Autoinhibition of Bcr-Abl through its SH3 domain (Q30164601)

9 June 2017

Autoinhibition of Bcr-Abl through its SH3 domain (English)

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9 June 2017

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Kristen M Smith

1

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PubMed ID

12887890

9 June 2017

Rinat Yacobi

series ordinal

2

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PubMed ID

12887890

9 June 2017

Richard A Van Etten

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3

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9 June 2017

1 July 2003

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9 June 2017

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9 June 2017

12

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9 June 2017

27-37

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9 June 2017

1

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A coiled-coil oligomerization domain of Bcr is essential for the transforming function of Bcr-Abl oncoproteins

9 June 2017

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12 December 2020

Activated c-Abl is degraded by the ubiquitin-dependent proteasome pathway

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12 December 2020

Deletion of an N-terminal regulatory domain of the c-abl tyrosine kinase activates its oncogenic potential

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12 December 2020

c-Abl is activated by growth factors and Src family kinases and has a role in the cellular response to PDGF

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12 December 2020

Phosphorylation and structure-based functional studies reveal a positive and a negative role for the activation loop of the c-Abl tyrosine kinase.

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12 December 2020

A myristoyl/phosphotyrosine switch regulates c-Abl

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12 December 2020

c-Abl has high intrinsic tyrosine kinase activity that is stimulated by mutation of the Src homology 3 domain and by autophosphorylation at two distinct regulatory tyrosines

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12 December 2020

The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity

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12 December 2020

A new link between the c-Abl tyrosine kinase and phosphoinositide signalling through PLC-gamma1

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12 December 2020

An intramolecular SH3-domain interaction regulates c-Abl activity

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12 December 2020

Crystal structure of the Src family tyrosine kinase Hck

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12 December 2020

The NH(2)-terminal coiled-coil domain and tyrosine 177 play important roles in induction of a myeloproliferative disease in mice by Bcr-Abl

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12 December 2020

Structural basis for the autoinhibition of c-Abl tyrosine kinase

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12 December 2020

Structural mechanism for STI-571 inhibition of abelson tyrosine kinase

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12 December 2020

Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop

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12 December 2020

SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence

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12 December 2020

In vitro transformation of immature hematopoietic cells by the P210 BCR/ABL oncogene product of the Philadelphia chromosome

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12 December 2020

The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia-like disease by bcr/abl.

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12 December 2020

Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL.

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12 December 2020

Autoinhibition of c-Abl

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12 December 2020

The Abl family kinases: mechanisms of regulation and signaling

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12 December 2020

Crossref

https://api.crossref.org/works/10.1016%2FS1097-2765%2803%2900274-0

7 January 2021

inferred from DOI database lookup

Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia

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12 December 2020

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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12 December 2020

BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner

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12 December 2020

The src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase

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12 December 2020

Cell signaling by receptor tyrosine kinases

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12 December 2020

Evidence for regulation of the human ABL tyrosine kinase by a cellular inhibitor

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12 December 2020

Activation of c-Abl kinase activity and transformation by a chemical inducer of dimerization

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12 December 2020

Amino acid substitutions within the leucine zipper domain of the murine coronavirus spike protein cause defects in oligomerization and the ability to induce cell-to-cell fusion

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12 December 2020

The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity

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12 December 2020

Mutational analysis of the regulatory function of the c-Abl Src homology 3 domain

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12 December 2020

Deletion of the ABL SH3 domain reactivates de-oligomerized BCR-ABL for growth factor independence

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12 December 2020

Studying the pathogenesis of BCR-ABL+ leukemia in mice

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12 December 2020

An actin-binding function contributes to transformation by the Bcr-Abl oncoprotein of Philadelphia chromosome-positive human leukemias

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12 December 2020

Introduction of a loss-of-function point mutation from the SH3 region of the Caenorhabditis elegans sem-5 gene activates the transforming ability of c-abl in vivo and abolishes binding of proline-rich ligands in vitro.

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12 December 2020

Effect of Bcr sequences on the cellular function of the Bcr-Abl oncoprotein.

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12 December 2020

Structure of the Bcr-Abl oncoprotein oligomerization domain

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12 December 2020

The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase

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12 December 2020

Detection of c-abl tyrosine kinase activity in vitro permits direct comparison of normal and altered abl gene products

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12 December 2020

10.1016/S1097-2765(03)00274-0

Identifiers

DOI

1 reference

9 June 2017

0 references

1 reference

PubMed ID

12887890