Target intelligence / Profile preview

Src family kinase and Abelson kinase (SFK and ABL)

Target
SFK and ABL
Molecular classification
Enzyme, Tyrosine kinase, Non-receptor tyrosine kinase, Protein kinase
01

Overview

Src family kinases and Abelson kinase (ABL) are non-receptor tyrosine kinases involved in key pathways regulating cellular proliferation, survival, migration, and cytoskeletal dynamics[1][2]. The Src family includes multiple homologous kinases (c-Src, Fyn, Lck, etc.) sharing a similar domain structure and regulatory mechanism[2]. Abelson kinase (c-Abl or ABL1) shares structural similarity with Src kinases, including SH3, SH2, and kinase domains, and additional unique regulatory regions[1]. Both SFK and ABL play vital roles in physiological signal transduction and are deregulated in various diseases, particularly cancers such as leukemia (for ABL fusion Bcr-Abl) and solid tumors (for SFK)[1][2]. Numerous drugs (notably tyrosine kinase inhibitors like imatinib) have been developed to therapeutically target these enzymes.

Other names
Src family kinase: "c-Src"Src kinaseindividual members such as "Fyn""Lck""Yes""Lyn""Hck""Blk""Fgr""Yrk"Abelson kinase: "c-Abl""ABL1""Abelson tyrosine-protein kinase 1""Bcr-Abl" (fusion)
02

Mechanism of action

Inhibition of tyrosine kinase activity; Blockade of ATP binding site; Disruption of downstream signal transduction pathways controlling proliferation and survival

03

Biological functions

Signal transductionCell proliferationCell survivalCytoskeletal reorganizationCell motilityCell cycle regulationApoptosis
04

Disease associations

CancerInflammationLeukemia (notably chronic myeloid leukemia for Bcr-Abl fusion)
05

Safety considerations

Off-target inhibition affecting normal kinasesCytopeniasFluid retentionCardiotoxicity (notably with some ABL inhibitors)Resistance due to kinase domain mutations
06

Interacting drugs

6 more in the full profile.

07

Biomarkers

Bcr-Abl fusion gene (Philadelphia chromosome) for chronic myeloid leukemia and targeted therapy selectionPhosphorylation status of SFK/ABL kinases

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