ライフサイエンスコーパス: tyrosine kinase domain

1 atter factor receptors but lack an intrinsic tyrosine kinase domain.

2 ustered around the ATP-binding pocket of the tyrosine kinase domain.

3 s, consisting primarily of the intracellular tyrosine kinase domain.

4 ation domain, but lacks both the SH2 and the tyrosine kinase domain.

5 rkA, suggesting that GM1 does not affect the tyrosine kinase domain.

6 ng molecules through a constitutively active tyrosine kinase domain.

7 n of the activation loop of the beta-subunit tyrosine kinase domain.

8 ) in the first part of the cytoplasmic split tyrosine kinase domain.

9 H3 and SH2 Src homology domains, but lacks a tyrosine kinase domain.

10 nerated mice with a germline ablation of the tyrosine kinase domain.

11 tially purified native IR and recombinant IR tyrosine kinase domain.

12 portion of the protein immediately after the tyrosine kinase domain.

13 C-terminal coding region of the cytoplasmic tyrosine kinase domain.

14 nerated mice (merkd) that lack the signaling tyrosine kinase domain.

15 The apoptotic mechanism requires the c-Kit tyrosine kinase domain.

16 eletion (termed T691stop) which includes the tyrosine kinase domain.

17 d allosteric regulation of the intracellular tyrosine kinase domain.

18 identity overall and 84% identity within the tyrosine kinase domain.

19 bers, contains a pseudo kinase in place of a tyrosine kinase domain.

20 gion is required for maximal activity of the tyrosine kinase domain.

21 ome-13 gene (ZNF198), are fused to the FGFR1 tyrosine-kinase domain.

22 ceptor while retaining the transmembrane and tyrosine kinase domains.

23 ces encoding the transmembrane, WW-like, and tyrosine kinase domains.

24 rkC receptor proteins containing full-length tyrosine kinase domains.

25 acks the extracytoplasmic, transmembrane and tyrosine kinase domains.

26 his event to activation of the intracellular tyrosine kinase domains.

27 signaling proteins possessing SH3, SH2, and tyrosine kinase domains.

28 lves formation of an asymmetric dimer of the tyrosine kinase domains.

29 3-ITD allelic ratio (P = .004) and IS in the tyrosine kinase domain 1 (TKD1, P = .06) were associated

30 adenosine triphosphate (ATP)-binding domain (tyrosine kinase domain 1 [TKD1]) of the fms-related tyro

31 1982T-->C, that resulted in Val654Ala in KIT tyrosine kinase domain 1.

32 rane domain (23%) and point mutations in the tyrosine kinase domain (10%).

33 concomitant activation of its intracellular tyrosine kinase domain [5] [6] [7].

34 n is located within a critical region of the tyrosine kinase-domain activation loop.

35 iFer is devoid of both the tyrosine kinase domain and a functional SH2 domain but d

36 es, and a nonsense mutation that removes the tyrosine kinase domain and all subsequent 3' regions of

37 ceptors (PDGFR), which have an intracellular tyrosine kinase domain and an extracellular region compr

38 ogenic Src was linked to the activity of its tyrosine kinase domain and attention turned to identifyi

39 o constitutive activation of the PDGF beta R tyrosine kinase domain and cellular transformation.

40 Since sKDR does not have a tyrosine kinase domain and does not dimerize, it is prin

41 EGFR gene sequencing of the tyrosine kinase domain and gene copy number assessments

42 d (HKD) construct of the HER-2 intracellular tyrosine kinase domain and have identified an optimal su

43 ence and second proline-rich domain from the tyrosine kinase domain and integrin-binding sequence.

44 -DNR) is a truncated receptor that lacks the tyrosine kinase domain and is devoid of signaling capabi

45 This molecule lacks a catalytic tyrosine kinase domain and is related to a previously id

46 icted to cause a p.R621H substitution in the tyrosine kinase domain and partial loss of FGFR3 functio

47 Crystallographic studies of the tyrosine kinase domain and proximal juxtamembrane region

48 nd neoplastic processes via signaling by its tyrosine kinase domain and subsequent activation of tran

49 t not in B82L-par cells, indicating that the tyrosine kinase domain and the auto-phosphorylation site

50 iochemical characterization of the human RET tyrosine kinase domain and the structure determination o

51 TDs result in constitutive activation of the tyrosine kinase domain and transform growth factor-depen

52 The truncated form of trkB, lacking the tyrosine kinase domain, and the low-affinity neurotrophi

53 atively long juxtamembrane sequence, a split tyrosine kinase domain, and two conserved intracellular

54 N-terminal segment followed by SH3, SH2, and tyrosine kinase domains, and a short C-terminal tail.

55 ivated by BCR-ABL segments distinct from its tyrosine kinase domain are essential for rescue of eryth

56 rane proteins bearing syk but not src family tyrosine kinase domains are capable of autonomously trig

57 Abl's SH3, SH2, and tyrosine kinase domains are joined via a linker to an F-

58 ly occurring mutants of the insulin receptor tyrosine kinase domain, Arg-1174 --> Gln and Pro-1178 --

59 h receptor containing the signal transducing tyrosine kinase domain as well as truncated forms lackin

60 show that this gene encodes a protein with a tyrosine kinase domain at the N-terminal end and a proli

61 We also present the structures of the RET tyrosine kinase domain bound to two inhibitors, the pyra

62 The functions of Arg required an intact tyrosine kinase domain but not the actin-binding motifs

63 ized by mutations in exons encoding the EGFR tyrosine kinase domain, but disease progression invariab

64 unctioning as an adaptor protein for the MET tyrosine kinase domain, can augment the HGF-MET signalin

65 yclonal and monoclonal antibodies to the ALK tyrosine kinase domain, consistent with ALK deregulation

66 f ABL regulatory domains outside the SH3-SH2-tyrosine kinase domain core.

67 we attenuated FGFR signaling by expressing a tyrosine kinase domain-deficient Fgfr1 (tFgfr1) gene con

68 the epidermal growth factor receptor (EGFR) tyrosine kinase domain determine responsiveness to EGFR

69 Other mutations within the FGFR3 tyrosine kinase domain (e.g., C1620A or C1620G [both res

70 opoietic receptor superfamily lack intrinsic tyrosine kinase domains for the intracellular transmissi

71 Partial cDNA sequences encoding the tyrosine kinase domains from six distinct members of the

72 oiled-coil domain that when fused to the RET tyrosine kinase domain had the ability to activate it, f

73 Activation of receptors that signal via tyrosine kinase domains has been thought to involve rece

74 racellular domains and intracellular protein tyrosine kinase domains have suggested mechanisms for gr

75 showed somatically acquired mutations in the tyrosine kinase domain in 12.4% of samples.

76 The constitutive activation of the tyrosine kinase domain in the carboxyl-terminal end of R

77 rve two prevalent conformations in which the tyrosine kinase domains interact asymmetrically.

78 The cytoplasmic tyrosine kinase domain is also a preferred target for sm

79 ructural studies show that the inactive EGFR tyrosine kinase domain is autoinhibited by intramolecula

80 the transmembrane helix and the cytoplasmic tyrosine kinase domain, is conserved among all insulin r

81 Although Itk also contains SH3, SH2 and tyrosine kinase domains, it lacks the corresponding regu

82 s are characterized by dual kinase domain: a tyrosine kinase domain (JH1) that is preceded by a pseud

83 k is that, in addition to a fully functional tyrosine kinase domain (JH1), Jak possesses a pseudokina

84 ons in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquire

85 e we report the crystal structure of the Lck tyrosine kinase domain (LCKK) in its activated state at

86 The deletion resulted in activation of the tyrosine kinase domain leading to constitutive tyrosine

87 it mesoderm induction by receptors bearing a tyrosine kinase domain mutation.

88 nternal tandem duplications (FLT3-ITD), FLT3 tyrosine kinase domain mutations (FLT3-TKD), MLL partial

89 nternal tandem duplications (P < .0001), and tyrosine kinase domain mutations (P = .02) were less fre

90 To determine whether EGFR tyrosine kinase domain mutations are early events in the

91 Both ITD and tyrosine kinase domain mutations at D835 were identified

92 n chronic myeloid leukemia, the emergence of tyrosine kinase domain mutations has historically been t

93 ALK tyrosine kinase domain mutations occurred in 8% of sampl

94 with epidermal growth factor receptor (EGFR) tyrosine kinase domain mutations require altered signali

95 (breakpoint cluster region/Abelson oncogene) tyrosine kinase domain mutations that impair imatinib bi

96 Moreover, 6 FGFR4 tyrosine kinase domain mutations were found among 7 of 9

97 ed in NSCLC patients with BAC, and that EGFR tyrosine kinase domain mutations were identified in larg

98 EGFR tyrosine kinase domain mutations were not identified, an

99 tations were mainly attributed to exon 8 and tyrosine kinase domain mutations, respectively.

100 ulation was impaired in two NSCLCs with EGFR tyrosine kinase domain mutations.

101 (n = 6) and in two different regions in the tyrosine kinase domain (n = 4).

102 ing antibodies or by genetic deletion of the tyrosine kinase domain neither prevented nor changed the

103 esently, no high resolution structure of the tyrosine kinase domain of Abl is available.

104 separate germline missense mutations in the tyrosine kinase domain of ALK that segregated with the d

105 ined by the presence of mutations within the tyrosine kinase domain of BCR-ABL, such mutations are no

106 c AMP-dependent protein kinase (RI) with the tyrosine kinase domain of c-Ret.

107 4, two groups reported that mutations in the tyrosine kinase domain of EGFR are strongly associated w

108 rbor somatic mutations in exons encoding the tyrosine kinase domain of EGFR experience significant tu

109 Our findings indicate that mutation of the tyrosine kinase domain of EGFR is an early event in the

110 are reversible competitive inhibitors of the tyrosine kinase domain of EGFR that bind to its adenosin

111 We show here that somatic deletions in the tyrosine kinase domain of EGFR were associated with incr

112 at WHSC1L1 mono-methylates lysine 721 in the tyrosine kinase domain of EGFR, and that this methylatio

113 e typically located after the C-helix of the tyrosine kinase domain of EGFR, may account for up to 4%

114 arboring somatic-activating mutations in the tyrosine kinase domain of EGFR.

115 Activation of the tyrosine kinase domain of either chimera repressed myoge

116 Although specific mutations in the tyrosine kinase domain of epidermal growth factor recept

117 Several somatic mutations within the tyrosine kinase domain of epidermal growth factor recept

118 l structure of PD 173074 in complex with the tyrosine kinase domain of FGF receptor 1 at 2.5 A resolu

119 yrosine autophosphorylation of the catalytic tyrosine kinase domain of FGF-receptor-1 (FGFR1) is medi

120 cribe the crystal structure of the activated tyrosine kinase domain of FGFR1 in complex with a phosph

121 Crystal structures of the tyrosine kinase domain of FGFR1 in complex with the two

122 6Lys) and c.1966A>G (p.Lys656Glu) within the tyrosine kinase domain of FGFR1, in two affected individ

123 641 amino acids of RAMP become joined to the tyrosine kinase domain of FGFR1.

124 MYM domains of ZNF198 and the intracellular tyrosine kinase domain of FGFR1.

125 echanism by which a missense mutation in the tyrosine kinase domain of FGFR2, described in the sporad

126 The crystal structure of the tyrosine kinase domain of fibroblast growth factor recep

127 surface receptor with strong homology to the tyrosine kinase domain of growth factor receptors, in pa

128 Activating mutations in the tyrosine kinase domain of HER2 (ErbB2) have been identif

129 We sequenced the tyrosine kinase domain of HER2 in 671 primary non-small

130 probes for the extracellular domain and the tyrosine kinase domain of human TrkC, we found by Northe

131 ere, we present the crystal structure of the tyrosine kinase domain of IGF1R (IGF1RK), in its unphosp

132 currently ongoing with agents targeting the tyrosine kinase domain of MET in sporadic and hereditary

133 RanBPM interacts with the tyrosine kinase domain of MET through its SPRY domain.

134 ere located in the ATP-binding region of the tyrosine kinase domain of MET.

135 on protein composed of the carboxyl terminal tyrosine kinase domain of NTRK1 and the amino terminal p

136 our novel EGFR somatic mutations in the EGFR tyrosine kinase domain of prostate cancer patients: G735

137 Activating mutations in the tyrosine kinase domain of receptor tyrosine kinases (RTK

138 cDNA sequencing of the receptor tyrosine kinase domain of the ALK gene was assessed in 4

139 ntified 14 different mutations affecting the tyrosine kinase domain of the colony stimulating factor

140 Somatic mutations were identified in the tyrosine kinase domain of the EGFR gene in eight of nine

141 Somatic mutations in the tyrosine kinase domain of the epidermal growth factor re

142 CLC) do not have activating mutations in the tyrosine kinase domain of the epidermal growth factor re

143 finger protein that binds to the cytoplasmic tyrosine kinase domain of the epidermal growth factor re

144 Somatic mutations in exons encoding the tyrosine kinase domain of the epidermal growth factor re

145 curred in NSCLC tumors with mutations in the tyrosine kinase domain of the epidermal growth factor re

146 f Cell provides compelling evidence that the tyrosine kinase domain of the epidermal growth factor re

147 hat the presence of somatic mutations in the tyrosine kinase domain of the epidermal growth factor re

148 A year has passed since mutations of the tyrosine kinase domain of the epidermal growth factor re

149 n and new endometrial cancer hotspots in the tyrosine kinase domain of the FGFR2 protein, one of whic

150 RanBPM has been reported to bind to the tyrosine kinase domain of the hepatocyte growth factor (

151 Missense mutations in the tyrosine kinase domain of the human insulin receptor fre

152 The tyrosine kinase domain of the insulin receptor is subjec

153 tyrosyl peptide substrate with the activated tyrosine kinase domain of the insulin receptor was studi

154 of the Grb14 BPS region in complex with the tyrosine kinase domain of the insulin receptor.

155 H2 domain in complex with the phosphorylated tyrosine kinase domain of the insulin receptor.

156 ish the structure of FGFR1K from that of the tyrosine kinase domain of the insulin receptor.

157 This compound activated the tyrosine kinase domain of the IR beta-subunit at concent

158 Oncogenic missense mutations of the tyrosine kinase domain of the MET gene have been identif

159 identified missense mutations located in the tyrosine kinase domain of the MET gene in the germline o

160 y, we demonstrated missense mutations in the tyrosine kinase domain of the MET proto-oncogene in HPRC

161 een shown to have germ-line mutations in the tyrosine kinase domain of the MET proto-oncogene.

162 e ETS-family member TEL fused to the protein-tyrosine kinase domain of the platelet-derived growth fa

163 ) induces dimerization and activation of the tyrosine kinase domain of the receptor, resulting in aut

164 e depigmentation in these species map to the tyrosine kinase domain of the receptor, whereas none hav

165 1271 of the insulin receptor, containing the tyrosine kinase domain of the receptor.

166 c oncogene is generated by the fusion of the tyrosine kinase domain of the RET proto-oncogene to the

167 lar domain, the transmembrane domain, or the tyrosine kinase domain of these receptors.

168 the major role of autophosphorylation in the tyrosine kinase domain of v-Fps is to increase the rate

169 olecule designed to bind specifically to the tyrosine kinase domain of VEGFR and inhibit angiogenesis

170 Also, genetic ablation of the tyrosine kinase domain of VEGFR-1 in the host did not re

171 VEGFR-1 blockade and genetic deletion of the tyrosine kinase domain of VEGFR-1 resulted in enhanced t

172 d mutagenesis deletes the C-terminal SH2 and tyrosine kinase domains of c-fes (referred to as c-fes(D

173 ding mode of this class of inhibitors to the tyrosine kinase domains of c-Src, PDGFr, FGFr, and EGFr

174 ant Phe-527) and in cells with the activated tyrosine kinase domains of the Drosophila insulin recept

175 Structural studies of the extracellular and tyrosine kinase domains of the epidermal growth factor r

176 fused to the transmembrane and intracellular tyrosine kinase domains of the PDGFbetaR.

177 IP1 joined in-frame to the transmembrane and tyrosine kinase domains of the PDGFbetaR.

178 iption factor to the C-terminal PTK (protein-tyrosine kinase) domain of the neurotrophin-3 receptor N

179 Somatic mutations in the EGFR tyrosine kinase domain play a critical role in the devel

180 ernal tandem duplication mutations, 23% FLT3-tyrosine kinase domain point mutations, and 2% both type

181 ed with poorer therapeutic responses and ABL tyrosine kinase domain point mutations.

182 For growth factor receptors with intrinsic tyrosine kinase domains, polyubiquitination is believed

183 ptors with truncations at the distal half of tyrosine kinase domain (residues 809-957) were not effic

184 of the quinazoline interaction with the EGFR tyrosine kinase domain should allow for an analysis of r

185 ceptor has a mutation (Ala-Thr(1134)) in its tyrosine kinase domain that disrupts insulin signaling.

186 Imatinib is an inhibitor of the Abl tyrosine kinase domain that is effective in the treatmen

187 , the Ang II type 1 receptor does not have a tyrosine kinase domain that mediates the cellular signal

188 stal structure of an asymmetric dimer of the tyrosine kinase domain, the JM region of an acceptor mon

189 canonical FGFRs that initiate signaling via tyrosine kinase domains, the short intracellular sequenc

190 y reported Met mutations, which occur in the tyrosine kinase domain, this missense mutation is locate

191 We demonstrated that SSB-1 bound to MET tyrosine kinase domain through its SPRY domain.

192 cations of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rearrangements of MYB w

193 xtamembrane domain or point mutations in the tyrosine kinase domain (TKD) appear to activate FLT3 in

194 ic dimerization mechanism in which a "donor" tyrosine kinase domain (TKD) contacts an "acceptor" TKD,

195 ly 25% and point mutations within the second tyrosine kinase domain (TKD) in approximately 7% of AML

196 The prognostic impact of tyrosine kinase domain (TKD) mutations of the fms-like t

197 rboring somatic, activating mutations in the tyrosine kinase domain (TKD) of the EGFR exhibit signifi

198 type of FLT3 mutation: point mutation in the tyrosine kinase domain (TKD) or internal tandem duplicat

199 tion of the recombinant EGF receptor protein-tyrosine kinase domain (TKD).

200 ve FGFR1, which lacks a major portion of the tyrosine kinase domain (TKD).

201 The fusion of the trk tyrosine kinase domain to a cell adhesion molecule may e

202 /ptc2 is activated through fusion of the Ret tyrosine kinase domain to the dimerization domain of ano

203 dominant negative FGF receptor, lacking the tyrosine kinase domain, together with RNA encoding vario

204 Two sites outside of the tyrosine kinase domain, Tyr(317) in the FERM domain and

205 R gene amplification or mutation of the EGFR tyrosine kinase domain was not altered in the resistant

206 Sequence representing the conserved tyrosine kinase domain was obtained by reverse transcrip

207 ones of the JAK1 and JAK2 genes encoding the tyrosine kinase domain were also isolated and compared w

208 cript encoding a receptor with the catalytic tyrosine kinase domain were expressed.

209 es, respectively, both reside within the ALK tyrosine kinase domain where they dramatically increased

210 mutations, such as D816V, which occur in the tyrosine kinase domain, whereas another involves mutatio

211 FLT3 is a trans-membrane receptor with a tyrosine kinase domain which, when activated, initiates

212 the conformational changes that activate the tyrosine kinase domain, which are normally initiated by

213 a fused BCR-ABL gene that activates the Abl tyrosine kinase domain within Bcr-Abl.

214 Whether the two phosphorylated tyrosine kinase domains within the receptor dimer functi