Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance. - Wikidata - wikimedia - TriplyDB

Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance.

Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance.

http://www.wikidata.org/entity/Q34695008

about

Activation of tyrosine kinases by mutation of the gatekeeper threonine Targeting Bcr–Abl by combining allosteric with ATP-binding-site inhibitors Towards a Molecular Understanding of the Link between Imatinib Resistance and Kinase Conformational Dynamics Abl kinase constructs expressed in bacteria: facilitation of structural and functional studies including segmental labeling by expressed protein ligation Targeting substrate-site in Jak2 kinase prevents emergence of genetic resistance Computational modeling of allosteric communication reveals organizing principles of mutation-induced signaling in ABL and EGFR kinases.Cell treatment and lysis in 96-well filter-bottom plates for screening Bcr-Abl activity and inhibition in whole-cell extracts.In vitro selection of a DNA-templated small-molecule library reveals a class of macrocyclic kinase inhibitors PH006, a novel and selective Src kinase inhibitor, suppresses human breast cancer growth and metastasis in vitro and in vivo.Novel dual Src/Abl inhibitors for hematologic and solid malignancies.An update on dual Src/Abl inhibitors.Src activates Abl to augment Robo1 expression in order to promote tumor cell migration.Energetic dissection of Gleevec's selectivity toward human tyrosine kinases.Mutation-specific control of BCR-ABL T315I positive leukemia with a recombinant yeast-based therapeutic vaccine in a murine model Evaluating the predictivity of virtual screening for ABL kinase inhibitors to hinder drug resistance A method for screening and validation of resistant mutations against kinase inhibitors Targeting invadopodia to block breast cancer metastasis The cancer treatment revolution Vav3 collaborates with p190-BCR-ABL in lymphoid progenitor leukemogenesis, proliferation, and survival.Sustained suppression of Bcr-Abl-driven lymphoid leukemia by microRNA mimics.SRC points the way to biomarkers and chemotherapeutic targets.The Src signaling pathway: a potential target in melanoma and other malignancies.Overcoming AC220 resistance of FLT3-ITD by SAR302503.Molecular drug targets in myeloproliferative neoplasms: mutant ABL1, JAK2, MPL, KIT, PDGFRA, PDGFRB and FGFR1.Nilotinib: optimal therapy for patients with chronic myeloid leukemia and resistance or intolerance to imatinib.BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors Overcoming resistance in chronic myelogenous leukemia.Current treatment options for adult patients with Philadelphia chromosome-positive acute lymphoblastic leukemia.Current status of agents active against the T315I chronic myeloid leukemia phenotype.Molecular dynamics simulations show that conformational selection governs the binding preferences of imatinib for several tyrosine kinases.Extensive analysis of the T315I substitution and detection of additional ABL mutations in progenitors and primitive stem cell compartment in a patient with tyrosine kinase inhibitor-resistant chronic myeloid leukemia.Theoretical Studies on Pyrazolo[3,4-d]pyrimidine Derivatives as Potent Dual c-Src/Abl Inhibitors Using 3D-QSAR and Docking Approaches.Quantitative monitoring by polymerase colony assay of known mutations resistant to ABL kinase inhibitors

P2860

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P2860

Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance.

http://www.wikidata.org/entity/Q34695008

description

2006 nî lūn-bûn

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2006 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2006 թվականի հունիսին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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Proceedings of the National Academy of Sciences of the United States of America

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Activity of dual SRC-ABL inhib ...... e dynamics in drug resistance.

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Bayard Clarkson

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Chester A Metcalf

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Darren R Veach

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David C Dalgarno

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Mohammad Azam

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Raji Sundaramoorthi

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Regine S Bohacek

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Valentina Nardi

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William C Shakespeare

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P2860

EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

A screen to identify drug resistant variants to target-directed anti-cancer agents

Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571)

Structural basis for the autoinhibition of c-Abl tyrosine kinase

Three-dimensional structure of the tyrosine kinase c-Src

Crystal structure of the Src family tyrosine kinase Hck

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia

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7027909

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