Reactome: A Curated Pathway Database

PKA phosphorylates GLI1

Stable Identifier
Homo sapiens
Locations in the PathwayBrowser

Although direct phosphorylation of GLI1 by PKA has not been demonstrated, deletion of the putative PKA sites abrogates the interaction of GLI1 with beta-TrCP and stabilizes GLI1 protein levels; similarly, treatment of GLI1-expressing cells with PKA inhibitors delays the kinetics of GLI1 degradation (Huntzicker et al, 2006). These data are consistent with a role for PKA-mediated phosphorylation in promoting the proteasome-dependent degradation of GLI1 in the absence of Hh signal, as is the case for GLI2 and GLI3 (Huntzicker et al, 2006; Tempe et al, 2006; Pan and Wang, 2007; Pan et al, 2009). Potential roles for CK2 and GSK3 in promoting the phosphorylation-dependent degradation of GLI1 have not been investigated.

Literature References
Participant Of
This entity is regulated by:
Title Physical Entity Activity
cAMP-dependent protein kinase activity of PKA catalytic subunit [ciliary base] PKA catalytic subunit [ciliary base] cAMP-dependent protein kinase activity (0004691)
Inferred From