cAMP dissociates PKA, promoting GLI processing

Stable Identifier
Reaction [binding]
Homo sapiens
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cAMP is a known regulator of PKA activity and works by binding to the regulatory subunits and promoting dissociation of the tetramer, freeing the active catalytic subunits (reviewed in Sassone-Corsi, 2012). In the Hh pathway in the absence of ligand, cAMP levels increase in response to the recruitment of GPR161 to the ciliary base by TULP3 and the IFT-A retrograde complex (Mukhopadhyay et al, 2010; Mukhopadhyay et al, 2013). Activated PKA then initiates the phosphorylation cascade that regulates processing and/or degradation of the GLI proteins (reviewed in Briscoe and Therond, 2013; Mukhopadhyay and Rohatgi, 2014).

Literature References
PubMed ID Title Journal Year
23209152 The cyclic AMP pathway

Sassone-Corsi, P

Cold Spring Harb Perspect Biol 2012
23332756 The ciliary G-protein-coupled receptor Gpr161 negatively regulates the Sonic hedgehog pathway via cAMP signaling

Scales, SJ, Wen, X, Rangell, L, Jackson, PK, Loktev, A, Mukhopadhyay, S, Ratti, N

Cell 2013
20889716 TULP3 bridges the IFT-A complex and membrane phosphoinositides to promote trafficking of G protein-coupled receptors into primary cilia

Lane, WS, Scales, SJ, Wen, X, Chih, B, Jackson, PK, Nelson, CD, Mukhopadhyay, S

Genes Dev. 2010
24845016 G-protein-coupled receptors, Hedgehog signaling and primary cilia

Rohatgi, R, Mukhopadhyay, S

Semin. Cell Dev. Biol. 2014
Orthologous Events
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