Difference between revisions of "Team:MIT"
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<span class="text-content"><span><br>Explore how our sensors interact logically by transfecting 4 to 5-unit genetic circuits into model cell cultures<br><br><br><br><br><br>Read more</span></span> | <span class="text-content"><span><br>Explore how our sensors interact logically by transfecting 4 to 5-unit genetic circuits into model cell cultures<br><br><br><br><br><br>Read more</span></span> | ||
Revision as of 19:50, 16 October 2016
This diagnostic process can be expedited by using the following synthetic biological tools to sense molecular markers in endometrial biopsy samples.
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Respond to malfunctioning of hormone sensing in endometriosis
Read more -
Identify cells in disease state through dysregulated miRNA activity
Read more -
Give the circuit a form of memory through a biological latch system
Read more -
Explore how our sensors interact logically by transfecting 4 to 5-unit genetic circuits into model cell cultures
Read more
Genetic circuit to sense endometriosis
Some of our team's achievements this year include:
- Developed novel estrogen and progesterone inducible synthetic mammalian promoters through bottom-up promoter engineering. These constructs could resolve the changes in estrogen and progesterone signaling characteristic of endometriosis
- Characterized the functionality of a miRNA sensing platform in TERT immortalized human endometrial stromal cells (tHESC). We are one of the first to characterize changes in miRNA activity in the cell line with and without estrogen.
- Characterized the functionality of a serine integrase (TP901) in a mammalian cell line. Recombinases like TP901 downstream of a tunable L7Ae - kturn system that we implemented could help process input from our estrogen, progesterone, and miRNA sensors and adjust output as per a patient's needs.
- Transfected larger 4 to 5 transcriptional unit genetic circuits that cascaded our devices together in order to explore how our sensors interact with one another.
