Abstract:
:Tumor necrosis factor alpha (TNF-α) is a cytokine which plays opposing roles in the context of infectious disease pathogenesis. TNF-α is essential for the development of a protective immune response to some pathogens, for example, Mycobacterium tuberculosis, by synergizing with other cytokines. However, exorbitant or uncontrolled TNF-α activity may also drive pathology and disease symptoms in many infectious diseases. In order to elucidate the beneficial and detrimental roles of TNF-α in tuberculosis (TB) and other diseases for which the guinea pig is the small animal model of choice, recombinant guinea pig (rgp)TNF-α has been produced using prokaryotic expression systems. However, it is unknown whether posttranslational modifications which cannot be made in the prokaryotic expression systems may be important for rgpTNF-α structure and function. Therefore, we carried out a comparative study by expressing rgpTNF-α in prokaryotic and eukaryotic expression systems and analyzed the eukaryotic-expressed rgpTNF-α for the presence of posttranslational modifications by subjecting it to NanoLC-MS/MS. We conclude that the eukaryotic-expressed rgpTNF-α lacks posttranslational modifications, and we found no significant difference in terms of the biological activity between prokaryotic- and eukaryotic-expressed rgpTNF-α. Taken together, results from our study show that a prokaryotic expression system can be used for generating large amounts of rgpTNF-α without concern for the biological integrity.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Dirisala VR,Jeevan A,Ly LH,McMurray DNdoi
10.1155/2015/619480subject
Has Abstractpub_date
2015-01-01 00:00:00pages
619480eissn
0962-9351issn
1466-1861journal_volume
2015pub_type
杂志文章abstract::Macrophages contribute to a continuous increase in blood pressure and kidney damage in hypertension, but their polarization status and the underlying mechanisms have not been clarified. This study revealed an important role for M2 macrophages and the YM1/Chi3l3 protein in hypertensive nephropathy in a mouse model of h...
journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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abstract::[This corrects the article DOI: 10.1155/2016/3214105.]. ...
journal_title:Mediators of inflammation
pub_type: 已发布勘误
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2012/498373
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/S0962935194000050
更新日期:1994-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2015/506041
更新日期:2015-01-01 00:00:00
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journal_title:Mediators of inflammation
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doi:10.1155/2016/2945650
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1080/09629350120093731
更新日期:2001-10-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1080/09629359890875
更新日期:1998-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
doi:10.1080/09629350120054518
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/MI/2006/31919
更新日期:2006-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/S0962935196000014
更新日期:1996-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2016/5302120
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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