Increasing levels of cdk-6 led that molecule and other key (or critical) cell cycle proteins to move into the nucleus to foster replication, but in the quiescent or non-replicating cell, the only ones that remained in the nucleus were inhibitors of replication. Understanding how and why those inhibiting proteins block replication could in turn lead to ways to block their activity, providing a novel approach for reviving beta cell regeneration, Dr. Fiaschi-Taesch said.
Dr. Stewart noted that the relocation of cell cycle proteins outside the nucleus in the beta cell might hold true for other kinds of cells.
"It makes me curious about whether we can turn replication back on in other cells that aren't known to regenerate, such as neurons," he said. "I'd also like to know why these proteins continue to be produced by the quiescent cell if they aren't playing a role in cell replication."
In the second Diabetes paper, the team described the intracellular localization of all the cell cycle proteins in the beta cell, a biochemical atlas that could guide other researchers.
|Contact: Anita Srikameswaran|
University of Pittsburgh Schools of the Health Sciences