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In our proposed detection model, we would construct a fusion protein where a linker, TEV protease cleavage site and transcription factor (in that order) are fused to the intracellular domain of LilrB2. We would also fuse a TEV protease to cofilin. In that way, when beta-amyloid oligomers bind to the receptor, thus activating it, the TEV protease on the recruited cofilin cleaves at the cleavage site releasing the transcription factor in to the cytosol. The cleaved portion will be guided to the nucleus of the cell and will go on to activate the subsequent processing module.
Big/open questions:
- How do we test our construct to see if neurodegeneration is still occurring or not?
To Do (non-experiemental/immediate):
- Finish making primers for LilrB2 and PirB fusion proteins.
- Possibly make primers to amplify LilrB2 and PirB stocks.
- Start GoldenGate reactions for LilrB2 and PirB (followed by gibsons; in the Experiment list)
Experiments:
| Experiment | Expected Results | Controls | Protocols | Parts | Started | Completed? |
|---|---|---|---|---|---|---|