Global Phosphoproteomics Reveals Crosstalk Between Bcr-Abl and Negative Feedback Mechanisms Controlling Src Signaling-Reference-Cited by-同舟云学术

Global Phosphoproteomics Reveals Crosstalk Between Bcr-Abl and Negative Feedback Mechanisms Controlling Src Signaling

Published:2011-03-29 Issue:166 Volume:4 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

Rubbi Liudmilla¹²³⁴,Titz Björn¹²³⁴,Brown Lauren¹²³⁴,Galvan Erica¹²³⁴,Komisopoulou Evangelia¹²³⁴,Chen Sharon S.¹²³⁴,Low Tracey¹²³⁴,Tahmasian Martik¹²³⁴,Skaggs Brian⁵,Müschen Markus⁶,Pellegrini Matteo⁷⁸,Graeber Thomas G.¹²³⁴⁸

Affiliation:

1. Crump Institute for Molecular Imaging, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

2. Institute for Molecular Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

3. Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

4. Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

5. Division of Rheumatology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

6. Department of Laboratory Medicine, University of California, San Francisco, CA 94143, USA.

7. Institute for Genomics and Proteomics; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, CA 90095, USA.

8. California NanoSystems Institute, University of California, Los Angeles, CA 90095, USA.

Abstract

Negative feedback fails to limit Src family kinase activity in the presence of Bcr-Abl, an oncoprotein that drives leukemia.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference75 articles.

1. Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia

2. Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice

3. Dasatinib in Imatinib-Resistant Philadelphia Chromosome–Positive Leukemias

4. Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase

5. Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases

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