SandboxPKA
From Proteopedia
| Line 2: | Line 2: | ||
<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 ( | + | |
| + | 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''' == | ||
Revision as of 21:49, 4 December 2012
Introduction
|
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
kjnkjkj
| |||||||||||
Catalytic domain
It is responsible of both, ATP binding as well as protein binding.
| |||||||||||
