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EGF — PKD2

Text-mined interactions from Literome

Hurd et al., Biochem Biophys Res Commun 2001 : Induced expression of constitutively active, but not kinase dead PKD , suppressed EGF stimulated c-Jun phosphorylation at Ser 63, demonstrating that activated PKD is sufficient to suppress c-Jun phosphorylation
Ma et al., Mol Cell Biol 2005 : Pharmacological experiments indicate that the EGF induced activation of PKD2 occurs independently of store depletion but requires the activity of phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K)
Gattone et al., Am J Kidney Dis 1991 (Polycystic Kidney Diseases) : Murine infantile polycystic kidney disease : a role for reduced renal epidermal growth factor
Lakshmanan et al., Biochem Biophys Res Commun 1993 (Disease Models, Animal...) : Since normal siblings do not acquire renal cystic disease despite expressing the variant 154 kDa EGF-prohormone while the affected littermates, which lack the normal 165 kDa EGF-prohormone, manifest renal cystic disease, we suggest that congenital polycystic kidney disease is due to an inborn defect in the synthesis and secretion of the normal 165 kDa renal EGF-prohormone