Team:Bay Area RSI

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You are provided with this team page template with which to start the iGEM season.  You may choose to personalize it to fit your team but keep the same "look." Or you may choose to take your team wiki to a different level and design your own wiki.  You can find some examples <a href="https://2008.igem.org/Help:Template/Examples">HERE</a>.
 
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|You can write a background of your team here. Give us a background of your team, the members, etc.  Or tell us more about something of your choosing.
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|''Every year over 1.2 million people suffer myocardial infarction (MI). The resulting heart damage requires new approaches for effective repair. Stem cell therapies provide hope. However none of the stem cell therapies currently in clinical trials addresses the need for efficient stem cell targeting to cardiac tissue or the need to replace efficiently dead tissue with new cardiomyocytes. To address these problems, we have built several genetic circuits that work sequentially to repair the heart. First, we have built an inducible differentiation circuit that closely resembles the endogenous differentiation pathway, to program cells to become cardiomyocytes. Second, we have built circuits that use the extracellular domains of chimeric proteins to target cells to damaged cardiac tissue. Upon binding, novel receptor-coupled intein-mediated signaling domains activate effector genes that then aid in integration, inhibition of cell death, and the alteration of the tissue microenvironment.  We have shown that both the targeting and signal transduction circuits work in cell culture models of MI.''
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''Every year over 1.2 million people suffer myocardial infarction (MI). The resulting heart damage requires new approaches for effective repair. Stem cell therapies provide hope. However none of the stem cell therapies currently in clinical trials addresses the need for efficient stem cell targeting to cardiac tissue or the need to replace efficiently dead tissue with new cardiomyocytes. To address these problems, we have built several genetic circuits that work sequentially to repair the heart. First, we have built an inducible differentiation circuit that closely resembles the endogenous differentiation pathway, to program cells to become cardiomyocytes. Second, we have built circuits that use the extracellular domains of chimeric proteins to target cells to damaged cardiac tissue. Upon binding, novel receptor-coupled intein-mediated signaling domains activate effector genes that then aid in integration, inhibition of cell death, and the alteration of the tissue microenvironment.''
 
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|align="center"|[[Team:Bay_Area_RSI | Team Example 2]]
 
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!align="center"|[[Team:Bay_Area_RSI/Project|The Project]]
!align="center"|[[Team:Bay_Area_RSI/Project|The Project]]
!align="center"|[[Team:Bay_Area_RSI/Parts|Parts Submitted to the Registry]]
!align="center"|[[Team:Bay_Area_RSI/Parts|Parts Submitted to the Registry]]
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!align="center"|[[Team:Bay_Area_RSI/Modeling|Modeling]]
 
!align="center"|[[Team:Bay_Area_RSI/Notebook|Notebook]]
!align="center"|[[Team:Bay_Area_RSI/Notebook|Notebook]]
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(''Or you can choose different headings.  But you must have a team page, a project page, and a notebook page.'')
 

Latest revision as of 03:32, 30 October 2008

Every year over 1.2 million people suffer myocardial infarction (MI). The resulting heart damage requires new approaches for effective repair. Stem cell therapies provide hope. However none of the stem cell therapies currently in clinical trials addresses the need for efficient stem cell targeting to cardiac tissue or the need to replace efficiently dead tissue with new cardiomyocytes. To address these problems, we have built several genetic circuits that work sequentially to repair the heart. First, we have built an inducible differentiation circuit that closely resembles the endogenous differentiation pathway, to program cells to become cardiomyocytes. Second, we have built circuits that use the extracellular domains of chimeric proteins to target cells to damaged cardiac tissue. Upon binding, novel receptor-coupled intein-mediated signaling domains activate effector genes that then aid in integration, inhibition of cell death, and the alteration of the tissue microenvironment. We have shown that both the targeting and signal transduction circuits work in cell culture models of MI.
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