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J Biol Chem. 2010 Dec 31;285(53):41675-85. doi: 10.1074/jbc.M110.179895. Epub 2010 Nov 1.

PDCD10/CCM3 acts downstream of {gamma}-protocadherins to regulate neuronal survival.

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  • 1Department of Molecular Biosciences, Northwestern University, Evanston, Illinois 60208, USA.

Abstract

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.

PMID:
21041308
PMCID:
PMC3009895
DOI:
10.1074/jbc.M110.179895
[PubMed - indexed for MEDLINE]
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