GenomeNet

Database: Pfam
Entry: bCoV_NS6
LinkDB: bCoV_NS6
Original site: bCoV_NS6 
#=GF ID   bCoV_NS6
#=GF AC   PF12133.12
#=GF DE   Betacoronavirus NS6 protein
#=GF PI   Sars6; Corona_NS6;
#=GF AU   Assefa S;0000-0003-2178-533X
#=GF AU   Bateman A;0000-0002-6982-4660
#=GF AU   Coggill P;0000-0001-5731-1588
#=GF AU   Chuguransky S;0000-0002-0520-0736
#=GF SE   PfamB-2188 (release 23.0)
#=GF GA   27.00 27.00;
#=GF TC   108.40 108.30;
#=GF NC   20.70 18.90;
#=GF BM   hmmbuild HMM.ann SEED.ann
#=GF SM   hmmsearch --cpu 4 -E 1000 -Z 75585367 HMM pfamseq
#=GF TP   Family
#=GF RN   [1]
#=GF RM   17108045
#=GF RT   Severe acute respiratory syndrome coronavirus protein 6
#=GF RT   accelerates murine coronavirus infections.
#=GF RA   Tangudu C, Olivares H, Netland J, Perlman S, Gallagher T;
#=GF RL   J Virol. 2007;81:1220-1229.
#=GF RN   [2]
#=GF RM   16310783
#=GF RT   The putative protein 6 of the severe acute respiratory
#=GF RT   syndrome-associated coronavirus: expression and functional
#=GF RT   characterization.
#=GF RA   Geng H, Liu YM, Chan WS, Lo AW, Au DM, Waye MM, Ho YY;
#=GF RL   FEBS Lett. 2005;579:6763-6768.
#=GF RN   [3]
#=GF RM   25907116
#=GF RT   Severe acute respiratory syndrome coronavirus protein 6 mediates
#=GF RT   ubiquitin-dependent proteosomal degradation of N-Myc (and STAT)
#=GF RT   interactor.
#=GF RA   Cheng W, Chen S, Li R, Chen Y, Wang M, Guo D;
#=GF RL   Virol Sin. 2015;30:153-161.
#=GF DR   INTERPRO; IPR022736;
#=GF DR   SO; 0100021; polypeptide_conserved_region;
#=GF CC   This entry represents non-structural protein NS6 (also known as
#=GF CC   non-structural protein 6, accessory protein 6, or X3 protein),
#=GF CC   which is highly conserved among SARS-related coronaviruses [2].
#=GF CC   (This is distinct from NSP6 which is encoded on the replicase
#=GF CC   polyprotein). Proteins in this family are typically between 42
#=GF CC   to 63 amino acids in length. NS6 is located in the endoplasmic
#=GF CC   reticulum [2]. It has been reported that NS6 can increase the
#=GF CC   cellular gene synthesis and it can also induce apoptosis through
#=GF CC   Jun N-terminal kinase and Caspase-3 mediated stress. This
#=GF CC   protein can modulate host antiviral responses by inhibiting
#=GF CC   synthesis and signalling of IFN-beta, via NS6 interaction with
#=GF CC   host N-Myc (and STAT) interactor (Nmi) protein and suppressing
#=GF CC   the translocation of signal transducer and activator of
#=GF CC   transcription 1 (STAT1) [3].
#=GF SQ   4
#=GS NS6_SARS/1-62         AC P59634.1
#=GS A0A0K1Z0N6_SARS/1-62  AC A0A0K1Z0N6.1
#=GS NS6_SARS2/1-61        AC P0DTC6.1
#=GS Q0Q480_SARS/1-62      AC Q0Q480.1
NS6_SARS/1-62                    MFHLVDFQVTIAEILIIIMRTFRIAIWNLDVIISSIVRQLFKPLTKKNYSELDDEEPMELDY
A0A0K1Z0N6_SARS/1-62             MFHLVDFQVTIAEILVIIMRTFRIAIWNLDMITSSIVTQLFKPLTKKKYSELDDEVPMEIDY
NS6_SARS2/1-61                   MFHLVDFQVTIAEILLIIMRTFKVSIWNLDYIINLIIKNLSKSLTENKYSQLDEEQPMEID-
Q0Q480_SARS/1-62                 MFHLVDFQVTIAEILIIIMRTFRIAIWNLDVLISSIVRQLFKPLTKKKYPQLDDEEPMELDY
#=GC seq_cons                    MFHLVDFQVTIAEILlIIMRTFRIAIWNLDhIISSIV+QLFKPLTKKKYSpLDDEpPMElDY
//
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