Abl gene

Abl gene

The abl gene is associated with chronic myelogenous leukemia (CML). The abl gene is located on the 9th chromosome. In CML, the gene is activated by being translocated within the bcr (breakpoint cluster region) gene on chromosome 22. This new abl/bcr (chimeric) gene encodes an unregulated, cytoplasm targeted tyrosine kinase which allows the cells to proliferate without being regulated by cytokines. This in turn allows the cell to become cancerous.

PBB_Summary
section_title =
summary_text = The ABL1 protooncogene 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 c-Abl 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 (MIM:151410) and ABL1 genes present in many cases of chronic myelogeneous 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 7-kb mRNA transcript, with alternatively spliced first exons spliced to the common exons 2-11. [cite web | title = Entrez Gene: ABL1 v-abl Abelson murine leukemia viral oncogene homolog 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=25| accessdate = ]

This gene is fused with the "bcr" gene in a Philadelphia chromosome, the characteristic abnormality in chronic myelogenous leukemia (CML) and rarely in some other leukemia forms. The "bcr-abl" transcript is also 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 with the agent imatinib mesylate, which occupies the "TK" domain and inhibits "bcr-abl"s influence on the cell cycle.

References

Further reading

* Clark, Stevens. "Publications." Research Papers 1986-1989.
* Dunitz, Martin. "Chronic Myeloid Leukaemia" 2001. Taylor & Francis, Limited. Published online via Ebrary.com
* Scott K Shore, Ramana V Tantravahi and E Premkumar Reddy. "Transforming pathways activated by the v-Abl tyrosine kinase" 9 Dec. 2002. PBB_Further_reading
citations =
*cite journal | author=Shaul Y |title=c-Abl: activation and nuclear targets. |journal=Cell Death Differ. |volume=7 |issue= 1 |pages= 10–6 |year= 2000 |pmid= 10713716 |doi= 10.1038/sj.cdd.4400626
*cite journal | author=Era T |title=Bcr-Abl is a "molecular switch" for the decision for growth and differentiation in hematopoietic stem cells. |journal=Int. J. Hematol. |volume=76 |issue= 1 |pages= 35–43 |year= 2002 |pmid= 12138893 |doi=
*cite journal | author=Pendergast AM |title=The Abl family kinases: mechanisms of regulation and signaling. |journal=Adv. Cancer Res. |volume=85 |issue= |pages= 51–100 |year= 2003 |pmid= 12374288 |doi=
*cite journal | author=Keung YK, Beaty M, Steward W, "et al." |title=Chronic myelocytic leukemia with eosinophilia, t(9;12)(q34;p13), and ETV6-ABL gene rearrangement: case report and review of the literature. |journal=Cancer Genet. Cytogenet. |volume=138 |issue= 2 |pages= 139–42 |year= 2003 |pmid= 12505259 |doi=
*cite journal | author=Saglio G, Cilloni D |title=Abl: the prototype of oncogenic fusion proteins. |journal=Cell. Mol. Life Sci. |volume=61 |issue= 23 |pages= 2897–911 |year= 2005 |pmid= 15583852 |doi= 10.1007/s00018-004-4271-0
*cite journal | author=Shaul Y, Ben-Yehoyada M |title=Role of c-Abl in the DNA damage stress response. |journal=Cell Res. |volume=15 |issue= 1 |pages= 33–5 |year= 2005 |pmid= 15686624 |doi= 10.1038/sj.cr.7290261
*cite journal | author=Yoshida K |title=Regulation for nuclear targeting of the Abl tyrosine kinase in response to DNA damage. |journal=Adv. Exp. Med. Biol. |volume=604 |issue= |pages= 155–65 |year= 2007 |pmid= 17695727 |doi=

ee also

* BCR gene

External links

*
* (ABL)
*

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