Targeting of the N-terminal coiled coil oligomerization interface by a helix-2 peptide inhibits unmutated and imatinib-resistant BCR/ABL.
about
The Philadelphia chromosome in leukemogenesisEmerging Role of Genomic Rearrangements in Breast Cancer: Applying Knowledge from Other CancersCurrent concepts in pediatric Philadelphia chromosome-positive acute lymphoblastic leukemiaThe effect of the dual Src/Abl kinase inhibitor AZD0530 on Philadelphia positive leukaemia cell linesReciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment.Translocation Biosensors - Cellular System Integrators to Dissect CRM1-Dependent Nuclear Export by Chemicogenomics.The nuclear translocation assay for intracellular protein-protein interactions and its application to the Bcr coiled-coil domainAllosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315IDisruption of Bcr-Abl coiled coil oligomerization by design.A coiled-coil mimetic intercepts BCR-ABL1 dimerization in native and kinase-mutant chronic myeloid leukemiaStructure, regulation, signaling, and targeting of abl kinases in cancer.BCR: a new target in resistance mediated by BCR/ABL-315I?T-cell receptor transfer into human T cells with ecotropic retroviral vectors.Cell-penetrating fusion peptides OD1 and OD2 interact with Bcr-Abl and influence the growth and apoptosis of K562 cells.Oleylamine-carbonyl-valinol inhibits auto-phosphorylation activity of native and T315I mutated Bcr-Abl, and exhibits selectivity towards oncogenic Bcr-Abl in SupB15 ALL cell lines.TAT-CC fusion protein depresses the oncogenicity of BCR-ABL in vitro and in vivo through interrupting its oligomerization.p185(BCR/ABL) has a lower sensitivity than p210(BCR/ABL) to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia.The gatekeeper mutation T315I confers resistance against small molecules by increasing or restoring the ABL-kinase activity accompanied by aberrant transphosphorylation of endogenous BCR, even in loss-of-function mutants of BCR/ABL.Improved coiled-coil design enhances interaction with Bcr-Abl and induces apoptosis.SOCS1 function in BCR-ABL mediated myeloproliferative disease is dependent on the cytokine environment.
P2860
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P2860
Targeting of the N-terminal coiled coil oligomerization interface by a helix-2 peptide inhibits unmutated and imatinib-resistant BCR/ABL.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Targeting of the N-terminal co ...... nd imatinib-resistant BCR/ABL.
@en
Targeting of the N-terminal co ...... nd imatinib-resistant BCR/ABL.
@nl
type
label
Targeting of the N-terminal co ...... nd imatinib-resistant BCR/ABL.
@en
Targeting of the N-terminal co ...... nd imatinib-resistant BCR/ABL.
@nl
prefLabel
Targeting of the N-terminal co ...... nd imatinib-resistant BCR/ABL.
@en
Targeting of the N-terminal co ...... nd imatinib-resistant BCR/ABL.
@nl
P2093
P50
P356
P1476
Targeting of the N-terminal co ...... and imatinib-resistant BCR/ABL
@en
P2093
Alena Hundertmark
Tim Beissert
Velina Kaburova
P304
P356
10.1002/IJC.23467
P577
2008-06-01T00:00:00Z