Team:ATOMS-Turkiye/deneme

From 2013.igem.org

(Difference between revisions)
 
(70 intermediate revisions not shown)
Line 2: Line 2:
{{:Team:ATOMS-Turkiye/Templates/Head}}
{{:Team:ATOMS-Turkiye/Templates/Head}}
-
{{:Team:ATOMS-Turkiye/Templates/SlidingFeatureWidget}}
+
<html>
 +
  <head>
 +
  </head>
 +
  <script>
 +
    function openPage(pg){
 +
      item = $("#slideshow items").children("div").eq(pg-1);
 +
      content=$("#slideshow #right");
 +
      content.stop();
 +
      content.fadeOut(200);
 +
      content.html(item.find("#text").html());
 +
      content.fadeIn(200);
 +
      image = item.find("#image");
 +
      image.css("position","relative");
 +
      imagebox = $("#slideshow").find( "#imagebox");
 +
      imagebox.stop(200);
 +
      imagebox.fadeOut(200);
 +
      //image.width(imagebox.width());
 +
      image.height(imagebox.height());
 +
      imagebox.html(image.clone());
 +
      imagebox.fadeIn(200);
 +
    }
 +
    function initSlideShow(a){
 +
      items=a.children("items");
 +
      l = items.children("div").length;
 +
      pager = a.find("#pager");
 +
      pages="<ul class='slide-pager'>";
 +
      for( i=1;i<=l;i++ )
 +
        pages+="<li onclick='openPage("+i+");' ><a href='#' class='no-action'>"+i+"</a></li> ";
 +
      pages+="</ul>"
 +
      pages = $(pages);
 +
      pages.children("li").hover(function(){openPage(parseInt($(this).text()));});
 +
      pager.html(pages);
 +
      openPage(1);
 +
    }
 +
   
 +
initBillboard=function (a){
 +
  a.find("li").first().addClass("rui-billboard-current");
 +
  a.find(".rui-billboard-button-prev").click(function(e){
 +
    b= a.find(".rui-billboard-current");
 +
    if(b.is(':animated'))
 +
      return;
 +
    b.css("left",0);
 +
    b.animate({
 +
        left: a.outerWidth(true)
 +
    },function(){$(this).removeClass("rui-billboard-current");});
 +
    b=b.prev("li");
 +
    if(b.length<1)
 +
    b=a.find("li").last();
 +
    b.addClass("rui-billboard-current");
 +
    b.css("left",-a.outerWidth(true));
 +
    b.animate({
 +
        left: 0
 +
    });
 +
  });
 +
  a.find(".rui-billboard-button-next").click(function(e){
 +
    b= a.find(".rui-billboard-current");
 +
    if(b.is(':animated'))
 +
      return;
 +
    b.stop();
 +
    b.css("left",0);
 +
    b.animate({
 +
        left: -a.outerWidth(true)
 +
    },function(){$(this).removeClass("rui-billboard-current");});
 +
    //b.removeClass("rui-billboard-current");
 +
    b=b.next("li");
 +
    if(b.length<1)
 +
    b=a.find("li").first();
 +
    b.stop();
 +
    b.addClass("rui-billboard-current");
 +
    b.css("left",a.outerWidth(true));
 +
    b.animate({
 +
    left: 0
 +
    });
 +
  });
 +
}
 +
    $(document).ready(function(){
 +
      initSlideShow( $("#slideshow") );
 +
      $(".no-action").click(function (e){e.preventDefault();return true;});
 +
      initBillboard( $(".rui-billboard"));
 +
    });
-
'''''PROJECT DESCRIPTION'''''
+
  </script>
 +
<div style="margin:4em;"width:50%;>
 +
<div id="slideshow" class="box" style="width:100%;height:300px;">
 +
      <items class='no-print'>
 +
        <div>
 +
          <image id="image" src="https://static.igem.org/mediawiki/2013/6/66/Oncoli-diagram-2.jpg"  />
 +
          <div id="text">
 +
            <p class='infocard'><b>Welcome to our model of Oncoli.</b><br/> The genetically engineered Nissle 1917 bacteria present in the lumen produce nanofactories which are responsible of recognizing and inducing the apoptosis mechanism of cancer cells.</p>
 +
          </div>
 +
        </div>
 +
        <div>
 +
          <image id="image" src="https://static.igem.org/mediawiki/2013/c/cb/Oncoli-diagram-3.jpg" />
 +
          <div id="text">
 +
            <p class='infocard'>The nanofactory complex produced by our bacteria is formed by three parts. These are: Anti-EpCAM , Protein G and our enzymes Luxs-pfs and His-link-enzyme. These nanofactories are released from bacteria into the lumen via signal peptides. Once the Anti-EpCAM’s present on the nanofactories bind to the EpCAM antigens present on the surface of epithelial cells, the enzymes Luxs-pfs and His-link-enzyme present within the nanofactories begin to use SAH in the lumen to produce AI-2: Quorum sensing material. </p>
 +
          </div>
 +
        </div>
 +
        <div>
 +
          <image id="image" src="https://static.igem.org/mediawiki/2013/2/26/Oncoli-diagram-4.jpg" />
 +
          <div id="text">
 +
            <p class='infocard'>Compared to normal cells, EpCAM antigens are expressed 100 times more on a cancer cell. Therefore the concentration of bound nanofactories on a cancer cell is 100 times greater.</p>
 +
          </div>
 +
        </div>
 +
        <div>
 +
          <image id="image" src="https://static.igem.org/mediawiki/2013/5/52/Oncoli-diagram-6.jpg" />
 +
          <div id="text">
 +
            <p class='infocard'>The AI-2 substance produced in the lumen by our nanofactories act like a chemo-attractant which trigger our Nissle 1917 bacteria to motions toward the cancer cells via the quorum sensing technique.</p>
 +
          </div>
 +
        </div>
 +
        <div>
 +
          <image id="image" src="https://static.igem.org/mediawiki/2013/b/b2/Oncoli-diagram-7.jpg" />
 +
          <div id="text">
 +
            <p class='infocard'>TAT-Apoptin: our killer protein is controlled by an inducible promoter called LsrR-lsrk. LsrR-lsrk is induced by AI-2 which is formed when our nanofactories bind to the cancer cells. Our bacteria build up around cancer cells and release our killer protein: TAT-Apoptin. </p>
 +
          </div>
 +
        </div>
 +
        <div>
 +
          <image id="image" src="https://static.igem.org/mediawiki/2013/5/58/Oncoli-diagram-11.jpg" />
 +
          <div id="text">
 +
            <p class='infocard'>The secreted TAT-APOPTIN complex, binds to the cancer cells and normal cells, penetrating into the membrane without causing any damage. When apoptin reaches a specific concentration in the cytoplasm of cancer cells, the period of apoptosis begins and the cancer cells are destroyed. However the normal cells remain unaffected as apoptin is cancer specific. </p>
 +
          </div>
 +
        </div>
 +
      </items>
 +
      <div id="left" style="position:relative;float:left;width:57.7%;height:100%;">
 +
        <div id="imagebox" style="position:relative;text-align:center;width:100%;height:100%;overflow:hidden;">
 +
          image here
 +
        </div>
 +
        <div id="pager" style="position:absolute;bottom:0;width:100%;">
 +
        </div>
 +
      </div>
 +
     
 +
      <div class="boxin" style="float:left;width:42.3%;height:100%;overflow:hidden;background: #233447;">
 +
        <div id="right" style="width:100%;height:100%;">
 +
          content here
 +
      </div>
 +
    </div>
 +
  </div>
 +
  </div>
 +
 
 +
<div class="tourview" style="background:url('https://static.igem.org/mediawiki/2013/thumb/e/e3/Oncoli-tour-main.png/800px-Oncoli-tour-main.png');-webkit-background-size: cover;-moz-background-size: cover;-o-background-size: cover;background-size: cover;">
 +
  <div style="padding-left:130px;padding-right:170px;padding-left:130px;padding-top:100px;padding-bottom:55px;height:135px;">
 +
  <a href="/Team:ATOMS-Turkiye/Tour:1" title="Take a tour"></a>
 +
  <a href="/Team:ATOMS-Turkiye/Tour:2"></a>
 +
  <a href="/Team:ATOMS-Turkiye/Tour:3"></a>
 +
  <a href="/Team:ATOMS-Turkiye/Tour:4"></a>
 +
  </div>
 +
</div>
-
'''Project Oncoli'''
 
-
It is not surprising at all if we name the cancer disease as our century’s health problem when it causes about 13% of all human deaths worldwide. It is also not surprising why a considerable amount of scientists working for decades to find an exact and efficient solution to this chaotic growing catastrophe. The more we improve ourselves in technology, the more we approaching the solution; but also we drifting apart by causing more cancer patients.
+
-
This year, we want to focus on the possibility of an efficient treatment for colon cancer by using the advantages of synthetic biology. Unlike our last year’s project about the easy diagnosis of cancer, we want to propose a better and safe remedy option at this year’s Jamboree. In our plan, we are willing to design a safe E.coli strain which is able to detect possible cancer cells and destroy them selectively by releasing a kind of apoptosis inducing protein. To empower the system and to have better results, our plan includes using the properties of quorum sensing.
+
</html>
-
With the ability to manipulate the gut flora without disturbing the body or without causing serious problems, we are looking forward to take a remarkable step about cancer treatment and attribute the society of science fairly.
+
 
 +
{{:Team:ATOMS-Turkiye/Sponsors}}

Latest revision as of 03:48, 5 October 2013

Welcome to our model of Oncoli.
The genetically engineered Nissle 1917 bacteria present in the lumen produce nanofactories which are responsible of recognizing and inducing the apoptosis mechanism of cancer cells.

The nanofactory complex produced by our bacteria is formed by three parts. These are: Anti-EpCAM , Protein G and our enzymes Luxs-pfs and His-link-enzyme. These nanofactories are released from bacteria into the lumen via signal peptides. Once the Anti-EpCAM’s present on the nanofactories bind to the EpCAM antigens present on the surface of epithelial cells, the enzymes Luxs-pfs and His-link-enzyme present within the nanofactories begin to use SAH in the lumen to produce AI-2: Quorum sensing material.

Compared to normal cells, EpCAM antigens are expressed 100 times more on a cancer cell. Therefore the concentration of bound nanofactories on a cancer cell is 100 times greater.

The AI-2 substance produced in the lumen by our nanofactories act like a chemo-attractant which trigger our Nissle 1917 bacteria to motions toward the cancer cells via the quorum sensing technique.

TAT-Apoptin: our killer protein is controlled by an inducible promoter called LsrR-lsrk. LsrR-lsrk is induced by AI-2 which is formed when our nanofactories bind to the cancer cells. Our bacteria build up around cancer cells and release our killer protein: TAT-Apoptin.

The secreted TAT-APOPTIN complex, binds to the cancer cells and normal cells, penetrating into the membrane without causing any damage. When apoptin reaches a specific concentration in the cytoplasm of cancer cells, the period of apoptosis begins and the cancer cells are destroyed. However the normal cells remain unaffected as apoptin is cancer specific.

image here

Sponsors

Oncoli-s-tozal.png Oncoli-s-sigma.jpg Oncoli-s-sentegen.png