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 PMID:27170117  

Megf10 Is a Receptor for C1Q That Mediates Clearance of Apoptotic Cells by Astrocytes.

Tal Iram | Zaida Ramirez-Ortiz | Michael H Byrne | Uwanda A Coleman | Nathan D Kingery | Terry K Means | Dan Frenkel | Joseph El Khoury
The Journal of neuroscience : the official journal of the Society for Neuroscience | 2016

Multiple EGF-like domains 10 (Megf10) is a class F scavenger receptor (SR-F3) expressed on astrocytes and myosatellite cells, and recessive mutations in humans result in early-onset myopathy, areflexia, respiratory distress, and dysphagia (EMARDD). Here we report that Megf10-deficient mice have increased apoptotic cells in the developing cerebellum and have impaired phagocytosis of apoptotic cells by astrocytes ex vivo We also report that cells transfected with Megf10 gain the ability to phagocytose apoptotic neurons and that Megf10 binds with high affinity to C1q, an eat-me signal for apoptotic cells. In contrast, cells expressing Megf10 with EMARDD mutations have impaired apoptotic cell clearance and impaired binding to C1q. Our studies reveal that Megf10 is a receptor for C1q and identify a novel role for Megf10 in clearance of apoptotic cells in the mammalian developing brain with potential relevance to EMARDD patients and other CNS disorders.

Pubmed ID: 27170117

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Associated grants

  • Agency: NIAID NIH HHS, United States
    Id: T32 AI007061
  • Agency: NIAID NIH HHS, United States
    Id: R01 AI084884
  • Agency: NIAID NIH HHS, United States
    Id: U24 AI082660
  • Agency: NIAID NIH HHS, United States
    Id: R01 AI119065
  • Agency: NIAMS NIH HHS, United States
    Id: K01 AR066716

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International Mouse Phenotyping Consortium (IMPC) (tool)

RRID:SCR_006158

Center that produces knockout mice and carries out high-throughput phenotyping of each line in order to determine function of every gene in mouse genome. These mice will be preserved in repositories and made available to scientific community representing valuable resource for basic scientific research as well as generating new models for human diseases.

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