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− | {{Team:ASIJ_Tokyo/ | + | {{ASIJ_Tokyo/CSS}} |
+ | {{:Team:ASIJ_Tokyo/bar}} | ||
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<html> | <html> | ||
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− | <style> | + | <style type="text/css"> |
/*page preset==============================================*/ | /*page preset==============================================*/ | ||
#content { | #content { | ||
− | + | width: 100%; | |
− | + | margin: auto; | |
+ | background: none; | ||
+ | border: none; | ||
+ | padding: 0; | ||
} | } | ||
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background-repeat: repeat, repeat; | background-repeat: repeat, repeat; | ||
background-size: 100%; | background-size: 100%; | ||
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padding: 0; | padding: 0; | ||
margin: 0; | margin: 0; | ||
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margin-right: 10%; | margin-right: 10%; | ||
} | } | ||
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footer { | footer { | ||
border-top: 2px dotted #fff; | border-top: 2px dotted #fff; | ||
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color: #88C1EF; | color: #88C1EF; | ||
} | } | ||
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#title h1 { | #title h1 { | ||
− | font-size: 90px; | + | font-size: 90px !important; |
color: #071f4e; | color: #071f4e; | ||
text-align: right; | text-align: right; | ||
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padding-top: 70px; | padding-top: 70px; | ||
padding-bottom: 0; | padding-bottom: 0; | ||
− | + | margin-bottom: -5px; | |
} | } | ||
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margin-right: 0; | margin-right: 0; | ||
margin-left: 0; | margin-left: 0; | ||
− | margin-top: | + | margin-top: 4%; |
margin-bottom: 5%; | margin-bottom: 5%; | ||
background: none; | background: none; | ||
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} | } | ||
− | #subtitle | + | #subtitle h2 { |
text-align: right; | text-align: right; | ||
color: #071f4e; | color: #071f4e; | ||
− | font-size: | + | font-size: 15px; |
line-height: 30px; | line-height: 30px; | ||
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padding-top: 0; | padding-top: 0; | ||
} | } | ||
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background-color: #88c1ef; | background-color: #88c1ef; | ||
padding: 50px; | padding: 50px; | ||
+ | } | ||
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+ | #abstract h3 { | ||
+ | text-align: center; | ||
+ | color: white; | ||
+ | font-size: 30px; | ||
+ | letter-spacing: 2px; | ||
+ | font-weight: 100; | ||
+ | margin-bottom: 15px; | ||
} | } | ||
#HQ_page p { | #HQ_page p { | ||
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font-size: 18px; | font-size: 18px; | ||
text-align: justify; | text-align: justify; | ||
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h6 { | h6 { | ||
font-size: 10px; | font-size: 10px; | ||
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font-weight: 100; | font-weight: 100; | ||
float: right; | float: right; | ||
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} | } | ||
+ | #igem { | ||
+ | height: 300px; | ||
+ | z-index: -2; | ||
+ | position: absolute; | ||
+ | top: 9%; | ||
+ | right: 27%; | ||
+ | } | ||
</style> | </style> | ||
<body background="https://static.igem.org/mediawiki/2018/b/b0/T--ASIJ_Tokyo--OfficialBackground.jpeg"> | <body background="https://static.igem.org/mediawiki/2018/b/b0/T--ASIJ_Tokyo--OfficialBackground.jpeg"> | ||
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<div class="wrapper"> | <div class="wrapper"> | ||
− | + | <img id="igem" src="https://static.igem.org/mediawiki/2018/8/81/T--ASIJ_Tokyo--%2Aigem_asij_logo%2A.png"> | |
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<table> | <table> | ||
<tr> | <tr> | ||
<td rowspan="2"> | <td rowspan="2"> | ||
− | <img id="liver" src="https://static.igem.org/mediawiki/2018/ | + | <img id="liver" src="https://static.igem.org/mediawiki/2018/7/7a/T--ASIJ_Tokyo--%2ALIVER%2A%28resized%29.png" height="375px" alt="liver"> |
<td id="title"><h1>A1-AT<br>de<span style="color:rgb(182, 9, 23)">LIVER</span>y </h1></td> | <td id="title"><h1>A1-AT<br>de<span style="color:rgb(182, 9, 23)">LIVER</span>y </h1></td> | ||
</td> | </td> | ||
</tr> | </tr> | ||
<tr> | <tr> | ||
− | <td id="subtitle">< | + | <td id="subtitle"><h2> Using CRISPR Technology to Combat Alpha-1 Antitrypsin Deficiency </h2></td> |
</tr> | </tr> | ||
</table> | </table> | ||
<div id="abstract"> | <div id="abstract"> | ||
<h3> ABSTRACT </h3> | <h3> ABSTRACT </h3> | ||
− | <p> Alpha-1 | + | <p> Alpha-1 antitrypsin (A1AT) deficiency is a genetic disorder that arises from a single base pair mutation in the SERPINA gene. The disease results in the production of a form of A1AT prone to polymerization, which builds up in liver cells and is unable to inhibit proteases in the lungs. The lack of antitrypsin leads to damage in both the liver and the lungs. Using CRISPR-Cas9 technology, we attempted to fix the point mutation in SERPINA1 so that proper antitrypsin can be produced. We will test our system in E. Coli cells using histidine tags, osmY secretion tags, and GFP as a reporter. We hope to design a liver organ bud using iPS cell technology to deliver functional antitrypsin through collaboration with Dr. Kagimoto of Healios Japan KK. |
</div> | </div> | ||
Latest revision as of 04:16, 17 October 2018
A1-AT |
|
Using CRISPR Technology to Combat Alpha-1 Antitrypsin Deficiency |
ABSTRACT
Alpha-1 antitrypsin (A1AT) deficiency is a genetic disorder that arises from a single base pair mutation in the SERPINA gene. The disease results in the production of a form of A1AT prone to polymerization, which builds up in liver cells and is unable to inhibit proteases in the lungs. The lack of antitrypsin leads to damage in both the liver and the lungs. Using CRISPR-Cas9 technology, we attempted to fix the point mutation in SERPINA1 so that proper antitrypsin can be produced. We will test our system in E. Coli cells using histidine tags, osmY secretion tags, and GFP as a reporter. We hope to design a liver organ bud using iPS cell technology to deliver functional antitrypsin through collaboration with Dr. Kagimoto of Healios Japan KK.