Novel Mechanism May Lead to New Targeted Pharmacological Cancer Treatment
Wednesday, March 28, 2012 - 13:30
in Health & Medicine
Inactivation of the retinoblastoma tumor suppressor protein (pRb) by phosphorylation triggers uncontrolled cell proliferation. Accordingly, activation of cyclin-dependent kinase (CDK)/cyclin complexes or downregulation of CDK inhibitors appears as a common event in human cancer. Now, a new study from the Sbarro Health Research Organization shows that Pin1 (protein interacting with NIMA (never in mitosis) A-), a peptidylprolyl isomerase involved in the control of protein phosphorylation, is an essential mediator for inactivation of the pRB.