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

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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...

Topics

Amino Acid Sequence
Animals
Cell Transformation, Neoplastic
Culture Media, Conditioned
Fusion Proteins, bcr-abl
Hematopoietic Cell Growth Factors
Hematopoietic Stem Cells
Humans
Mice
Mice, Inbred BALB C
Mice, Nude

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Molecular Sequence Data

Mutagenesis, Site-Directed

Phenotype

Phosphorylation

Point Mutation

Protein Processing, Post-Translational

Recombinant Fusion Proteins

Source

Open in PubMed

Identifiers

PMID: 7579359

Genes

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7579359-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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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 ↗

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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 ↗

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

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