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Article

Phosphorylation of tyrosine 393 in the kinase domain of Bcr-Abl influences the sensitivity towards imatinib in vivo.

Leukemia - 1 Sept 2003

Miething C, Mugler C, Grundler R, Hoepfl J, Bai R-Y, Peschel C, Duyster J

Abstract excerpt

The Bcr-Abl fusion protein arising through the t(9;22)(q34;q11) reciprocal translocation is the causative agent in chronic myeloid leukemia and a subset of acute lymphocytic leukemia. Imatinib mesylate is a specific inhibitor of the Bcr-Abl kinase and has shown promising results in clinical studies. The structural relation between the Bcr-Abl oncogene and the tyrosine kinase inhibitor imatinib has recently been...

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Source

Identifiers

PMID: 12970766
DOI: 10.1038/sj.leu.2403040

Genes

F3

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.

Related research

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

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Phosphorylation of tyrosine 393 in the kinase domain of Bcr-Abl influences the sensitivity towards imatinib in vivo.PMID 12970766Read ↗

Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinibSemantic proximity Read ↗

Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.Semantic proximity Read ↗

The BCR-ABL Story: Bench to Bedside and BackSemantic proximity Read ↗

SGX393 inhibits the CML mutant Bcr-Abl T315I and preempts in vitro resistance when combined with nilotinib or dasatinibSemantic proximity Read ↗

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

The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase.Semantic proximity Read ↗

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

Crystal Structure of the T315I Abl Mutant in Complex with the Aurora Kinases Inhibitor PHA-739358Semantic proximity Read ↗

The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib.Semantic proximity Read ↗

The gatekeeper mutation T315I confers resistance against small molecules by increasing or restoring the ABL-kinase activity accompanied by aberrant transphosphorylation of endogenous BCR, even in loss-of-function mutants of BCR/ABL.Semantic proximity Read ↗

Involvement of Jak2 tyrosine phosphorylation in Bcr-Abl transformation.Semantic proximity Read ↗

In vivo antiproliferative effect of NS-187, a dual Bcr-Abl/Lyn tyrosine kinase inhibitor, on leukemic cells harbouring Abl kinase domain mutations.Semantic proximity Read ↗

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