PDCD10/CCM3 acts downstream of γ-Protocadherins to regulate neuronal survival

Chengyi Lin, Shuxia Meng, Tina Zhu, Xiaozhong Wang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


γ-Protocadherins (PCDH-γ) regulate neuronal survival in the vertebrate central nervous system. The molecular mechanisms of how PCDH-γ mediates this function are still not understood. In this study, we show that through their common cytoplasmic domain, different PCDH-γ isoforms interact with an intracellular adaptor protein named PDCD10 (programmed cell death 10). PDCD10 is also known as CCM3, a causative genetic defect for cerebral cavernous malformations in humans. Using RNAi-mediated knockdown, we demonstrate that PDCD10 is required for the occurrence of apoptosis upon PCDH-γ depletion in developing chicken spinal neurons. Moreover, overexpression of PDCD10 is sufficient to induce neuronal apoptosis. Taken together, our data reveal a novel function for PDCD10/CCM3, acting as a critical regulator of neuronal survival during development.

Original languageEnglish (US)
Pages (from-to)41675-41685
Number of pages11
JournalJournal of Biological Chemistry
Issue number53
StatePublished - Dec 31 2010

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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