Difference between revisions of "Team:UST Beijing/Background"

 
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               <li><a href="https://2018.igem.org/Team:UST_Beijing/Background">Background</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/Background">Background</a ></li>
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               <li><a href="https://static.igem.org/mediawiki/2018/e/e9/T--UST_Beijing--experiment.pdf">Experiments</a ></li>
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               <li><a href="https://2018.igem.org/Team:UST_Beijing/Experiments">Experiments</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/Notebook">Notebook</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/Notebook">Notebook</a ></li>
 
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           <li><a href="https://static.igem.org/mediawiki/2018/6/63/T--UST_Beijing--model.pdf">Model</a ></li>
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           <li><a href="https://2018.igem.org/Team:UST_Beijing/Model">Model</a ></li>
 
           <li><a href="https://2018.igem.org/Team:UST_Beijing/Parts">Parts</a ></li>
 
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           <li><a href="https://2018.igem.org/Safety/Final_Safety_Form?team_id=2537">Safety</a ></li>
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           <li class="dropdown"><a href="javascript:{}">Awards</a >
 
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               <li><a href="https://2018.igem.org/Team:UST_Beijing/Attributions">Attribution</a ></li>
 
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               <li><a href="https://2018.igem.org/Team:UST_Beijing/Collaborations">Collaboration</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/Collaborations">Collaboration</a ></li>
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              <li><a href="https://static.igem.org/mediawiki/2018/5/5a/T--UST_Beijing--Demonstrate.pdf">Demonstrate</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/InterLab">InterLab</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/InterLab">InterLab</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/Human_Practices">HumanPractice</a ></li>
 
               <li><a href="https://2018.igem.org/Team:UST_Beijing/Human_Practices">HumanPractice</a ></li>
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              <li><a href="https://2018.igem.org/Team:UST_Beijing/Improve">Improve</a ></li>
 
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         <div>
 
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             <h1><span>Cholesterol</span></h1>
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             <h2><span>Cholesterol</span></h2>
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             <p>an essential component of membrane structure, but gradually  
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             <h3>an essential component of membrane structure, but gradually  
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               accumulates in arteries of human body, which results in
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               accumulates in arteries of human body, which becomes the top one killer mechanism of human life: <span>atherosclerosis</span></h3>
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              the number one killer mechanism of human life:</p>
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             <h2><span> An alarming health threat: Atherosclerosis</span></h2>
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            <p><span>atherosclerosis</span></p>
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             <h3>Shown on the right are the cholesterol structure and pie charts of epidemic statistics of atherosclerosis-related mortality in China (black area: atherosclerosis-related death).</h3>
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             <h1><span> An alarming health threat: Atherosclerosis</span></h1>
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             <p>Shown on the right are the cholesterol structure and pie charts of Epidemic statistics of atherosclerosis-related mortality in China</p>
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         <h2><span>Pathology of Atheroscleosis</span></h2>
 
         <h2><span>Pathology of Atheroscleosis</span></h2>
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         <p>Artery atherosclerosis refers to arteries accumulated with cholesterol resulting in blockage of blood flow. Cholesterol is the main culprit of cardio-cerebrovascular disease. In heart it causes heart attack. In brain it causes blockage stroke.</p>
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         <h3>Cholesterol is the main culprit of cardio-and cerebro-vascular disease. Artery atherosclerosis refers to arteries accumulated with cholesterol resulting in blockage of blood flow. In heart it causes heart attack. In brain it causes blockage stroke.</h3>
 
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         <h2><span>Molecular Mechanism of Atherosclerosis Formation</span></h2>
 
         <h2><span>Molecular Mechanism of Atherosclerosis Formation</span></h2>
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         <p>Because of foam cell apoptosis, which is formed by macrophages overloading cholesterol, cholesterol is deposited on the inner wall of artery.</p>
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         <h3>Because of foam cell apoptosis, which is formed by macrophages overloading cholesterol, cholesterol is deposited on the inner wall of artery.</h3>
 
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         <h2><span>Nuclear receptor LXR as therapeutic target against atherosclerosis</span></h2>
 
         <h2><span>Nuclear receptor LXR as therapeutic target against atherosclerosis</span></h2>
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         <p>Live X receptor(LXR) functions as a master regulation switch, which can accelerate the transport of cholesterol and prevent the formation of foam cells.</p>
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         <h3>Live X receptor(LXR) functions as a master regulation switch, which can accelerate the transport of cholesterol and prevent the formation of foam cells.</h3>
 
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        <h2><span> Actions of LXR </span></h2>
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        <h3>LXRs have a typical nuclear receptor structure. Upon bound by agonists (such as ginseno-sterols), LXRs would recruit co-activators (shown in the animation, only a fragment of coactivator peptide is displayed)and activate the transcription of a target gene.</h3>
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  <blockquote><p>Ginseng triterpenes' structure is similar to that of cholesterol, that is to say, it has the potential of regulating LXRs.
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  <h3>Ginseng triterpenes' structure is similar to that of cholesterol, therefore it has the potential of regulating LXRs.
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       LXRs is a typical nuclear receptor. In the presence of co-activators, regulated by agonists (such as ginsenoside), LXRs could binds
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       LXRs is a typical nuclear receptor. In the presence of co-regulators, bound by agonists (such as ginsenosides), LXRs could be demobilized to specific site on a target gene promoter region to activate transcription of the target gene. Ginsenosides or like could therefore regulate the metabolism of cholesterol. </h3>
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special site on target gene promoter region to repress or active the transcription of the target gene.
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      So to sum up, ginsenosides could regulate the metabolism of cholesterol. We devote to finding a better way to solve the two remaining problems.
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    Here is the foothold of our project postulates.</p></blockquote>
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         <div class="item_description"><h1><span>Atherosclerosis formation is delayed<br>by ginsenosides in vivo</span></h1></div>
 
         <div class="item_description"><h1><span>Atherosclerosis formation is delayed<br>by ginsenosides in vivo</span></h1></div>
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Latest revision as of 15:28, 16 October 2018

Team:UST_Beijing/Collaborations

Cholesterol

an essential component of membrane structure, but gradually accumulates in arteries of human body, which becomes the top one killer mechanism of human life: atherosclerosis

An alarming health threat: Atherosclerosis

Shown on the right are the cholesterol structure and pie charts of epidemic statistics of atherosclerosis-related mortality in China (black area: atherosclerosis-related death).

Pathology of Atheroscleosis

Cholesterol is the main culprit of cardio-and cerebro-vascular disease. Artery atherosclerosis refers to arteries accumulated with cholesterol resulting in blockage of blood flow. In heart it causes heart attack. In brain it causes blockage stroke.

Molecular Mechanism of Atherosclerosis Formation

Because of foam cell apoptosis, which is formed by macrophages overloading cholesterol, cholesterol is deposited on the inner wall of artery.

Nuclear receptor LXR as therapeutic target against atherosclerosis

Live X receptor(LXR) functions as a master regulation switch, which can accelerate the transport of cholesterol and prevent the formation of foam cells.

Actions of LXR

LXRs have a typical nuclear receptor structure. Upon bound by agonists (such as ginseno-sterols), LXRs would recruit co-activators (shown in the animation, only a fragment of coactivator peptide is displayed)and activate the transcription of a target gene.

Ginseng triterpenes' structure is similar to that of cholesterol, therefore it has the potential of regulating LXRs. LXRs is a typical nuclear receptor. In the presence of co-regulators, bound by agonists (such as ginsenosides), LXRs could be demobilized to specific site on a target gene promoter region to activate transcription of the target gene. Ginsenosides or like could therefore regulate the metabolism of cholesterol.

Ginsenoside TR1 modulates
LXR biological activity

Atherosclerosis formation is delayed
by ginsenosides in vivo

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