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EGF — PKD1
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
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