Judy L. Meinkoth

TL;DR: It is proposed that PP-1 specifically dephosphorylates CREB at Ser-133 and inhibits cAMP-dependent transcription, and this phosphatase is the major regulator of CREB activity in camp-responsive cells.

TL;DR: It is shown that stable expression of either constitutively active Akt or Bcl-2 inhibits apoptosis, but only B cl-2 prevents the release of cytochrome c from mitochondria, suggesting that Akt regulates apoptosis at a postmitochondrial level.

TL;DR: VPA and VPA analogs induce differentiation in hematopoietic cell lines in a p21-dependent manner, and the order of potency for induction of differentiation parallels the potencies for inhibition in vitro, supporting the argument that differentiation caused by VPA is mediated through inhibition of HDACs.

TL;DR: This study probed cross-talk between cAMP signaling and the phosphatidylinositol 3-kinase/PKB pathways by monitoring the specific roles that Epac and PKA play individually in regulating PKB activity and suggests a complex regulatory scheme in which Epacand PKA mediate the opposing effects of cAMP on PKB regulation.

TL;DR: It is reported that cAMP stimulates proliferation through both protein kinase A (PKA)-dependent and PKA-independent signaling pathways and that phosphatidylinositol 3-kinase (PI3K) is required for cAMP-stimulated mitogenesis.