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Article

Hyperphosphorylation of polycystin-2 at a critical residue in disease reveals an essential role for polycystin-1-regulated dephosphorylation.

Human molecular genetics - 15 May 2013

Streets Andrew J, Wessely Oliver, Peters Dorien J M, Ong Albert C M

Abstract excerpt

Mutations in PKD1 (85%) or PKD2 (15%) account for almost all cases of autosomal dominant polycystic kidney disease (ADPKD). The ADPKD proteins, termed as polycystin-1 (PC1) and polycystin-2 (PC2), interact via their C-termini to form a receptor-ion channel complex whose function and regulation are not fully understood. Here, we report the first phosphorylated residue (Ser(829)) in PC2, whose dephosphorylation is...

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Source

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Identifiers

PMID: 23390129
DOI: 10.1093/hmg/ddt031
PMCID: PMC3633370

Genes

PKD1
PKD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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