Another piece of the p27Kip1 puzzle

Forskningsoutput: TidskriftsbidragÖversiktsartikel

Abstract

How extracellular signals communicate with the cell cycle is poorly understood. In this issue, two papers (Grimmler et al., 2007; Chu et al., 2007) address this problem by reporting phosphorylation of the cyclin-dependent kinase inhibitor p27Kip1 on a tyrosine residue by nonreceptor tyrosine kinases, which decreases p27 stability. This new mechanism could explain how cells enter the cell cycle from a quiescent state.

Detaljer

Författare
Externa organisationer
  • National Cancer Institute at Frederick
Originalspråkengelska
Sidor (från-till)241-244
TidskriftCell
Volym128
Utgåva nummer2
StatusPublished - 2007 jan 26
PublikationskategoriForskning
Peer review utfördJa
Externt publiceradJa