Team:ATOMS-Turkiye/deneme

From 2013.igem.org

(Difference between revisions)
 
(68 intermediate revisions not shown)
Line 3: Line 3:
<html>
<html>
-
    <script>
+
  <head>
-
      function openPage(pg){
+
  </head>
-
        item = $("#slideshow items").children("div").eq(pg-1);
+
  <script>
-
        content=$("#slideshow #right");
+
    function openPage(pg){
-
        content.fadeOut(200);
+
      item = $("#slideshow items").children("div").eq(pg-1);
-
        content.html(item.find("#text").html());
+
      content=$("#slideshow #right");
-
        content.fadeIn(200);
+
      content.stop();
-
        image = item.find("#image");
+
      content.fadeOut(200);
-
        image.css("position","relative");
+
      content.html(item.find("#text").html());
-
        image.css("z-index","-1");
+
      content.fadeIn(200);
-
        imagebox = $("#slideshow").find( "#imagebox");
+
      image = item.find("#image");
-
        imagebox.fadeOut(200);
+
      image.css("position","relative");
-
        //image.width(imagebox.width());
+
      imagebox = $("#slideshow").find( "#imagebox");
-
        image.height(imagebox.height()-$("#pager").height());
+
      imagebox.stop(200);
-
        imagebox.html(image.clone());
+
      imagebox.fadeOut(200);
-
        imagebox.fadeIn(200);
+
      //image.width(imagebox.width());
-
      }
+
      image.height(imagebox.height());
-
      function initSlideShow(a){
+
      imagebox.html(image.clone());
-
        items=a.children("items");
+
      imagebox.fadeIn(200);
-
        items.hide();
+
    }
-
        l = items.children("div").length;
+
    function initSlideShow(a){
-
        pager = a.find("#pager");
+
      items=a.children("items");
-
        pages="<ul style='list-style:none;display:block;list-style-type: none;margin:0;padding=4;'>";
+
      l = items.children("div").length;
-
        for( i=1;i<=l;i++ )
+
      pager = a.find("#pager");
-
          pages+="<li onclick='openPage("+i+");' style='display: inline;'>"+i+"</li> ";
+
      pages="<ul class='slide-pager'>";
-
        pager.html(pages);
+
      for( i=1;i<=l;i++ )
-
        openPage(1);
+
        pages+="<li onclick='openPage("+i+");' ><a href='#' class='no-action'>"+i+"</a></li> ";
-
       }
+
      pages+="</ul>"
-
      $(document).ready(function(){
+
      pages = $(pages);
-
        initSlideShow( $("#slideshow") );
+
       pages.children("li").hover(function(){openPage(parseInt($(this).text()));});
-
       
+
      pager.html(pages);
-
       });
+
       openPage(1);
-
     </script>
+
     }
-
<div id="slideshow" style="width:50%;height:300px;
+
      
      
-
     box-shadow: 0px 0px 5px 2px rgba(119, 119, 119, 0.55);
+
initBillboard=function (a){
-
-moz-box-shadow: 0px 0px 5px 2px rgba(119, 119, 119, 0.55);
+
  a.find("li").first().addClass("rui-billboard-current");
-
-webkit-box-shadow: 0px 0px 5px 2px rgba(119, 119, 119, 0.55);">
+
  a.find(".rui-billboard-button-prev").click(function(e){
-
       <items>
+
     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"));
 +
    });
 +
 
 +
  </script>
 +
<div style="margin:4em;"width:50%;>
 +
<div id="slideshow" class="box" style="width:100%;height:300px;">
 +
       <items class='no-print'>
         <div>
         <div>
-
           <image id="image" src="RENDER.jpg"  />
+
           <image id="image" src="https://static.igem.org/mediawiki/2013/6/66/Oncoli-diagram-2.jpg"  />
           <div id="text">
           <div id="text">
-
             deneme1
+
             <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>
         </div>
         <div>
         <div>
-
           <image id="image" src="bg.jpg" />
+
           <image id="image" src="https://static.igem.org/mediawiki/2013/c/cb/Oncoli-diagram-3.jpg" />
           <div id="text">
           <div id="text">
-
             deneme2
+
             <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>
         </div>
         </div>
       </items>
       </items>
-
       <div id="left" style="position:relative;float:left;width:50%;height:100%;">
+
       <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%;z-index:-1;">
+
         <div id="imagebox" style="position:relative;text-align:center;width:100%;height:100%;overflow:hidden;">
           image here
           image here
         </div>
         </div>
Line 63: Line 132:
       </div>
       </div>
        
        
-
       <div style="float:left;width:50%;height:100%;background:#dfdfdf;">
+
       <div class="boxin" style="float:left;width:42.3%;height:100%;overflow:hidden;background: #233447;">
-
         <div id="right" style="width:100%;height:100%;background:#dfdfdf;">
+
         <div id="right" style="width:100%;height:100%;">
           content here
           content here
-
        </div>
 
       </div>
       </div>
     </div>
     </div>
-
    <script>
+
  </div>
-
        initSlideShow( $("#slideshow") );
+
  </div>
-
    </script>
+
 
 +
<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>
 +
 
 +
 
 +
 +
 
</html>
</html>
 +
 +
{{: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

Retrieved from "http://2013.igem.org/Team:ATOMS-Turkiye/deneme"