Pathways - manually collected, often from reviews:
OpenBEL Selventa BEL large corpus:
RPS6KB1
→
PDPK1
(directlyIncreases, PDPK1 Activity, RPS6KB1 Activity)
Sato et al., Oncogene 2002* Evidence: We then examined the change of the kinase activity of p70S6K which was known to be phosphorylated and activated by PDK1 (Vanhaesebroeck and Alessi, 2000).....treatment of the cells with UCN-01 suppressed p70S6K kinase activity in a dose-dependent manner.
OpenBEL Selventa BEL large corpus:
RPS6KB1
→
PDPK1
(directlyIncreases, PDPK1 Activity, RPS6KB1 Activity)
Evidence: Because PDK1 has been shown to phosphorylate p70S6 kinase directly [56], one might have assumed that activation of mTOR was dispensable in some settings of p70S6K activation. That might still be the case; alternatively, it might be that p70S6K must first be primed by another kinase, such as mTOR, before being activated by PDK1 [57,58]
OpenBEL Selventa BEL large corpus:
RPS6KB1
→
PDPK1
(directlyIncreases, PDPK1 Activity, RPS6KB1 Activity)
Vanhaesebroeck et al., Biochem J 2000* Evidence: PDK1 has now been shown to play a central role in activating many of the AGC subfamily members (reviewed in [150,151]). Apart from phosphorylating PKB on Thr308, PDK1 phosphorylates the equivalent residues on PKC isoforms [48,152,153], p70-S6K [32,154], the three isoforms of SGK [27,28,155] and PKA [156] (Figure 6).