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Article

The SH2-containing adapter protein GRB10 interacts with BCR-ABL.

Oncogene - 27 Aug 1998

Bai R Y, Jahn T, Schrem S, Munzert G, Weidner K M, Wang J Y, Duyster J

Abstract excerpt

Bcr-Abl is an oncogenic tyrosine kinase expressed in tumor cells of CML and a subset of ALL which in its unregulated and activated state is thought to cause cell transformation and leukemia. Bcr-Abl contains several autophosphorylation sites which serve as potential docking sites for SH2-containing signaling molecules. Mutational analysis has indicated that these autophosphorylation sites play a critical role in...

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Source

Identifiers

PMID: 9747873
DOI: 10.1038/sj.onc.1202024

Genes

BCR
GRB10

Provenance

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

Source receipt: pubmed, retrieved 7 Sept 2026.

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Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

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The SH2-containing adapter protein GRB10 interacts with BCR-ABL.PMID 9747873Read ↗

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BCR: a promiscuous fusion partner in hematopoietic disordersSemantic proximity Read ↗

Crk and Abi1: Binary Molecular Switches That Regulate Abl Tyrosine Kinase and Signaling to the CytoskeletonSemantic proximity Read ↗

Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits LeukemogenesisSemantic proximity Read ↗

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Genetic approaches to defining signaling by the CML-associated tyrosine kinase BCR-ABL.Semantic proximity Read ↗

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