SandboxPKA: Difference between revisions
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<Structure load='1opl' size='400' frame='true' align='right' caption='ABL1 homo-dimer complex' scene='SandboxPKA/Abl1_homo-dimer_complex/1'' /> | <Structure load='1opl' size='400' frame='true' align='right' caption='ABL1 homo-dimer complex' scene='SandboxPKA/Abl1_homo-dimer_complex/1'' /> | ||
The c-Abl protein 1 (ABL1), also known as Abelson kinase, is a non-receptor tyrosine kinase that plays a role in many key processes linked to cell growth and survival. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. In more than 90% cases, chronic myelogeneous leukemia (CML) is caused by chromosomal abnormality resulting in the formation of a so-called Philadelphia chromosome. It is caused by (9 | |||
The c-Abl protein 1 (ABL1), also known as Abelson kinase, is a non-receptor tyrosine kinase that plays a role in many key processes linked to cell growth and survival. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. In more than 90% cases, chronic myelogeneous leukemia (CML) is caused by chromosomal abnormality resulting in the formation of a so-called Philadelphia chromosome. It is caused by fusion between Abelson (Abl) tyrosine kinase gene at chromosome 9 and break point cluster (Bcr) gene at chromosome 22, resulting in the chimeric oncogene Bcr-Abl and a constitutively active Bcr-Abl tyrosine kinase. | |||
== '''Structure''' == | == '''Structure''' == | ||