here, we define two kinase-phosphatase switches that operate at different po

239 ue targets, including phosphatidylinositol 3-kinase (PI3K) and cyclin-dependent kinases.

240 rentially used downstream phosphoinositide 3-kinase (PI3K) pathways, whereas FGFR2b relied on downstr

241 We also identify active phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling in early human embryos

242 tion requires type II phosphatidylinositol 4 kinase (PI4KII)-dependent early endosomal sorting and ac

243 osine monophosphate (cAMP)-dependent protein kinase (PKA), leading to activation of the PKA pathway,

244 Type 1 cGMP-dependent protein kinases (PKGs) play important roles in human cardiovascu

245 s zygote, we show that the mitotic Polo-like kinase PLK-1 phosphorylates the lamin LMN-1 to promote t

246 ies demonstrate that the Drosophila PLK Polo kinase (Polo) is inhibited by the female meiosis-specifi

247 n the minimum EBE was fused with a thymidine-kinase promoter but could be restored by fusion with the

248 f the endothelial-specific receptor tyrosine kinase promoter Tie2.

249 eal a unique mode of regulation of a protein kinase, provide the first example of a bacterial kinase

250 Although their Histidine Kinase receptors are substantially localised to the endo

251 or suppressor or Chek2 DNA damage checkpoint kinase rescued Smc5 cKO neurodevelopmental defects.

252 Mec1/ATR kinase is one of the primary sensor kinases responsible for orchestrating DNA damage respons

253 Loss of either of these kinases results in paralysis and worm death in a mammali

254 Receptor-like cytoplasmic kinases (RLCKs) such as ZED1, interact with ZAR1 and pro

255 Receptor-like protein kinases (RLKs) play key roles in regulating plant growth

256 Here, we demonstrate that the Ras->Raf->rho kinase (ROCK) pathway in MBn suppresses ARM consolidatio

257 ulation of plasma membrane receptor tyrosine kinases (RTKs), such as the epidermal growth factor rece

258 ced TCL1A enhanced phospho-activation of TCR kinases, second-messenger generation, and JAK/STAT or NF

259 The Src family kinases (SFKs) Src, Lyn, and Fyn are essential for plate

260 lates the serum and glucocorticoid inducible kinase SGK1.

261 PI3K lipid kinases signal through the PI3K/Akt pathway, regulating

262 litinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activator of transcription

263 in integrin-paxillin-phosphatidylinositol 3-kinase signaling in vivo.

264 IL22 were prevented with inhibitors of Janus kinase signaling to signal transducer and activator of t

265 atory response and mitogen-activated protein kinase signaling.

266 , and the ABA-independent subclass 1 protein kinases SnRK2.1, SnRK2.4, SnRK2.5, SnRK2.9, and SnRK2.10

267 es the abscisic acid (ABA)-activated protein kinases SnRK2.2, SnRK2.3, SnRK2.6, SnRK2.7, and SnRK2.8,

268 The kinase-specific positional amino acid preferences are le

269 Using the tyrosine kinase Src as a model, we demonstrate efficient regulati

270 of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to the plasma membrane and promotes activat

271 lanoma progression via a function as an NRAS kinase, suggested by Yin et al. (2019) in Cell.

272 evolution of redox regulation in the protein kinase superfamily and may open new avenues for targetin

273 sts counteract the cytotoxic effects of HER2 kinase-targeted therapy in a subset of HER2(+) breast ca

274 e eSimoa method for the detection of protein kinases, telomerase, histone H3 methyltransferase SET7/9

275 These kinases terminate IL-17 signaling by phosphorylating the

276 he binding motif for endogenous Src tyrosine kinase that constitutively inhibits I(Kv1.5) Disrupting

277 ein kinase 1 (CDPK1) is an essential Ser/Thr kinase that controls invasion and egress by the protozoa

278 e HipA toxin functions as a serine/threonine kinase that inhibits cell growth, while the HipB antitox

279 se, provide the first example of a bacterial kinase that requires IP6 for its activation, and may aid

280 sine kinase (BTK) is a non-receptor tyrosine kinase that signals downstream of Fc receptors and plays

281 enomic stability relies on DNA damage sensor kinases that detect DNA lesions and phosphorylate an ext

282 ivation is under control of multiple protein kinases that either promote or inhibit origin activation

283 nel of 260 kinases as well as surfaced other kinases that it potently inhibits.

284 We identified Drosophila Tao kinase, the ortholog of the ASD risk gene Taok2, as a re

285 Netrin-1 induces Fak kinase to inactivate Gsk3alpha/beta and stabilize beta-c

286 and activates the transmembrane RET tyrosine kinase to signal through intracellular Akt/Erk pathways.

287 We predict 27 potential circadian kinases to participate in phosphorylating these sites, i

288 ition of the p38, CK2, CDK, AXL, and PIKFYVE kinases to possess antiviral efficacy, representing pote

289 5 in SCLC, linking the activity of these two kinases to the control of cell survival and lipid metabo

290 ir intracellular activation by host cellular kinases to yield ultimately the bioactive nucleoside ana

291 protein Nck (noncatalytic region of tyrosine kinase) to the CD3e subunit of the TCR.

292 human gliomas such as the receptor tyrosine kinases, TP53 and cell-cycle pathways, and IDH1 R132.

293 The dual protein kinase-transcription factor, ERK5, is an emerging drug t

294 s a potent inhibitor of tropomyosin receptor kinase (TRK) A, B, and C, which has been shown to have a

295 Tropomyosin-receptor kinases (TRKs) are essential for the development of the

296 Tropomyosin receptor kinases (TRKs) are promising cancer therapeutic targets.

297 cuitries in breast cancer cells and that the kinase TTK is important in acute myeloid leukemia.

298 While most kinases upstream of the yeast histone methylation enzyme

299 g disease resistance-related wall-associated kinase (WAK), Catharanthus roseus receptor-like kinase (

300 tors of cell cycle such as Wee1-like protein kinase (WEE1).