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Deletion of SNAP-23 Results in Pre-Implantation Embryonic Lethality in Mice

  1. Author:
    Suh, Y. H. S. Y. H.
    Yoshimoto-Furusawa, A.
    Weih, K. A.
    Tessarollo, L.
    Roche, K. W.
    Mackem, S.
    Roche, P. A.
  2. Author Address

    [Suh, YH Suh, YH; Weih, KA; Roche, PA] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA [Suh, YH Suh, YH; Roche, KW] NINDS, Receptor Biol Sect, NIH, Bethesda, MD 20892 USA [Suh, YH Suh, YH] Ajou Univ, Sch Med, Dept Pharmacol, Grad Program Neurosci, Suwon 441749, South Korea [Tessarollo, L] NCI, Mouse Canc Genet Program, CCR, NIH, Frederick, MD 21701 USA [Yoshimoto-Furusawa, A; Mackem, S] NCI, Canc & Dev Biol Lab, CCR, NIH, Frederick, MD 21701 USA;Suh, YH (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA;paul.roche@nih.gov
    1. Year: 2011
    2. Date: Mar
  1. Journal: Plos One
    1. 6
    2. 3
    3. Pages: 7
  2. Type of Article: Article
  3. Article Number: e18444
  4. ISSN: 1932-6203
  1. Abstract:

    SNARE-mediated membrane fusion is a pivotal event for a wide-variety of biological processes. SNAP-25, a neuron-specific SNARE protein, has been well-characterized and mouse embryos lacking Snap25 are viable. However, the phenotype of mice lacking SNAP-23, the ubiquitously expressed SNAP-25 homolog, remains unknown. To reveal the importance of SNAP-23 function in mouse development, we generated Snap23-null mice by homologous recombination. We were unable to obtain newborn SNAP-23-deficient mice, and analysis of pre-implantation embryos from Snap23(Delta/wt) matings revealed that Snap23-null blastocysts were dying prior to implantation at embryonic day E3.5. Thus these data reveal a critical role for SNAP-23 during embryogenesis.

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External Sources

  1. DOI: 10.1371/journal.pone.0018444
  2. WOS: 000289054600052

Library Notes

  1. Fiscal Year: FY2010-2011
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