Design, expression and characterization of a novel coexpression system of two antiarthritic molecules
Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion prot...
Ausführliche Beschreibung
Autor*in: |
Zhang, Wei [verfasserIn] |
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Artikel |
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Sprache: |
Englisch |
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2013 |
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Anmerkung: |
© Springer-Verlag Berlin Heidelberg 2013 |
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Übergeordnetes Werk: |
Enthalten in: Applied microbiology and biotechnology - Springer-Verlag, 1984, 97(2013), 14 vom: 06. März, Seite 6301-6314 |
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Übergeordnetes Werk: |
volume:97 ; year:2013 ; number:14 ; day:06 ; month:03 ; pages:6301-6314 |
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DOI / URN: |
10.1007/s00253-013-4787-z |
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Katalog-ID: |
OLC2050751338 |
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10.1007/s00253-013-4787-z doi (DE-627)OLC2050751338 (DE-He213)s00253-013-4787-z-p DE-627 ger DE-627 rakwb eng 570 VZ 12 ssgn BIODIV DE-30 fid Zhang, Wei verfasserin aut Design, expression and characterization of a novel coexpression system of two antiarthritic molecules 2013 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. TNFR-Fc CTLA4-FasL Adeno-associated virus vector Rheumatoid arthritis Wang, Fang aut Yan, Jinqi aut Zhang, Xiaojun aut Wang, Yu aut Jiang, Yunbo aut Wang, Lin aut Xu, Yuanji aut Yu, Jiyun aut Enthalten in Applied microbiology and biotechnology Springer-Verlag, 1984 97(2013), 14 vom: 06. März, Seite 6301-6314 (DE-627)129942634 (DE-600)392453-1 (DE-576)015507750 0175-7598 nnns volume:97 year:2013 number:14 day:06 month:03 pages:6301-6314 https://doi.org/10.1007/s00253-013-4787-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-TEC SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_23 GBV_ILN_70 GBV_ILN_130 GBV_ILN_267 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4082 GBV_ILN_4277 GBV_ILN_4305 AR 97 2013 14 06 03 6301-6314 |
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10.1007/s00253-013-4787-z doi (DE-627)OLC2050751338 (DE-He213)s00253-013-4787-z-p DE-627 ger DE-627 rakwb eng 570 VZ 12 ssgn BIODIV DE-30 fid Zhang, Wei verfasserin aut Design, expression and characterization of a novel coexpression system of two antiarthritic molecules 2013 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. TNFR-Fc CTLA4-FasL Adeno-associated virus vector Rheumatoid arthritis Wang, Fang aut Yan, Jinqi aut Zhang, Xiaojun aut Wang, Yu aut Jiang, Yunbo aut Wang, Lin aut Xu, Yuanji aut Yu, Jiyun aut Enthalten in Applied microbiology and biotechnology Springer-Verlag, 1984 97(2013), 14 vom: 06. März, Seite 6301-6314 (DE-627)129942634 (DE-600)392453-1 (DE-576)015507750 0175-7598 nnns volume:97 year:2013 number:14 day:06 month:03 pages:6301-6314 https://doi.org/10.1007/s00253-013-4787-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-TEC SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_23 GBV_ILN_70 GBV_ILN_130 GBV_ILN_267 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4082 GBV_ILN_4277 GBV_ILN_4305 AR 97 2013 14 06 03 6301-6314 |
allfields_unstemmed |
10.1007/s00253-013-4787-z doi (DE-627)OLC2050751338 (DE-He213)s00253-013-4787-z-p DE-627 ger DE-627 rakwb eng 570 VZ 12 ssgn BIODIV DE-30 fid Zhang, Wei verfasserin aut Design, expression and characterization of a novel coexpression system of two antiarthritic molecules 2013 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. TNFR-Fc CTLA4-FasL Adeno-associated virus vector Rheumatoid arthritis Wang, Fang aut Yan, Jinqi aut Zhang, Xiaojun aut Wang, Yu aut Jiang, Yunbo aut Wang, Lin aut Xu, Yuanji aut Yu, Jiyun aut Enthalten in Applied microbiology and biotechnology Springer-Verlag, 1984 97(2013), 14 vom: 06. März, Seite 6301-6314 (DE-627)129942634 (DE-600)392453-1 (DE-576)015507750 0175-7598 nnns volume:97 year:2013 number:14 day:06 month:03 pages:6301-6314 https://doi.org/10.1007/s00253-013-4787-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-TEC SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_23 GBV_ILN_70 GBV_ILN_130 GBV_ILN_267 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4082 GBV_ILN_4277 GBV_ILN_4305 AR 97 2013 14 06 03 6301-6314 |
allfieldsGer |
10.1007/s00253-013-4787-z doi (DE-627)OLC2050751338 (DE-He213)s00253-013-4787-z-p DE-627 ger DE-627 rakwb eng 570 VZ 12 ssgn BIODIV DE-30 fid Zhang, Wei verfasserin aut Design, expression and characterization of a novel coexpression system of two antiarthritic molecules 2013 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. TNFR-Fc CTLA4-FasL Adeno-associated virus vector Rheumatoid arthritis Wang, Fang aut Yan, Jinqi aut Zhang, Xiaojun aut Wang, Yu aut Jiang, Yunbo aut Wang, Lin aut Xu, Yuanji aut Yu, Jiyun aut Enthalten in Applied microbiology and biotechnology Springer-Verlag, 1984 97(2013), 14 vom: 06. März, Seite 6301-6314 (DE-627)129942634 (DE-600)392453-1 (DE-576)015507750 0175-7598 nnns volume:97 year:2013 number:14 day:06 month:03 pages:6301-6314 https://doi.org/10.1007/s00253-013-4787-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-TEC SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_23 GBV_ILN_70 GBV_ILN_130 GBV_ILN_267 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4082 GBV_ILN_4277 GBV_ILN_4305 AR 97 2013 14 06 03 6301-6314 |
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10.1007/s00253-013-4787-z doi (DE-627)OLC2050751338 (DE-He213)s00253-013-4787-z-p DE-627 ger DE-627 rakwb eng 570 VZ 12 ssgn BIODIV DE-30 fid Zhang, Wei verfasserin aut Design, expression and characterization of a novel coexpression system of two antiarthritic molecules 2013 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. TNFR-Fc CTLA4-FasL Adeno-associated virus vector Rheumatoid arthritis Wang, Fang aut Yan, Jinqi aut Zhang, Xiaojun aut Wang, Yu aut Jiang, Yunbo aut Wang, Lin aut Xu, Yuanji aut Yu, Jiyun aut Enthalten in Applied microbiology and biotechnology Springer-Verlag, 1984 97(2013), 14 vom: 06. März, Seite 6301-6314 (DE-627)129942634 (DE-600)392453-1 (DE-576)015507750 0175-7598 nnns volume:97 year:2013 number:14 day:06 month:03 pages:6301-6314 https://doi.org/10.1007/s00253-013-4787-z lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-TEC SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_23 GBV_ILN_70 GBV_ILN_130 GBV_ILN_267 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4082 GBV_ILN_4277 GBV_ILN_4305 AR 97 2013 14 06 03 6301-6314 |
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Enthalten in Applied microbiology and biotechnology 97(2013), 14 vom: 06. März, Seite 6301-6314 volume:97 year:2013 number:14 day:06 month:03 pages:6301-6314 |
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TNFR-Fc CTLA4-FasL Adeno-associated virus vector Rheumatoid arthritis |
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Zhang, Wei @@aut@@ Wang, Fang @@aut@@ Yan, Jinqi @@aut@@ Zhang, Xiaojun @@aut@@ Wang, Yu @@aut@@ Jiang, Yunbo @@aut@@ Wang, Lin @@aut@@ Xu, Yuanji @@aut@@ Yu, Jiyun @@aut@@ |
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design, expression and characterization of a novel coexpression system of two antiarthritic molecules |
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Design, expression and characterization of a novel coexpression system of two antiarthritic molecules |
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Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. © Springer-Verlag Berlin Heidelberg 2013 |
abstractGer |
Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. © Springer-Verlag Berlin Heidelberg 2013 |
abstract_unstemmed |
Abstract The complexity of rheumatoid arthritis (RA) pathogenesis makes combined blockade of multiple targets an attractive therapeutic strategy. The combination therapy with anti-TNF plus anti-T-cell has been mostly reported to provide greater efficacy than anti-TNF alone. TNFR (p75)-Fc fusion protein, which has been proven effective in clinics, is chosen as the TNF antagonist in this study. CTLA4-FasL fusion molecule, which has been well characterized in our previous studies for its suppressive effect in rat arthritis model, is chosen as the T-cell antagonist. In this study, furin cleavage site and 2A self-processing sequence were introduced to link upstream TNFR-Fc and downstream CTLA4-FasL and mediate separate coexpression of the two fusion proteins in a single recombinant adeno-associated virus (rAAV) vector. Using this expression system, we generated two fusion proteins with same size as their individual counterparts in vitro and in vivo, and the proteins desirably retained their parent biological activities. In vivo results demonstrated that furin-2A technology is able to regulate separate coexpression of these proteins under arthritic inflammatory conditions. This study describes a single rAAV vector for production of two antiarthritic molecules antagonizing both TNF and T cells, which may serve as an attractive expression system for RA gene therapy. © Springer-Verlag Berlin Heidelberg 2013 |
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