#=GF ID   Mx_ML
#=GF AC   PF17536.6
#=GF DE   Matrix and Matrix long proteins N-terminal
#=GF AU   El-Gebali S;0000-0003-1378-5495
#=GF SE   PRODOM:PD124289
#=GF GA   25.00 25.00;
#=GF TC   25.10 56.00;
#=GF NC   24.90 19.90;
#=GF BM   hmmbuild HMM.ann SEED.ann
#=GF SM   hmmsearch -E 1000 -Z 75585367 --cpu 4 HMM pfamseq
#=GF TP   Family
#=GF RN   [1]
#=GF RM   19812269
#=GF RT   Thogoto virus ML protein is a potent inhibitor of the interferon
#=GF RT   regulatory factor-7 transcription factor.
#=GF RA   Buettner N, Vogt C, Martinez-Sobrido L, Weber F, Waibler Z,
#=GF RA   Kochs G;
#=GF RL   J Gen Virol. 2010;91:220-227.
#=GF RN   [2]
#=GF RM   27411929
#=GF RT   pH-dependent conformational changes of a Thogoto virus matrix
#=GF RT   protein reveal mechanisms of viral assembly and uncoating.
#=GF RA   Yang M, Feng F, Liu Y, Wang H, Yang Z, Hou W, Liang H;
#=GF RL   J Gen Virol. 2016;97:2149-2156.
#=GF DR   INTERPRO; IPR035212;
#=GF DR   SO; 0100021; polypeptide_conserved_region;
#=GF CC   This entry represents the N-terminal fragment of family members
#=GF CC   such as the Matrix (Mx) and Matrix protein long (ML) proteins.
#=GF CC   They are found in Thogoto virus (THOV), a tick-transmitted
#=GF CC   orthomyxovirus with a genome consisting of six single-stranded
#=GF CC   RNA segments that encode seven structural proteins [1]. Matrix
#=GF CC   proteins of the family Orthomyxoviridae are major structural
#=GF CC   components of the viral capsid, located below the viral lipid
#=GF CC   membrane and provide protection for viral ribonucleoproteins
#=GF CC   (vRNPs) [2]. They serve as a major participant during the
#=GF CC   processes of virus invasion and budding. Furthermore, they play
#=GF CC   specific roles throughout the viral life cycle, usually by
#=GF CC   interacting with other viral components or host cellular
#=GF CC   proteins [2]. ML protein, an extended version of the viral M
#=GF CC   protein, is a viral IFN antagonist. ML is essential for virus
#=GF CC   growth and pathogenesis in an IFN-competent host. In the
#=GF CC   presence of ML the activation and/or action of the interferon
#=GF CC   regulatory factor-3 (IRF-3) is severely affected. This effect
#=GF CC   depends on direct interaction of ML with the transcription
#=GF CC   factor IIB (TFIIB). ML suppresses IRF-7 in a similar manner as
#=GF CC   it suppresses IRF-3. Studies have revealed that ML associates
#=GF CC   with IRF-7 and prevents IRF-7 dimerization and interaction with
#=GF CC   TRAF6 [1]. Structural analysis revealed that N-terminal fragment
#=GF CC   of M protein (MN) undergoes conformational changes that result
#=GF CC   in specific, pH-dependent inter-molecular interactions.
#=GF CC   Comparison of THOV MN and influenza A virus (IAV) MN region,
#=GF CC   showed low sequence identity. However, superimposition of the
#=GF CC   two structures in neutral condition, showed that both matrix
#=GF CC   proteins contain nine helices connected with same topology.
#=GF CC   Since the matrix layer of IAV disassembles in acidic endosome at
#=GF CC   the beginning of infection and repacks in the neutral cytoplasm,
#=GF CC   a change of pH might be a key regulator for the capsid
#=GF CC   assembly/disassembly transition during these processes. Hence,
#=GF CC   pH-dependent conformational transition model was studied in THOV
#=GF CC   MN, where interactions such as hydrogen bonds and hydrophobic
#=GF CC   interactions are suggested to be involved in THOV matrix
#=GF CC   assembly [2].
#=GF SQ   5
#=GS ML_THOGV/3-151          AC Q80A33.1
#=GS A0A0C5IEG2_9ORTO/6-147  AC A0A0C5IEG2.1
#=GS X2CUE6_9ORTO/2-152      AC X2CUE6.1
#=GS M1_THOGV/3-151          AC Q77D96.1
#=GS A0A2Z6BEX1_9ORTO/7-148  AC A0A2Z6BEX1.1
ML_THOGV/3-151                     .....SNLPVRSFSEVCCAEARAAIIQMENNPDETVCNRIWKIHRDLQSSDLTTTVQVMMVYRFISKRVPEGCFAILSGVNTGMYNPRELKRSYVQSLSSGTSCEFLRSLDKLAKNLLAVHVCSDVKMSLNKRQVIDFISGEEDPTLHTAEHLT.............
A0A0C5IEG2_9ORTO/6-147             .aagn------SLDTLCIGRISPHVREMEYCHSDKTCNRIWKTVRDEPTYSTEELLQVALVYKYVTKRAPEAFILISQRLKGGKYDPQNVKKCFKQKDGLREISEYICSLDKEGKMVLSSMLVLSS-QVLNKTVLVELIAG-------------lsgknkcdv....
X2CUE6_9ORTO/2-152                 ..aak---PLLSLSSLCSEDAVHAIAQMENAPEEAICNRIWKMHRDQAHSSPLLLAQLMLCYKFLLHKTPEGATATLARFPTSMYNAKELKKEFLSRNTTVQVCDMVQKLDELGVLVLAVQLCTDVRYSITKPILAEFLSRAK-----------eggglsmdpehla
M1_THOGV/3-151                     .....SNLPVRSFSEVCCAEARAAIIQMENNPDETVCNRIWKIHRDLQSSDLTTTVQVMMVYRFISKRVPEGCFAILSGVNTGMYNPRELKRSYVQSLSSGTSCEFLRSLDKLAKNLLAVHVCSDVKMSLNKRQVIDFISGEEDPTLHTAEHLT.............
A0A2Z6BEX1_9ORTO/7-148             agnsi--------DMICSPRVIPHVREMEQCHSEKTCLRLWKLVRDDNTYSSEELIQVALMYKYVTKRQPESFISLTHKMKQGKYDPPSIKRCFRQQDGLRAISDYIRSLDKEGKMVLACMLIQSSQ-VLNRTVLVELIGGIA-----------gksthdll.....
#=GC seq_cons                      ..su....PlhShSplCsu-ApsAItQMENsP-EslCNRIWKlHRDpsoSSsppLlQVMLVYKFloKRsPEGshAILu+lsTGMYNP+ELKRsFlQpsoosslCEalRSLDKLGKhVLAVpLCoDV+hSLNKslLlEFISGtc............tut.ph......
//