Difference between revisions of "Team:SCUT-China/Description"

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<h2> Project Description </h2>
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<p>Tell us about your project, describe what moves you and why this is something important for your team.</p>
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<br />
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<h5>What should this page contain?</h5>
 
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<ul>
 
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<li> A clear and concise description of your project.</li>
 
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<li>A detailed explanation of why your team chose to work on this particular project.</li>
 
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<li>References and sources to document your research.</li>
 
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<li>Use illustrations and other visual resources to explain your project.</li>
 
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</ul>
 
  
  
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<div id="descriptionContainer">
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<h4>Advice on writing your Project Description</h4>
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    <h1 id="descriptionTitle">Project description</h1>
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    <div id="descriptionContent">
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        <div class="part part-head">
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            <h2>Content</h2>
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            <h3>1. Overview</h3>
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            <h3>2. Background</h3>
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            <h3>3. Project</h3>
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            <h4>3.1 Over Expression of sGC</h4>
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            <h4>3.2 Silence the PDE5A</h4>
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            <h4>3.3 On-Off: Hypoxia-Inducible Promoter</h4>
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        </div>
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        <div class="part">
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            <h3>Overview</h3>
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            <p>According to the data from WHO, cardiovascular diseases are the main leading cause of death globally. Cyclic guanosine monophosphate (cGMP) is a critical second messenger molecule.It can transduce nitric-oxide and natriuretic-peptide-coupled signaling and remit the myocardial hypertrophy by relaxing the blood vessels. This summer, we tried to use synthetic biology to modify the cGMP metabolic pathway in a human cell line. We hope that our work would provide the proof of principle for future gene therapy.</p>
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            <img src="image/2015-SCUT-China-homeoverview.png" class="img" />
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            <p>Soluble guanylate cyclase (sGC) is an enzyme that synthesize cGMP from GTP. We up-regulate sGC by overexpressing its α and β subunits  in a mammalian cell line. However, elevated levels of cGMP leads to the feed-back expression of PDE5a, a cGMP-specific phosphodiesteras that degrades cGMP. Thus, we further modified the pathway by silencing the PDE5a. To achieve controllable up-regulation of cGMP level in the cell, we designed a hypoxia-inducible operon, HRE, as a switch to up regulate cGMP only in hypoxia situation.</p>
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        </div>
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        <div class="part">
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            <h3>Overview</h3>
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            <p>According to the data from WHO, cardiovascular diseases are the main leading cause of death globally. Cyclic guanosine monophosphate (cGMP) is a critical second messenger molecule.It can transduce nitric-oxide and natriuretic-peptide-coupled signaling and remit the myocardial hypertrophy by relaxing the blood vessels. This summer, we tried to use synthetic biology to modify the cGMP metabolic pathway in a human cell line. We hope that our work would provide the proof of principle for future gene therapy.</p>
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            <img src="image/2015-SCUT-China-homeoverview.png" class="img" />
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            <p>Soluble guanylate cyclase (sGC) is an enzyme that synthesize cGMP from GTP. We up-regulate sGC by overexpressing its α and β subunits  in a mammalian cell line. However, elevated levels of cGMP leads to the feed-back expression of PDE5a, a cGMP-specific phosphodiesteras that degrades cGMP. Thus, we further modified the pathway by silencing the PDE5a. To achieve controllable up-regulation of cGMP level in the cell, we designed a hypoxia-inducible operon, HRE, as a switch to up regulate cGMP only in hypoxia situation.</p>
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        </div>
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    </div>
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</div>
  
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<p>
 
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We encourage you to put up a lot of information and content on your wiki, but we also encourage you to include summaries as much as possible. If you think of the sections in your project description as the sections in a publication, you should try to be consist, accurate and unambiguous in your achievements.
 
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</p>
 
  
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<p>
 
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Judges like to read your wiki and know exactly what you have achieved. This is how you should think about these sections; from the point of view of the judge evaluating you at the end of the year.
 
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</p>
 
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<br />
 
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<h4>References</h4>
 
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<p>iGEM teams are encouraged to record references you use during the course of your research. They should be posted somewhere on your wiki so that judges and other visitors can see how you though about your project and what works inspired you.</p>
 
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<h4>Inspiration</h4>
 
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<p>See how other teams have described and presented their projects: </p>
 
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<ul>
 
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<li><a href="https://2014.igem.org/Team:Imperial/Project"> Imperial</a></li>
 
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<li><a href="https://2014.igem.org/Team:UC_Davis/Project_Overview"> UC Davis</a></li>
 
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<li><a href="https://2014.igem.org/Team:SYSU-Software/Overview">SYSU Software</a></li>
 
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</ul>
 
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</div>
 
 
</html>
 
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Revision as of 12:53, 15 September 2015

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Project description

Content

1. Overview

2. Background

3. Project

3.1 Over Expression of sGC

3.2 Silence the PDE5A

3.3 On-Off: Hypoxia-Inducible Promoter

Overview

According to the data from WHO, cardiovascular diseases are the main leading cause of death globally. Cyclic guanosine monophosphate (cGMP) is a critical second messenger molecule.It can transduce nitric-oxide and natriuretic-peptide-coupled signaling and remit the myocardial hypertrophy by relaxing the blood vessels. This summer, we tried to use synthetic biology to modify the cGMP metabolic pathway in a human cell line. We hope that our work would provide the proof of principle for future gene therapy.

Soluble guanylate cyclase (sGC) is an enzyme that synthesize cGMP from GTP. We up-regulate sGC by overexpressing its α and β subunits  in a mammalian cell line. However, elevated levels of cGMP leads to the feed-back expression of PDE5a, a cGMP-specific phosphodiesteras that degrades cGMP. Thus, we further modified the pathway by silencing the PDE5a. To achieve controllable up-regulation of cGMP level in the cell, we designed a hypoxia-inducible operon, HRE, as a switch to up regulate cGMP only in hypoxia situation.

Overview

According to the data from WHO, cardiovascular diseases are the main leading cause of death globally. Cyclic guanosine monophosphate (cGMP) is a critical second messenger molecule.It can transduce nitric-oxide and natriuretic-peptide-coupled signaling and remit the myocardial hypertrophy by relaxing the blood vessels. This summer, we tried to use synthetic biology to modify the cGMP metabolic pathway in a human cell line. We hope that our work would provide the proof of principle for future gene therapy.

Soluble guanylate cyclase (sGC) is an enzyme that synthesize cGMP from GTP. We up-regulate sGC by overexpressing its α and β subunits  in a mammalian cell line. However, elevated levels of cGMP leads to the feed-back expression of PDE5a, a cGMP-specific phosphodiesteras that degrades cGMP. Thus, we further modified the pathway by silencing the PDE5a. To achieve controllable up-regulation of cGMP level in the cell, we designed a hypoxia-inducible operon, HRE, as a switch to up regulate cGMP only in hypoxia situation.