Abl gene

Jump to navigation Jump to search

WikiDoc Resources for Abl gene


Most recent articles on Abl gene

Most cited articles on Abl gene

Review articles on Abl gene

Articles on Abl gene in N Eng J Med, Lancet, BMJ


Powerpoint slides on Abl gene

Images of Abl gene

Photos of Abl gene

Podcasts & MP3s on Abl gene

Videos on Abl gene

Evidence Based Medicine

Cochrane Collaboration on Abl gene

Bandolier on Abl gene

TRIP on Abl gene

Clinical Trials

Ongoing Trials on Abl gene at Clinical Trials.gov

Trial results on Abl gene

Clinical Trials on Abl gene at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Abl gene

NICE Guidance on Abl gene


FDA on Abl gene

CDC on Abl gene


Books on Abl gene


Abl gene in the news

Be alerted to news on Abl gene

News trends on Abl gene


Blogs on Abl gene


Definitions of Abl gene

Patient Resources / Community

Patient resources on Abl gene

Discussion groups on Abl gene

Patient Handouts on Abl gene

Directions to Hospitals Treating Abl gene

Risk calculators and risk factors for Abl gene

Healthcare Provider Resources

Symptoms of Abl gene

Causes & Risk Factors for Abl gene

Diagnostic studies for Abl gene

Treatment of Abl gene

Continuing Medical Education (CME)

CME Programs on Abl gene


Abl gene en Espanol

Abl gene en Francais


Abl gene in the Marketplace

Patents on Abl gene

Experimental / Informatics

List of terms related to Abl gene

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Abelson murine leukemia viral oncogene homolog 1 also known as ABL1 is a protein that, in humans, is encoded by the ABL1 gene (previous symbol ABL) located on chromosome 9. c-Abl is sometimes used to refer to the version of the gene found within the mammalian genome, while v-Abl refers to the viral gene.


The ABL1 proto-oncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of ABL1 protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. The t(9;22) translocation results in the head-to-tail fusion of the BCR and ABL1 genes, leading to a fusion gene present in many cases of chronic myelogenous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for ABL1. The ABL1 gene is expressed as either a 6- or a 7-kb mRNA transcript, with alternatively spliced first exons spliced to the common exons 2-11.[1]

Clinical significance

ABL1 kinase domain (blue) in complex with the second-generation Bcr-Abl tyrosine-kinase inhibitor nilotinib (red)

Mutations in the ABL1 gene are associated with chronic myelogenous leukemia (CML). In CML, the gene is activated by being translocated within the BCR (breakpoint cluster region) gene on chromosome 22. This new fusion gene, BCR-ABL, encodes an unregulated, cytoplasm-targeted tyrosine kinase that allows the cells to proliferate without being regulated by cytokines. This, in turn, allows the cell to become cancerous.

This gene is a partner in a fusion gene with the BCR gene in the Philadelphia chromosome, a characteristic abnormality in chronic myelogenous leukemia (CML) and rarely in some other leukemia forms. The BCR-ABL transcript encodes a tyrosine kinase, which activates mediators of the cell cycle regulation system, leading to a clonal myeloproliferative disorder. The BCR-ABL protein can be inhibited by various small molecules. One such inhibitor is imatinib mesylate, which occupies the tyrosine kinase domain and inhibits BCR-ABL's influence on the cell cycle. Second generation BCR-ABL tyrosine-kinase inhibitors are also under development to inhibit BCR-ABL mutants resistant to imatinib.

See also


  1. "Entrez Gene: ABL1 v-abl Abelson murine leukemia viral oncogene homolog 1".

External links