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About:
HLA-DMB restricts human T-cell leukemia virus type-1 (HTLV-1) protein expression via regulation of ATG7 acetylation
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research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
title
HLA-DMB restricts human T-cell leukemia virus type-1 (HTLV-1) protein expression via regulation of ATG7 acetylation
Creator
Wang, Hui
Yang, Bo
Wang, Jie
Liu, Lu
Gao, Zhitao
Guo, Zhixiang
Liu, Yanzi
Lu, Guangjian
Ma, Lingling
Song, Di
Yang, Shuai
Zhang, Chenguang
source
PMC
abstract
The roles of autophagy in viral infection are complicated. While autophagy has been shown to function in host antiviral defense by eliminating intracellular viruses and regulating adaptive immunity, several viruses have evolved molecular mechanisms to get benefits from it. The deltaretrovirus human T-cell leukemia virus type-1 (HTLV-1) has been reported to profit its replication from enhancing autophagosome accumulation. Here, we reported that HLA-DMB (generally referred to here as DMB), the beta chain of the non-classical MHC-II protein HLA-DM, had strong expression in HTLV-1-transformed T-cell lines and could be induced in Hela, PMA-differentiated THP1 (PMA-THP1) or primary human monocytes by HTLV-1 infection. Immunoblot and real-time PCR assays demonstrated that overexpression of DMB decreased HTLV-1 protein expression while the knockdown of DMB increased HTLV-1 protein expression. Immunoblot and confocal microscopy assays indicated that overexpression of DMB decreased HTLV-1 induced autophagosome accumulation while the knockdown of DMB yielded the opposite effects. Coimmunoprecipitation and immunoprecipitation experiments suggested DMB interacted with autophagy-related gene (ATG) 7 and increased the acetylation of ATG7. Taken together, these results suggested DMB modulated HTLV-1 protein expression through regulation of autophagosome accumulation and our findings suggested a new mechanism by which the host cells defended against HTLV-1 infection.
has issue date
2017-10-31
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)
bibo:doi
10.1038/s41598-017-14882-z
bibo:pmid
29089548
has license
cc-by
sha1sum (hex)
4aa092956fea94f9487d129b4a05a8704b73d0fc
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https://doi.org/10.1038/s41598-017-14882-z
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HLA-DMB restricts human T-cell leukemia virus type-1 (HTLV-1) protein expression via regulation of ATG7 acetylation
has PubMed Central identifier
PMC5663917
has PubMed identifier
29089548
schema:publication
Sci Rep
resource representing a document's body
covid:4aa092956fea94f9487d129b4a05a8704b73d0fc#body_text
is
schema:about
of
named entity 'replication'
named entity 'DMB'
named entity 'complicated'
named entity 'DMB'
named entity 'DMB'
named entity 'ATG7'
named entity 'HLA-DMB'
named entity 'REFERRED TO'
named entity 'OPPOSITE'
covid:arg/4aa092956fea94f9487d129b4a05a8704b73d0fc
named entity 'ANTIVIRAL'
named entity 'DMB'
named entity 'REGULATION'
named entity 'NON-'
named entity 'THESE'
named entity 'EXPERIMENTS'
named entity 'HOST CELLS'
named entity 'RESTRICTS'
named entity 'HUMAN T-CELL LEUKEMIA'
named entity 'MOLECULAR'
named entity 'DECREASED'
named entity 'PROTEIN EXPRESSION'
named entity 'COIMMUNOPRECIPITATION'
named entity 'THP1'
named entity 'PROTEIN '
named entity 'EFFECTS'
named entity 'CHAIN'
named entity 'IMMUNOBLOT'
named entity 'ACETYLATION'
named entity 'STRONG'
named entity 'OPEN'
named entity 'LEUKEMIA VIRUS'
named entity 'LEUKEMIA VIRUS'
named entity 'ADAPTIVE IMMUNITY'
named entity 'OUR'
named entity 'NEW'
named entity 'ENHANCING'
named entity 'HUMAN T-CELL LEUKEMIA'
named entity 'ACETYLATION'
named entity 'VIRUS TYPE'
named entity 'PROTEIN EXPRESSION'
named entity 'GENE'
named entity 'FINDINGS'
named entity 'EVOLVED'
named entity 'CELL LINES'
named entity 'MHC-II'
named entity 'HELA'
named entity 'HTLV-1 INFECTION'
named entity 'DELTARETROVIRUS'
named entity 'TAKEN'
named entity 'HTLV-1'
named entity 'HERE'
named entity 'ATG7'
named entity 'REAL-TIME PCR '
named entity 'CLASSICAL'
named entity 'VIRUSES'
named entity 'IMMUNOPRECIPITATION'
named entity 'INTERACTED'
named entity 'AUTOPHAGOSOME'
named entity 'T-CELL'
named entity 'OVEREXPRESSION'
named entity 'COULD BE'
named entity 'BENEFITS'
named entity 'INDICATED'
named entity 'MODULATED'
named entity 'HUMAN MONOCYTES'
named entity 'ROLES'
named entity 'HOST'
named entity 'INCREASED'
named entity 'AUTOPHAGY'
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