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          Institute: MPI für molekulare Zellbiologie und Genetik     Collection: MPI-CBG Publications 2013 (arch)     Display Documents



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ID: 688540.0, MPI für molekulare Zellbiologie und Genetik / MPI-CBG Publications 2013 (arch)
Mouse SAMHD1 has antiretroviral activity and suppresses a spontaneous cell-intrinsic antiviral response.
Authors:Behrendt, Raymond; Schumann, Tina; Gerbaulet, Alexander; Nguyen, Laura A; Schubert, Nadja; Alexopoulou, Dimitra; Berka, Ursula; Lienenklaus, Stefan; Peschke, Katrin; Gibbert, Kathrin; Wittmann, Sabine; Lindemann, Dirk; Weiss, Siegfried; Dahl, Andreas; Naumann, Ronald; Dittmer, Ulf; Kim, Baek; Mueller, Werner; Gramberg, Thomas; Roers, Axel
Date of Publication (YYYY-MM-DD):2013
Title of Journal:Cell Reports
Volume:4
Issue / Number:4
Start Page:689
End Page:696
Copyright:not available
Audience:Experts Only
Intended Educational Use:No
Abstract / Description:Aicardi-Goutières syndrome (AGS), a hereditary autoimmune disease, clinically and biochemically overlaps with systemic lupus erythematosus (SLE) and, like SLE, is characterized by spontaneous type I interferon (IFN) production. The finding that defects of intracellular nucleases cause AGS led to the concept that intracellular accumulation of nucleic acids triggers inappropriate production of type I IFN and autoimmunity. AGS can also be caused by defects of SAMHD1, a 3' exonuclease and deoxynucleotide (dNTP) triphosphohydrolase. Human SAMHD1 is an HIV-1 restriction factor that hydrolyzes dNTPs and decreases their concentration below the levels required for retroviral reverse transcription. We show in gene-targeted mice that also mouse SAMHD1 reduces cellular dNTP concentrations and restricts retroviral replication in lymphocytes, macrophages, and dendritic cells. Importantly, the absence of SAMHD1 triggered IFN-β-dependent transcriptional upregulation of type I IFN-inducible genes in various cell types indicative of spontaneous IFN production. SAMHD1-deficient mice may be instrumental for elucidating the mechanisms that trigger pathogenic type I IFN responses in AGS and SLE.
External Publication Status:published
Document Type:Article
Version Comment:Automatic journal name synchronization
Communicated by:Lib
Affiliations:MPI für molekulare Zellbiologie und Genetik
Identifiers:LOCALID:5638
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