Abstract
Progression through the cell cycle is mediated
by the sequential activation of a number
of cyclins that form active kinase complexes
when bound to one of several
cyclin-dependent kinases (CDKs). In GI,
these kinases phosphorylate, amongst
others, the retinoblastoma protein, which,
when phosphorylated, releases the E2F
transcription factor, which, in turn, drives
cells into S phase. CDKs can be
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