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AQP2 — PRKAR2A

Text-mined interactions from Literome

Hasler et al., J Am Soc Nephrol 2005 : These results indicate that in collecting duct principal cells : ( 1 ) a short-term increase of extracellular osmolarity decreases AQP2 expression through inhibition of AQP2 gene transcription ; ( 2 ) a long-term increase of extracellular tonicity, but not osmolarity, enhances AQP2 expression via stimulation of AQP2 gene transcription ; and ( 3 ) long-term hypertonicity and PKA increases AQP2 expression through synergistic but independent mechanisms
Li et al., J Am Soc Nephrol 2006 (Diabetes Insipidus, Nephrogenic...) : Surprising, the effect of lithium was cAMP independent ; it did not alter AVP stimulated cAMP production or PKA dependent phosphorylation of AQP2 or cAMP responsive element binding protein
Umenishi et al., Biochim Biophys Acta 2006 : PKA activity was stimulated by AVP but PKA inhibitors did not block the upregulation of AQP2 expression
Bouley et al., J Am Soc Nephrol 2011 : Pharmacologic inhibition of protein kinase A (PKA) and deficiency of a critical PKA phosphorylation site on AQP2 both prevented calcitonin induced membrane accumulation of AQP2