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Fig. 3 | Molecular Medicine

Fig. 3

From: Autosomal dominant polycystic kidney disease and pioglitazone for its therapy: a comprehensive review with an emphasis on the molecular pathogenesis and pharmacological aspects

Fig. 3

The mechanism of STAT signaling by Polycystin-1. In autosomal dominant polycystic kidney disease (ADPKD), mutation of the PKD1 can lead to either the reduced or overexpression of polycystin-1. The over-expression of polycystin-1 (membrane-anchored) stimulates the activation of STAT1/3 by its phosphorylation of tyrosine. *Polycystin-1 binds to JAK2 that suggests polycystin-1 mediated regulation of JAK2 is attributable to the STAT1 activation. The other half of the figure is showing another model adopting which polycystin-1 regulates STAT proteins. In the ADPKD state, the 30 kilodalton (kDa) cytoplasmic (C) tail of polycystin-1 is released into the cytoplasm after cleavage and translocate to the nucleus where it interacts with the transcriptional co-activator P100 and STAT6 and co activates the STAT6. The remaining membrane-anchored portion (15 kDa) of polycystin-1 inhibits the STAT6 as it loses the ability to activate STAT6 (Ma et al. 2005)

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