Computational Plasmid Design for SMAD7 Production in Liver Fibrosis

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3 weeks

Duration

Synthetic Biology

Industry

Date

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Problem Statement

While the TGF-β pathway is a primary driver of liver fibrosis, broad inhibition of this pathway often results in severe, unintended side effects across the body. There is a critical need for a highly localized genetic intervention that can effectively halt fibrotic progression strictly within damaged liver cells without disrupting healthy tissue function.
While the TGF-β pathway is a primary driver of liver fibrosis, broad inhibition of this pathway often results in severe, unintended side effects across the body. There is a critical need for a highly localized genetic intervention that can effectively halt fibrotic progression strictly within damaged liver cells without disrupting healthy tissue function.
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Methods

To develop the therapeutic plasmid, I computationally designed a synthetic genetic circuit in Benchling featuring a fibrotic-specific promoter linked directly to the SMAD7 gene. I used python to simulate the plasmid's regulatory dynamics and edited the sequence to ensure it would only activate in response to targeted disease markers.

Experience

Designing computational genetic circuits to upregulate SMAD7 expression was a meaningful project because it explored a targeted, synthetic biology approach to halting liver fibrosis. By computationally modeling these genetic circuits to respond exclusively to specific fibrotic markers, I engineered a dynamic system aimed at safely blocking the disease-driving TGF-β pathway without triggering systemic side effects. This experience deepened my understanding of complex gene regulatory networks and demonstrated how computational design can be leveraged to create highly specific, programmable therapies for chronic conditions.

Contact

Have a project in mind or want to collaborate?

Have a project in mind or want to collaborate?

allisonlyp.huang@gmail.com

I usually reply within 24–48 hours.

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