Team:Penn/Project2
From 2013.igem.org
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Eventually, it could even give clinical researchers the means to restore healthy methylation | Eventually, it could even give clinical researchers the means to restore healthy methylation | ||
levels in many insofar-untreatable epigenetic diseases.</p> | levels in many insofar-untreatable epigenetic diseases.</p> | ||
- | <img src="https://googledrive.com/host/0B4ZBZOYYKBzEMzM5dWpRQWNvb1k" style="height: | + | <img src="https://googledrive.com/host/0B4ZBZOYYKBzEMzM5dWpRQWNvb1k" style="height: 75px; display: inline; float: right; margin: 5px;"/> |
- | <img src="https://googledrive.com/host/0B4ZBZOYYKBzEek95VVUyMkltSHc" style="height: | + | <img src="https://googledrive.com/host/0B4ZBZOYYKBzEek95VVUyMkltSHc" style="height: 75px; float: right; margin: 5px;/> |
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Revision as of 00:31, 11 August 2013
Abstract
The code of life is much more than a sequence of A's, G's, C's and T's; a suite of epigenetic mechanisms, ranging from chromatin remodeling to non-coding RNAs, affect gene expression and cellular function.
Synthetic biologists and geneticists are accustomed to turning genes on and off at will, but the tools don’t exist to easily manipulate epigenetic patterns. We are developing a novel fusion protein that enables site-specific methylation, which can repress promoter activity with high precision.