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Team:AITM-Nepal
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<li><a class="navbar-option" href="https://2013.igem.org/Team:AITM-Nepal">Home</a></li> | <li><a class="navbar-option" href="https://2013.igem.org/Team:AITM-Nepal">Home</a></li> | ||
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<li><a href="https://2013.igem.org/Team:AITM-Nepal/Part1" class="navbar-option">Part 1</a></li> | <li><a href="https://2013.igem.org/Team:AITM-Nepal/Part1" class="navbar-option">Part 1</a></li> | ||
<li><a href="https://2013.igem.org/Team:AITM-Nepal/Part2" class="navbar-option">Part 2</a></li> | <li><a href="https://2013.igem.org/Team:AITM-Nepal/Part2" class="navbar-option">Part 2</a></li> | ||
<li><a href="https://2013.igem.org/Team:AITM-Nepal/Part3" class="navbar-option">Part 3</a></li> | <li><a href="https://2013.igem.org/Team:AITM-Nepal/Part3" class="navbar-option">Part 3</a></li> | ||
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Canonical small interfering RNA (siRNA) duplexes are potent activators of the mammalian innate immune system. The induction of innate immunity by siRNA is dependent on siRNA structure and sequence, method of delivery, and cell type. The delivery of siRNA in a packaged outer membrane vesicle of gram negative bacteria is the theme of our work. The toll like receptor-7/8 activation by siRNA in order to boost the production of Interferon type -1 molecules to inhibit the viral and outer membrane LPS structure to activate Toll like receptor -4 to inhibit bacterial pathogens is the objective of this work. The delivery is made dependent on the peptide fragment which mediated the fusogenic mechanism so as to escape the endosomal compartment once endocytosed inside host(mamalian) cell. Thus freeing the siRNA to silence the myD88 transcript in host cytoplasm making RISC complex and hence, activating TLR-7/8 in endosomal membrane formerly. | Canonical small interfering RNA (siRNA) duplexes are potent activators of the mammalian innate immune system. The induction of innate immunity by siRNA is dependent on siRNA structure and sequence, method of delivery, and cell type. The delivery of siRNA in a packaged outer membrane vesicle of gram negative bacteria is the theme of our work. The toll like receptor-7/8 activation by siRNA in order to boost the production of Interferon type -1 molecules to inhibit the viral and outer membrane LPS structure to activate Toll like receptor -4 to inhibit bacterial pathogens is the objective of this work. The delivery is made dependent on the peptide fragment which mediated the fusogenic mechanism so as to escape the endosomal compartment once endocytosed inside host(mamalian) cell. Thus freeing the siRNA to silence the myD88 transcript in host cytoplasm making RISC complex and hence, activating TLR-7/8 in endosomal membrane formerly. | ||
Contact us: aitmnepal2013@gmail.com | Contact us: aitmnepal2013@gmail.com | ||
| - | + | <br> | |
| + | <h2>Sponsors:</h2> | ||
| + | <hr> | ||
| + | <a href="http://www.cmdn.org.np/main/"><img src="https://static.igem.org/mediawiki/2013/7/78/Cmdnlogo.jpg"></a> | ||
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Latest revision as of 20:07, 21 November 2014
Our Project:
ImmunEcoli
This is the first approach for Synthetic Biology from Nepal. We are a team of Undergrads of Biotechnology from Asian Institute of Technology and Management. This year we are trying to engineer ''Escherichia coli'' which will be used as a carrier and immune modulation point using Outer Membrane Vesicle (OMVs). ''Escherichia coli'', being a model organism, is easier to work with , especially for the purpose of genetically engineered realm. Canonical small interfering RNA (siRNA) duplexes are potent activators of the mammalian innate immune system. The induction of innate immunity by siRNA is dependent on siRNA structure and sequence, method of delivery, and cell type. The delivery of siRNA in a packaged outer membrane vesicle of gram negative bacteria is the theme of our work. The toll like receptor-7/8 activation by siRNA in order to boost the production of Interferon type -1 molecules to inhibit the viral and outer membrane LPS structure to activate Toll like receptor -4 to inhibit bacterial pathogens is the objective of this work. The delivery is made dependent on the peptide fragment which mediated the fusogenic mechanism so as to escape the endosomal compartment once endocytosed inside host(mamalian) cell. Thus freeing the siRNA to silence the myD88 transcript in host cytoplasm making RISC complex and hence, activating TLR-7/8 in endosomal membrane formerly. Contact us: aitmnepal2013@gmail.comSponsors:
