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Article

The SH2 domain of P210BCR/ABL is not required for the transformation of hematopoietic factor-dependent cells.

Blood - 15 Nov 1995

Ilaria R L, Van Etten R A

Abstract excerpt

Src-homology region 2 (SH2) domains, by binding to tyrosine-phosphorylated sequences, mediate specific protein-protein interactions important in diverse signal transduction pathways. Previous studies have shown that activated forms of the Abl tyrosine kinase, including P210BCR/ABL of human chronic myelogenous leukemia, require the SH2 domain for the transformation of fibroblasts. To determine whether SH2 is also...

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PMID: 7579359

Genes

BCR

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

The SH2 domain of P210BCR/ABL is not required for the transformation of hematopoietic factor-dependent cells.PMID 7579359Read ↗

SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence.Semantic proximity Read ↗

Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene.Semantic proximity Read ↗

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-kinaseSemantic proximity Read ↗

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

Rac2 GTPase deficiency depletes BCR-ABL+ leukemic stem cells and progenitors in vivoSemantic proximity Read ↗

The tetramerization domain-independent Ras activation by BCR-ABL oncoprotein in hematopoietic cells.Semantic proximity Read ↗

Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene.Semantic proximity Read ↗

The CRKL Adaptor Protein Transforms Fibroblasts and Functions in Transformation by the BCR-ABL OncogeneSemantic proximity Read ↗

Src family kinases phosphorylate the Bcr-Abl SH3-SH2 region and modulate Bcr-Abl transforming activity.Semantic proximity Read ↗

The CRISPR/Cas9 system efficiently reverts the tumorigenic ability of BCR/ABL in vitro and in a xenograft model of chronic myeloid leukemia.Semantic proximity Read ↗

Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis.Semantic proximity Read ↗

Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasia.Semantic proximity Read ↗

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