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1 Abelson (Abl) family tyrosine kinases have been implicat
2 Abelson (Abl) tyrosine kinase is an important cellular e
3 Abelson family kinases (Abls) are key regulators of cell
4 Abelson family kinases (AFKs; Abl1, Abl2) are non-recept
5 Abelson murine leukemia virus (A-MuLV) is an acute trans
6 Abelson murine leukemia virus (Ab-MLV) arose from a reco
7 Abelson murine leukemia virus (Ab-MLV) encodes the v-Abl
8 Abelson murine leukemia virus (Ab-MLV) mutants expressin
9 Abelson murine leukemia virus (Ab-MLV) transforms NIH 3T
10 Abelson murine leukemia virus encodes the related oncoge
11 Abelson murine leukemia virus transforms pre-B cells in
12 Abelson murine leukemia virus, which encodes v-Abl/p160,
13 Abelson murine leukemia virus-transformed cell lines hav
14 Abelson non-receptor tyrosine kinases are also found in
15 Abelson tyrosine kinase may also help regulate myosin II
16 Abelson-transformed pre-B cell lines derived from these
18 ally, forces applied to E-cadherin activated Abelson (Abl) tyrosine kinase to phosphorylate vinculin;
20 cipitation analyses of bone marrow cells and Abelson murine leukemia virus-transformed pre-B cell lin
21 ELISA) using less than 5 muL of sample, and Abelson tyrosine kinase activity was detectable in sampl
22 e analyzed the solution conformations of apo Abelson tyrosine kinase (c-Abl) and c-Abl complexes with
24 c arena (eg, breakpoint cluster region [BCR]/Abelson [ABL] kinase inhibitors in chronic myeloblastic
26 The v-Abl protein tyrosine kinase encoded by Abelson murine leukemia virus (Ab-MLV) induces pre-B-cel
28 The v-Abl protein tyrosine kinase encoded by Abelson murine leukemia virus (Ab-MLV) induces transform
30 re-B cell transformation process mediated by Abelson murine leukemia virus (Ab-MLV), we examined the
36 of the nonreceptor tyrosine kinase cellular Abelson (c-Abl), and c-Abl inhibitors, including imatini
37 y, we investigated the roles of the cellular Abelson tyrosine kinase (c-Abl) and the related protein
38 9ARF was previously shown to be required for Abelson murine leukemia virus transformation of primary
40 e most common breakpoint cluster region gene-Abelson murine leukemia viral oncogene homolog 1 (BCR-AB
41 in, the Src homology 3 (SH3) domain of human Abelson tyrosine kinase (Abl), was fused to green fluore
44 ronavirus replication in which we identified Abelson (Abl) kinase inhibitors, including the anticance
48 found Ikaros localized to heterochromatin in Abelson-transformed pre-B lymphocytes by using immunogol
49 e Tp53 tumor suppressor gene plays a role in Abelson virus transformation, conformation-specific mono
54 at the conserved nonreceptor tyrosine kinase Abelson (Abl) contributes to rapid embryonic wound closu
55 ctivation of the nonreceptor tyrosine kinase Abelson (Abl) contributes to the development of leukemia
57 t to a possible role for the tyrosine kinase Abelson in cell-cell adhesive junctions in both the CNS
58 edicted that the nonreceptor tyrosine kinase Abelson murine leukemia viral oncogene (c-Abl) is a puta
59 gene encoding the Drosophila tyrosine kinase Abelson substantially enhanced the severity of the CNS p
60 he small GTPase RAB5 and the tyrosine kinase Abelson tyrosine-protein kinase (ABL), to modulate endoc
62 Frazzled (Fra), and the signaling molecules Abelson tyrosine kinase (Abl), the guanine nucleotide-ex
67 by genetic and pharmacological inhibition of Abelson kinase (Abl) both in Dscam-overexpressing neuron
68 The absence of p53 shortens the latency of Abelson disease induction but does not affect the freque
69 nsformed by temperature-sensitive mutants of Abelson murine leukemia virus and PCR was used to identi
70 nsformed by temperature-sensitive mutants of Abelson virus that undergo kappa and lambda gene rearran
71 ansforming activity of the v-Abl oncogene of Abelson murine leukemia virus (A-MuLV) in immortal cell
72 ine kinase, encoded by the v-Abl oncogene of Abelson murine leukemia virus induces transformation of
75 ay central roles in the multistep process of Abelson murine leukemia virus (Ab-MLV) transformation.
76 s to the oncogenic Gag-Abl fusion protein of Abelson Murine Leukaemia Virus and found that in contras
77 ligated subdomains of the SH(32) segment of Abelson kinase in solution, using the orientational depe
78 mology type 3 and 2 domains (SH3 and SH2) of Abelson protein tyrosine kinase, which constitute the re
79 inhibition by imatinib and gene silencing of Abelson (Abl) tyrosine kinase reduced the lysosomal pH i
82 (CML) patients, a breakpoint cluster region-Abelson (BCR-ABL1) value >10% at 3 months of therapy is
83 o therapy with the breakpoint cluster region-Abelson murine leukemia (BCR/ABL) kinase inhibitor imati
84 to engraftment of breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-AB
87 rom the oncogenic break point cluster region/Abelson murine leukemia viral oncogene homolog 1 translo
88 opment of BCR-ABL (breakpoint cluster region/Abelson oncogene) tyrosine kinase domain mutations that
89 uence length polymorphism analysis to screen Abelson virus-transformed pre-B cells for evidence of LO
93 s transformed with the temperature-sensitive Abelson-murine leukemia virus, we show that large quanti
94 ALL) is associated with activated JAK/STAT, Abelson kinase (ABL), and/or phosphatidylinositol 3-kina
96 specifically identified the imatinib target, Abelson tyrosine-protein kinase 2 (Abl2), as required fo
110 cooperative interactions between Eya and the Abelson (Abl) tyrosine kinase during development of the
112 ein CT10 regulator of kinase (CrkII) and the Abelson-interacting protein Abi1, a component of the WAV
113 ene occurs during the generation of both the Abelson murine leukemia virus and the bcrabl fusion gene
114 The v-Abl tyrosine kinase encoded by the Abelson murine leukemia virus (A-MuLV) can either stimul
115 ncoprotein, a tyrosine kinase encoded by the Abelson murine leukemia virus, is a multi-step process r
116 ortant in the cellular events induced by the Abelson murine leukemia virus, the effects of IL-4 and I
120 show a previously unappreciated role for the Abelson (Abl) family kinases (Abl and Arg) in endothelia
122 nant genetic suppressors of mutations in the Abelson tyrosine kinase (Abl), suggesting that Ena and A
123 as a genetic suppressor of mutations in the Abelson tyrosine kinase and subsequently was shown to be
124 inant genetic suppressor of mutations in the Abelson tyrosine kinase and, more recently, as a member
126 all molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor
130 which represent the mammalian members of the Abelson family of nonreceptor protein tyrosine kinases (
131 c-Abl represent the mammalian member of the Abelson family of nonreceptor protein tyrosine kinases.
132 c-Abl represent the mammalian members of the Abelson family of nonreceptor protein-tyrosine kinases.
133 rg is a ubiquitously expressed member of the Abelson family of nonreceptor protein-tyrosine kinases.
135 he effects of the combined inhibition of the Abelson kinase (c-Abl) and platelet-derived growth facto
136 id cells, introduction and expression of the Abelson leukemia virus causes growth factor independence
138 of apoptosis is an important feature of the Abelson murine leukemia virus (Ab-MLV) transformation pr
139 used to prepare NMR sample quantities of the Abelson protein tyrosine kinase-SH(32) domain pair, in w
141 Two novel dosage-sensitive modifiers of the Abelson tyrosine kinase (Abl) mutant phenotype have been
143 that the N-terminal cap (NCap) region of the Abelson tyrosine kinase (c-Abl) is important for maintai
144 es of model protein-peptide complexes of the Abelson tyrosine kinase SH3 domain (abl-SH3) and the S-P
147 s study, we show for the first time that the Abelson (Abl) kinases regulate proximal signaling downst
148 nt genetic and biochemical evidence that the Abelson (Abl) tyrosine kinase and its substrate Enabled
150 2(dok) bind through their PTB domains to the Abelson tyrosine kinase in a kinase-dependent manner in
152 covered as the proto-oncogene from which the Abelson leukemia virus derived its Gag-v-Abl oncogene, r
158 blished lambda5(-/-)/VpreB1(-/-)/VpreB2(-/-) Abelson virus-transformed cell lines and reconstituted t
159 rovide insights into the mechanisms by which Abelson non-receptor tyrosine kinases relay information
160 in bone marrow B cells after infection with Abelson murine leukemia retrovirus (Ab-MLV), and in huma
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