ライフサイエンスコーパス: kinase domain

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

2 subsequent trans-autophosphorylation of the kinase domain.

3 tally determined PHTH-binding surface on the kinase domain.

4 he active site and on the distal side of the kinase domain.

5 result in an abnormal over-activation of its kinase domain.

6 dehydrogenase) (ACT) domain upstream of the kinase domain.

7 ns localize to the ATP-binding pocket of the kinase domain.

8 n distinct domains, a predicted nuclease and kinase domain.

9 ne phosphorylation sites within the receptor kinase domain.

10 PKN1's effects on SRF relied on its kinase domain.

11 ated S365 and S729 sites that flank the BRAF kinase domain.

12 promote autophosphorylation of the Aurora A kinase domain.

13 domain and blocking dimerization of the BRAF kinase domain.

14 conventional Src inhibitors that target the kinase domain.

15 d and inhibit a constitutively dimerized PKR kinase domain.

16 he PI3-kinase regulatory domain (PRD) or the kinase domain.

17 phosphorylating downstream proteins via its kinase domain.

18 ation domain (AF-1) thereby masking the TAK1 kinase domain.

19 hosphorylation at His(183) in its C-terminal kinase domain.

20 r-348 to an allosteric binding pocket on the kinase domain.

21 cs, kinetics, and accessible states of BTK's kinase domain.

22 sphorylated, but not unphosphorylated, IRAK4 kinase domain.

23 ATP-binding site (helices H9 and H11) of the kinase domain.

24 redundant, as they share a highly conserved kinase domain.

25 h the ATP-binding site of the CKI1 histidine kinase domain.

26 thout affecting the overall structure of the kinase domain.

27 cine-serine rich (GS) domain adjacent to the kinase domain.

28 including the coding sequence for the entire kinase domain.

29 e find that TRPM7 regulates SOCE through its kinase domain.

30 hers spread between the N and C lobes of the kinase domain.

31 ity via phosphorylation of sites outside the kinase domain.

32 ve because of secondary mutations in the Kit kinase domain.

33 uires direct binding of the inhibitor to the kinase domain.

34 by redox-sensitive cysteine residues in the kinase domain.

35 has to transmit the signal to the C-terminal kinase domain.

36 SH2-kinase linker, and a C-terminal tyrosine kinase domain.

37 es linking alpha-helices G and H of the Wee1 kinase domain.

38 residues, Ig domain, Fn3 domain and a second kinase domain.

39 Multiple UNC-89 isoforms contain two protein kinase domains.

40 ile retaining the transmembrane and tyrosine kinase domains.

41 cs simulations of their fully phosphorylated kinase domains.

42 ucts and compared the tails with the ordered kinase domains.

43 L. that encodes a protein with two putative kinase domains.

44 d fibronectin domains and one or two protein kinase domains.

45 ium exchange behavior when compared with the kinase domains.

46 isoforms, which consist of SH3 and guanylate kinase domains.

47 l solenoid tightly packs against the FAT and kinase domains.

48 mutations frequently targeted the GTPase and kinase domains.

49 ike kinase subfamilies have focused on their kinase domains.

50 All CaMKIIs consist of a kinase domain, a regulatory segment, a variable linker r

51 nts, which reveal a structural mechanism for kinase domain activation in SHK.

52 lobe regulates receptor phosphorylation and kinase domain activation.

53 xplained by a nonconserved amino acid in the kinase domain active site that impairs its phosphorylati

54 te Ser366 in the STING tail cannot reach the kinase-domain active site of bound TBK1, which suggests

55 r protein kinase that contains an N-terminal kinase domain and a C-terminal regulatory region consist

56 e traced to ancestral members that contain a kinase domain and a calmodulin-like domain.

57 AC signaling by artificially dimerizing Mps1 kinase domain and a cytosolic KNL1 phosphodomain, the ki

58 RbkR proteins are composed of the riboflavin kinase domain and a DNA-binding winged helix-turn-helix-

59 large, multidomain protein which contains a kinase domain and GTPase domain among other regions.

60 difference in the linker region between the kinase domain and holoenzyme hub, implying linker length

61 ads to activation of the CERK1 intracellular kinase domain and induction of plant innate immunity in

62 n of intramolecular interactions between the kinase domain and its N-terminal regulatory region indep

63 clinical JAK inhibitors target the tyrosine kinase domain and lack mutation and pathway selectivity.

64 Multiple variants in the kinase domain and one variant in the extracellular domai

65 Interaction between kinase domain and regulatory light chain (RLC) substrate

66 diated by direct ARRB1 binding to the VEGFR3 kinase domain and resulted in decreased VEGFR3 internali

67 ligand recognition and communication to the kinase domain and reveal the sensitivity of the system t

68 jor regulatory mechanism embedded within the kinase domain and show that the DFG motif serves as a co

69 nase active site that uses residues from the kinase domain and the juxtamembrane region.

70 terface formed between the large lobe of the kinase domain and the regulator of G protein signaling h

71 ally expressed protein kinase (SPEG) has two kinase-domains and is a critical cardiac regulator.

72 V mutations, which are located within ERK3's kinase domain, and are shown to exist in several cancers

73 s activation status, the conformation of its kinase domain, and clinically relevant inhibitors.

74 that mutations in the N-terminal end of the kinase domain are more disruptive of protein function.

75 RET gene rearrangements retaining the kinase domain are oncogenic drivers in papillary thyroid

76 a global selection for fusion functionality: kinase domains are nearly 2-fold more enriched in DEEPES

77 While most kinase domains are ordered independently, approximately

78 a interacts physically with Atg1 through its kinase domain, as well as with Atg6 and Vps34.

79 ystal structure of the human wild-type BMPR2 kinase domain at 2.35 angstrom resolution.

80 Despite the presence of a kinase domain at the N-terminus, no COP1-independent rol

81 solved three crystal structures of the IRAK4 kinase domain (at <=2.6 angstrom resolution), in its unp

82 Surrogates for the LRRK2 kinase domain based on checkpoint kinase 1 (CHK1) mutant

83 uencing, only five distinct mutations in the kinase domain behave as dominant-negative mutations in z

84 , we report the crystal structure of HIPK2's kinase domain bound to CX-4945, a casein kinase 2alpha (

85 f the Par-3 phosphorylation site from aPKC's kinase domain but does not disrupt the Par-3 PDZ2-aPKC P

86 uptake requires PDPK1 phosphorylation of the kinase domain but not mTORC2 phosphorylation of the HM d

87 d by engaging an allosteric site on the HER3 kinase domain, but this site is not required when HER3 i

88 d bifunctional channels to contain their own kinase domains, but how these channel-kinases are regula

89 The N-terminal LOK kinase domain can then access a site 40 residues distal

90 ent the first crystal structure of the HIPK2 kinase domain, complexed with the small-molecule inhibit

91 nd Her2 and highlight their influence on the kinase domain conformations and active site accessibilit

92 urified recombinant full-length proteins and kinase domain constructs differed substantially in phosp

93 to 1.87 angstrom resolution and a RET(G810A) kinase domain crystal structure to 1.99 angstrom resolut

94 The HIPK2 kinase domain crystallized in the active conformation, w

95 dy, x-ray crystal structures of the Aurora A kinase domain delineate redox-sensitive cysteine residue

96 tructural analysis of a phosphorylated B-Raf kinase domain dimer in complex with dimeric 14-3-3, at a

97 the full-length protein is preserved via the kinase domain dimerization interface in all variants, fu

98 Myddosome signaling complex, inducing IRAK4 kinase domain dimerization, autophosphorylation, and act

99 at combines an ion channel with an intrinsic kinase domain, enabling it to modulate cellular function

100 equence alignment (MSA) of 497 human protein kinase domains excluding atypical kinases.

101 he sequence and structure of the UWO241 Stt7 kinase domain exhibits substantial alterations, which we

102 In contrast, the Raf kinase domain extends into the cytoplasm and its assembl

103 es (PIKKs), is composed of conserved FAT and kinase domains (FATKINs) along with solenoid structures

104 kinase activation process in which the IRAK4 kinase domain first homodimerizes in the Myddosome, lead

105 We noted that the overall kinase domain fold of HIPK2 closely resembles that of ev

106 Additionally, the IRAK1 kinase domain forms heterodimers with the phosphorylated

107 omain is responsive to ligands that bind the kinase domain forms yet a third type of stress-independe

108 the prevailing assumption has been that the kinase domain fragment (deltaKD) freed from autoinhibito

109 a caspase-cleaved, proteasome-resistant NIK kinase domain fragment that amplifies pathogenic NF-kapp

110 brane causes steric clashes that release the kinase domain from autoinhibition, allowing it to underg

111 KRAS and the plasma membrane, unleashing the kinase domain from autoinhibition.

112 nase domain of VPS15, and releases the VPS34 kinase domain from the inhibited conformation.

113 spectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains.

114 nding partners for a number of this family's kinase domains have been identified, the catalytic neces

115 collapsed activation loop (a-loop) and an IN kinase domain helix 11 (kalpha11).

116 g of a second MIT stabilizes the VPS34 lipid kinase domain in an active conformation that has an unre

117 be the crystal structures of the native HPK1 kinase domain in both nonphosphorylated and doubly phosp

118 We present a model of cRaf kinase domain in complex with a heterogeneous membrane b

119 ort the crystal structure of the human IRAK1 kinase domain in complex with a small molecule inhibitor

120 first structural characterization of the Axl kinase domain in complex with a small-molecule macrocycl

121 we report a biochemical analysis of the ASK1 kinase domain in conjunction with its N-terminal thiored

122 SH3-SH2 domains perturb the dynamics of the kinase domain in the context of the full length protein.

123 addition, PUB13 could ubiquitinate the LYK5 kinase domain in vitro.

124 of phosphorylation at the latch interface of kinase domains in regulating EGFR dimerization.

125 A new phylogeny of the protein kinase domains in the human genome based on our alignmen

126 etween the Cdc42-binding CRIB domain and the kinase domain, inhibits PAK1 targeting to cell-cell junc

127 introducing point mutations in the GRK5 RHD-kinase domain interface, we show with both in silico and

128 mode of RET that is poised to bring the two kinase domains into close proximity for cross-phosphoryl

129 tion by bringing the thioredoxin-binding and kinase domains into close proximity.

130 tation, as well as a truncation of the LRRK2 kinase domain, into marmoset embryonic and induced pluri

131 While the IRAK4 kinase domain is capable of homodimerization in the unph

132 hosphorylated state, we found that the IRAK1 kinase domain is constitutively monomeric regardless of

133 rved proline in the CMGC insert of the DYRK1 kinase domain is hydroxylated by PHD1, and this event pr

134 e new families of pseudokinases in which the kinase domain is repurposed for noncanonical nucleotide

135 function are unclear, the importance of the kinase domain is strongly implicated, since 2 of the 5 m

136 the three members of the TAM family, the Axl kinase domain is the only one that has so far eluded str

137 d that S-acylation adjacent to receptor-like kinase domains is common, affecting ~25% of Arabidopsis

138 entral hub complex, while positioning of the kinase domains is highly flexible, revealing dynamic hol

139 JH2 stimulates the activity of the adjacent kinase domain (JH1) resulting in myeloproliferative diso

140 ith both a Ras of complex (ROC) domain and a kinase domain (KD) and, therefore, exhibits both GTPase

141 t the interactions between the PH domain and kinase domain (KD) are important for maintaining Akt in

142 TKIs) may select for drug-resistant BCR-ABL1 kinase domain (KD) mutants.

143 We identified kinase domain (KD) mutations that abolish kinase activit

144 lic nucleotide-binding domains (CNBs), and a kinase domain (KD), are arranged when the enzyme is inac

145 ating kinase 1 (ASK1) inhibitor bound to its kinase domain led to the design and synthesis of the nov

146 ur via apoptosis, but required Mixed Lineage Kinase Domain Like (MLKL) and activation of Signal trans

147 threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and generally manifests with m

148 Characterization of infected mixed lineage kinase domain-like (MLKL) and tumor necrosis factor rece

149 roptotic effector pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) by the upstream protein kinase

150 t RIP3-dependent activation of mixed lineage kinase domain-like (MLKL) leading to necroptosis.

151 f necrosis, is executed by the mixed lineage kinase domain-like (MLKL) protein, which is triggered by

152 ein-3 (NLRP3) inflammasome and mixed lineage kinase domain-like (MLKL) protein-dependent tubule necro

153 g protein kinase-3 (RIPK3) and mixed lineage kinase domain-like (MLKL) proteins.

154 Mixed Lineage Kinase domain-Like (MLKL), a key player in necroptosis,

155 icated in MSU crystal killing, mixed lineage kinase domain-like (MLKL), did not prevent MSU crystal-i

156 protein kinase (RIPK) 1/3- and mixed-lineage kinase domain-like (MLKL)-dependent necroptosis.

157 eam effector, the pseudokinase mixed lineage kinase domain-like (MLKL).

158 Blocking necroptosis using mixed lineage kinase domain-like deficient mice or necrostatin-1s trea

159 id not increase phosphorylated mixed lineage kinase domain-like in RIP3(-/-) mice.

160 This approach revealed that mixed lineage kinase domain-like protein (MLKL), a key terminal mediat

161 e-3 (RIPK3) phosphorylation of mixed-lineage kinase domain-like protein (MLKL), which results in disr

162 ions, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which then disrupts c

163 RIPK3 and the effector protein mixed-lineage kinase domain-like protein (MLKL).

164 in kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL).

165 teracting proteins 1 and 3 and mixed lineage kinase domain-like protein necroptotic signaling with th

166 ein kinase-3 and its substrate mixed-lineage kinase domain-like protein play a crucial role.

167 eonine-protein kinase 3)-MLKL (mixed lineage kinase domain-like protein)-dependent programmed necropt

168 increased RIPK1 expression and mixed lineage kinase domain-like pseudokinase (MLKL) activation in hum

169 the formation of a RIPK1-RIPK3-mixed lineage kinase domain-like pseudokinase (MLKL) signaling complex

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

171 pha/beta receptor signaling or mixed lineage kinase domain-like pseudokinase (MLKL)-dependent necropt

172 lasma membrane localization of mixed lineage kinase domain-like pseudokinase (MLKL).

173 cting protein kinase-1), MLKL (mixed lineage kinase domain-like pseudokinase) protein, and caspase-3.

174 that lead to the activation of mixed lineage kinase domain-like pseudokinase.

175 PK3, and a pseudo-kinase MLKL (Mixed Lineage Kinase domain-Like) associated in a multi-protein comple

176 the downstream effector MLKL (Mixed Lineage Kinase Domain-Like).

177 ally lead to the activation of mixed lineage kinase domain-like.

178 that membrane interaction of monomeric cRaf kinase domain likely orchestrates the Raf activation pro

179 our-point one, ezrin, radixin, moesin (FERM)-kinase domain linker, which contains autophosphorylation

180 bility and greater dynamic nature of the Axl kinase domain may account for its poor crystallizability

181 with different phenotypes than those in the kinase domain (MEN2B-like mutations).

182 Through TYK2 kinase domain mutants and a TYK2 980I knock-in mouse mod

183 n DIPG associated cytoplasmic ACVR1 receptor kinase domain mutants, G328V and R206H, are reexamined i

184 constitutive PDGFRbeta signaling caused by a kinase domain mutation (D849V) develop lethal autoinflam

185 t of new recommendations on the frequency of kinase domain mutation analysis to improve patient clini

186 We detected a kinase domain mutation in 25 (21%) of 121 patients.

187 We identified a kinase domain mutation in four (10%) of 41 patients with

188 with chronic myeloid leukaemia for BCR-ABL1 kinase domain mutation.

189 to our knowledge, we report the presence of kinase domain mutations after only 3 months of therapy,

190 esistant ROS1 positive cancer with secondary kinase domain mutations especially G2032R mutation which

191 to examine the clinical effects of low-level kinase domain mutations identified using NGS in patients

192 Kinase domain mutations in BCR-ABL1 are associated with

193 nd consistently detected early appearance of kinase domain mutations that would not otherwise be dete

194 We screened patients for BCR-ABL1 kinase domain mutations using NGS, irrespective of patie

195 Low-level kinase domain mutations were first identified in 17 (68%

196 quencing (NGS) allows detection of low-level kinase domain mutations, but its relevance in clinical p

197 cancers through genomic events like tyrosine kinase domain mutations, juxtamembrane splicing mutation

198 echanism is the acquisition of on-target TRK kinase domain mutations, which interfere with drug bindi

199 focal MET or HGF gene amplification, or MET kinase domain mutations.

200 lications and resistance-conferring tyrosine kinase domain mutations.

201 ral resistance mechanisms, such as secondary kinase-domain mutations (e.g., ROS1-G2032R) have been id

202 rmined the X-ray co-crystal structure of RET kinase domain-nintedanib complex to 1.87 angstrom resolu

203 ional SELEX approach was applied against the kinase domain of a group of c-KIT proteins (c-KIT(WT), c

204 acellular S1P directly bound to the purified kinase domain of aPKC and relieved autoinhibitory constr

205 The intracellular kinase domain of BRI1 is an active kinase and also encap

206 Newman algorithm-based community maps of the kinase domain of cAMP-dependent protein kinase A allow f

207 We show that the kinase domain of cRaf has three distinct membrane-intera

208 for ER-associated Bak and interacts with the kinase domain of DAPk1 to form Bik-DAPk1-ERK1/2-Bak comp

209 Utilizing a human cell line in which the kinase domain of DNA-PKcs is inactivated, we show here t

210 from a random RNA pool that can bind to the kinase domain of each target with high affinity and can

211 1 mono-methylates lysine 721 in the tyrosine kinase domain of EGFR, and that this methylation leads t

212 t Y155 is phosphorylated in vitro by the Tyr kinase domain of epidermal growth factor (EGF) receptor.

213 ons to probe the activation mechanism of the kinase domain of Fibroblast Growth Factor Receptor (FGFR

214 lso stabilize a distinct conformation of the kinase domain of GRK2 compared with previous complexes w

215 CaM binds primarily to the small lobe of the kinase domain of GRK5 near elements critical for recepto

216 Here we report on the structure of the kinase domain of human NEK1 in its apo- and ATP-mimetic

217 emergence of resistance mutations within the kinase domain of its target, Abl.

218 R-induced allelic variation in the conserved kinase domain of MPK6.

219 mation and inserts into a groove between the kinase domain of one TBK1 subunit and the scaffold and d

220 e discover that Smurf1 directly binds to the kinase domain of PIPKIgamma via its C2 domain while Lysi

221 We further show that the kinase domain of PKD dimerizes in a concentration-depend

222 inase domain, we ask the following: does the kinase domain of Raf has potential to interact with memb

223 ues in the amino (N)-terminal portion of the kinase domain of RAF isoforms are responsible for this d

224 x that directly interacts with the histidine kinase domain of RcsC.

225 (2020) show how missense mutations in the kinase domain of TBK1 differentially affect disease onse

226 we find a recurrent missense mutation in the kinase domain of the ALPK1 gene in spiradenomas and spir

227 on domain and the cytosolic protein tyrosine kinase domain of the insulin receptor was not affected b

228 where each autoinhibitory domain covers the kinase domain of the other monomer.

229 ic oncoproteins often contain the C-terminal kinase domain of the RTK joined in cis to various N-term

230 served TORC1 subunit that interacts with the kinase domain of TOR.

231 to sequences outside of-but adjacent to-the kinase domain of TrkA.

232 we report the 2.2 A crystal structure of the kinase domain of Trl1 from the fungal pathogen Candida a

233 Here we show that the C-terminal kinase domain of TRPM6 is cleaved from the channel domai

234 of the VPS15 scaffold, displaces the protein kinase domain of VPS15, and releases the VPS34 kinase do

235 -)) binds to a hydrophobic pocket within the kinase domain of WNKs to inhibit its activity.

236 pathways, the binding and inhibition of the kinase domain of ZAP-70, and GAP inhibition of the p21(r

237 en mutations in the fibronectin type III and kinase domains of EPHB1 were compared with wild-type EPH

238 The HisRS-like and kinase domains of GCN2 show conformational changes upon

239 ns bacterial phytochrome (DrBphP-PCM) to the kinase domains of neurotrophin receptors resulted in opt

240 asymmetric dimer is a "latch" formed between kinase domains of the binding partners.

241 R domain of BIR3 is fused to the cytoplasmic kinase domains of the SERK-dependent LRR-RKs BRASSINOSTE

242 demonstrate that KAT2A/2B acetylate the PLK4 kinase domain on residues K45 and K46.

243 es identified potential binding sites on the kinase domain, one of which was validated biochemically.

244 Deletion of either kinase domain or death domain in the T cell compartment

245 the ATP or peptide binding-sites within the kinase domain, or are important for protein stability, s

246 r interactions between the SH3 and guanylate kinase domains play a role in the stability of beta1a wh

247 tion of certain clinically relevant BCR-ABL1 kinase domain point mutants and further sensitized Ba/F3

248 ere, by analyzing mice with juxtamembrane or kinase domain point mutations that increase PDGFRalpha a

249 dem duplication mutations, 23% FLT3-tyrosine kinase domain point mutations, and 2% both types.

250 vanescent fields reflect the changes in EGFR kinase domain polarization upon ligand binding.

251 the effector protein SAV1, each increase the kinase domain proximity and autophosphorylation of MST2.

252 ncentrations of ATP prevent formation of RAF kinase-domain (RAF(KD)) dimers that are critical for act

253 rotein truncation and loss of the C-terminal kinase domain (Raf1-tr).

254 ed that increasing the proximity of adjacent kinase domains, rather than formation of a specific prot

255 In a much slower second step, the kinase domains rearrange internally.

256 e propose that the conformation of the LRRK2 kinase domain regulates its interactions with microtubul

257 c changes that are propagated throughout the kinase domain remains poorly understood.

258 identified, the catalytic necessity of these kinase domains remains unknown.

259 how PD-linked mutations that lie within the kinase domain result in hPINK1 loss-of-function and prov

260 ciprocality, and annotates gene partners for kinase domain retention.

261 nd autophosphorylation at CusS's cytoplasmic kinase domain(s).

262 n and extends the activation loop within the kinase domain, shifting the equilibrium toward the activ

263 s with purified cyt b6f and recombinant Stt7 kinase domain show that cyt b6f enhances Stt7 autophosph

264 osphorylated and phosphorylated forms of the kinase domains show no apparent structural change that c

265 al and clinical significance, only the IRAK4 kinase domain structure has been determined among the fo

266 possessing gain of function mutations in the kinase domain such as the most prevalent G2019S mutation

267 osed of a dual specificity (Ser/Thr and Tyr) kinase domain tethered to a calmodulin-like domain (CLD)

268 eric conformational shifts in regions of the kinase domain that are critical for catalysis.

269 cquisition of an additional mutation in EGFR kinase domain that confers resistance to TKIs.

270 hanges within the catalytic machinery of the kinase domain that distinguish them from their canonical

271 kinase c-ros oncogene 1 (ROS1), which has a kinase domain that is physiologically related to anaplas

272 We identify mutations in the kinase domain that lead to elevated levels of PI(3,5)P2

273 turn promotes conformational changes in the kinase domain that result in nuclear translocation of ER

274 lly disordered conformation of the IRE1alpha kinase domain that would be incompatible with back-to-ba

275 phosphodiesterase and central polynucleotide kinase domains that heal the broken ends to generate the

276 een the VPS15 protein kinase and VPS34 lipid kinase domains that restrict the conformation of the VPS

277 The phosphorylated IRAK4 kinase domain then forms heterodimers with the IRAK1 kin

278 We show that binding of ATP stabilizes the kinase domain, thereby altering the unfolding hierarchy.

279 LT3 mutation: point mutation in the tyrosine kinase domain (TKD) or internal tandem duplication (ITD)

280 ts with point mutations of the FLT3 tyrosine kinase domain (TKD), but the biological mechanism underl

281 death domain and phosphorylates TSC2 via its kinase domain to mediate mTORC1 activation in CD8(+) T c

282 and optogenetic recruitment of the PI3K C2A kinase domain to the TGN-induced deltaR export downstrea

283 motifs and domains found in association with kinase domains to illustrate their origin, organization,

284 quences of disordered linkers connecting the kinase domains to the oligomeric hubs of the holoenzyme.

285 ein with separate surfaces of the C-terminal kinase domain, to co-operatively inhibit kinase activati

286 oiled coil linker and the attached histidine kinase domains undergo a left handed rotation within mic

287 nding event activates the intracellular EGFR kinase domain via (dimer-dependent) asymmetric dimerizat

288 ated in the C-terminal lobe of the activator kinase domain was important to potentiate dimerization.

289 evealed the dynamic architecture of inactive kinase domains was co-opted in the activated dimer but t

290 Since the catalytic domain of Raf is its kinase domain, we ask the following: does the kinase dom

291 ains at rationally selected locations in the kinase domain, we created the photoswitchable kinases ps

292 adjacent to the latch binding region on the kinase domain, we propose that phosphorylation strengthe

293 structural consequences throughout the BAK1 kinase domain, whereas glutathionylation of C353 in the

294 terminal pleckstrin homology (PH) domain and kinase domain, which is relieved by C-tail phosphorylati

295 its binding to the insert loop within PERK's kinase domain, which is, itself, phosphorylated at multi

296 Moreover, separation of the sensor and kinase domains, which deactivates catalysis, increased t

297 phosphorylation of SPEG activates its second kinase-domain, which in turn phosphorylates sarcoplasmic

298 sol and nucleus, we further engineered a Fyn kinase domain with light-inducible nuclear localization

299 midazole inhibitors in complex with the EGFR kinase domain with X-ray crystallography.

300 omain then forms heterodimers with the IRAK1 kinase domain within the Myddosome, leading to its subse