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Department of Pediatrics
University of Iowa, Ph.D.
Apoptosis, Retinoblastoma, E2F, PI3K, Cancer
The Hallstrom laboratory is studying the cellular mechanisms
controlling Rb/E2F induced apoptosis during normal proliferation
and in cancer development. Rb regulation of cell cycle progression
and tumorigenesis is dependent on its control of E2F transcription
factor function, a family of proteins that control expression
of genes required for proliferation. E2F1, in particular,
forms a link between the deregulation of Rb pathway activity
and induction of p53-dependent apoptosis. E2F1 apoptosis induction
is believed to serve a tumor-suppressive mechanism by eliminating
cells that have sustained an oncogenic mutation which activates
the Rb pathway.
We are studying several mechanisms that regulate E2F1’s capacity to induce proliferation or apoptosis. One mode of regulation is the binding of Jab1/CSN5, which promotes E2F1 induction of apoptosis but not proliferation. Second, PI3K activation during normal growth stimulation inhibits expression of a subset of E2F1 apoptotic target genes.