Difference between revisions of "Team:SMMU-China/Part Collection"

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<h3 class="inner-h">References</h3>
 
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<li>Bingham A J, Ooi L, Kozera L, et al. The Repressor Element 1-Silencing Transcription Factor Regulates Heart-Specific Gene Expression Using Multiple Chromatin-Modifying Complexes[J]. Molecular & Cellular Biology, 2007, 27(11):4082.</li>
 
<li>Bingham A J, Ooi L, Kozera L, et al. The Repressor Element 1-Silencing Transcription Factor Regulates Heart-Specific Gene Expression Using Multiple Chromatin-Modifying Complexes[J]. Molecular & Cellular Biology, 2007, 27(11):4082.</li>
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<li>4. Lu Y M, Shioda N, Han F, et al. DY-9760e inhibits endothelin-1-induced cardiomyocyte hypertrophy through inhibition of CaMKII and ERK activities[J]. Cardiovascular Therapeutics, 2009, 27(1):17–27.</li>
 
<li>4. Lu Y M, Shioda N, Han F, et al. DY-9760e inhibits endothelin-1-induced cardiomyocyte hypertrophy through inhibition of CaMKII and ERK activities[J]. Cardiovascular Therapeutics, 2009, 27(1):17–27.</li>
 
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Revision as of 11:22, 7 October 2018

Part Collection

Abstract

This year is the first year which SMMU-iGEM 2018 team becomes a family member of iGEM. We have designed 14 parts, including 6 basic parts. All of the parts are designed ourselves and most of them have been tested to insure their reliability.

As a team focusing on real-world problem, heart faliure, we found it is hard to control the process of disease through traditional drug threopy, implanted cardiac assist devices or surgical treatments. In synthetic biology, one central route is to construct a controllable biological network which could express in the environment of heart failure. We designed a targeting device, CaRTIN (Cardiomyocyte RyR2 Targeting Intra-Nanobody), to implement RyR2-specific inhibition of phosphorylation.

In this year, we investigated the potential of adeno-associated virus (AAV)-9-mediated cardiac expression of AR185 which is one of the isolated nanobodies from a phage display library of variable domains of camellidae heavy chain-only antibodies (VHH) to combat post-ischemic heart failure. To achieve controlled intra-nanobody release, a BNP promoter based platform were also accessed. Our results established a role of CaRTIN as a promising therapeutic approach for heart failure.

Our members are involved in the construction of the parts, and has achieved some results. The functions of all components are tested and validated under controlled laboratory conditions and normal conditions, and data and phenomena demonstrate that they are valid. At the same time, all components are standardized, which makes them a convenient and powerful tool for others.

Design and Function of Ca2+RTIN

See More

To see their specific function, you can click the number link below to browse the specific page on parts.igem.org.

We listed Biobricks belong to Part Collection below.

Name Type Description Designer Length
BBa_K2865000 Regulatory BNP promoter, heart failure inducible Chuqi Wang 508
BBa_K2865001 Coding AR185, nanobody inhibiting RyR2 phosphorylation Chuqi Wang
BBa_K2865002 Project [AAV9]-Left-ITR Chuqi Wang 175
BBa_K2865003 Project [AAV9]-Right-ITR Chuqi Wang
BBa_K2865004 Terminator SV40 poly(A) Chuqi Wang
BBa_K2865005 Coding eGFP Hu Miao 726
BBa_K2865006 Composite CMV promoter-eGFP-poly(A) Hu Miao
BBa_K2865008 Composite BNP promoter-eGFP-poly(A) Hu Miao
BBa_K2865009 Composite BNP-AR185-Poly(A) Hu Miao
BBa_K2865010 Composite CMV-AR185-Poly(A) Hu Miao
BBa_K2865012 Composite Left ITR-BNP-AR185-Poly(A)-Right ITR Hu Miao
BBa_K2865013 Composite Left ITR-CMV-AR185-Poly(A)-Right ITR Hu Miao
BBa_K2865014 Composite Left ITR-CMV-eGFP-Poly(A)-Right ITR Hu Miao
BBa_K2865015 Composite Left ITR-BNP-eGFP-Poly(A)-Right ITR Hu Miao

References

  1. Bingham A J, Ooi L, Kozera L, et al. The Repressor Element 1-Silencing Transcription Factor Regulates Heart-Specific Gene Expression Using Multiple Chromatin-Modifying Complexes[J]. Molecular & Cellular Biology, 2007, 27(11):4082.
  2. Sergeeva I A, Christoffels V M. Regulation of expression of atrial and brain natriuretic peptide, biomarkers for heart development and disease[J]. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2013, 1832(12):2403-2413.
  3. Kerkelä R, Ilves M, Pikkarainen S, et al. Key roles of endothelin-1 and p38 MAPK in the regulation of atrial stretch response.[J]. American Journal of Physiology Regulatory Integrative & Comparative Physiology, 2011, 300(1):R140.
  4. 4. Lu Y M, Shioda N, Han F, et al. DY-9760e inhibits endothelin-1-induced cardiomyocyte hypertrophy through inhibition of CaMKII and ERK activities[J]. Cardiovascular Therapeutics, 2009, 27(1):17–27.
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