לוח שנה משולב

Our group studies the consequences of ribosomal protein deficiencies in mammals. Initially, we demonstrated that inducible deletion of the ribosomal protein S6 gene in the liver of adult mice inhibits the synthesis of the 40S ribosomal subunit as well as proliferation of liver cells following partial hepatectomy, despite seemingly unaffected protein synthesis. These observations suggested the existence of a novel checkpoint, downstream of the deficiency in ribosome biogenesis. We and several other research groups have recently provided convincing evidence for the existence of this checkpoint and demonstrated that the p53 tumor suppressor is its critical component. Our research interests focus on understanding the molecular basis of this checkpoint response and determining its role in pathogenesis of various diseases, including developmental abnormalities and cancer.