Two-factor dependent cell cycle kinase CDK6 kinase CDK4 and is widely considered to have almost the same function, so when a problem occurs in which a kinase, another kinase kinases can make problems. Recently, Veterinary Medicine Universitys new work challenges this view, the new work suggests that, with different CDK4, CDK6 also has the role of promoting blood vessel growth.
In human cancers often appear one or more protein is highly expressed in cancers such as lymphoma often found cell cycle-dependent kinase CDK6 factor overdose. Now shown, CDK6 is a multi-protein complex part of the complex of promoting INK4 family members (p16INK4a gene) production, thereby inhibiting tumor growth. In other words, the cells have a built-in mechanism to help themselves cope with excess CDK6.
When p16INK4a missing, often lead to lymphoma or leukemia. The high level of flood CDK6 may directly stimulate cell division. Scientists find another complex protein kinase CDK6 contain also another factor that can contribute to vascular endothelial growth factor-A generation, which increases the growth of blood vessels in the growth process to ensure that the tumor can be obtained in sufficient energy and oxygen.
Vetmeduni scientists have proved that when it lacks its kinase activity when, CDK6 can still play it on the p16INK4a gene regulation and the effects of VEGF-A, that CDK6 protein kinase mutations, its functional inactivation still retains the form of regulation and p16INK4a VEGF-A gene expression ability.
Because so many CDK6 type of cancer involved, CDK6 is a potential target for the fight against cancer, many laboratories are trying to design specific inhibitors. However, their efforts are focused on inhibiting CDK6 kinase function. New research has shown that now, CDK6 has an additional, non-dependent kinase mode of action to increase the production of blood vessels. Therefore, if they are to be effective in the treatment of cancer, the latter design of CDK6 inhibitor will need to stop kinase CDK6.
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