Mechanism? Fusions sequester adapters like Grb2 in cyto and prevent translocation to active EGFR at membrane. Previously shown for EML4-ALK, below for TPM3-ROS, same for (almost) all fusions tested

🚨New preprint(1/2)! We show that RTK fusion oncoproteins broadly suppress EGFR signaling. How? Sequestration of adapters as the shared principle.

Led by superb PhD student Carol Gao.

www.biorxiv.org/content/10.1...

Implications for drug tolerance/resistance, and includes one big surprise🫧.👇

We also developed a "universal" Aviatar that can localize to any GFP-tagged compartment using a weak nanobody, and we used it to localize to stress granules through endogenously-tagged G3BP1

Aviatar regulated actin polymerization at the membrane and revealed compartment-specific differences of RTK fragments commonly mislocalized in cancer

Aviatar can target any desired compartment for which a weak binder can be found. We show common targets: plasma membrane, endosomes, Golgi, ER, and microtubules.

Proteins often bind targets using avidity, the combined interaction strength of multiple weak binders. Now we’ve harnessed this principle for compact, *single*-component optogenetic tools for translocation. Lead by phenom PhD student @dennishuang.bsky.social #synbiosky🧵

📝 tinyurl.com/aviatar

New preprint! We found dynamic signal processing (IFFL) in a single protein, which pulses in response to step inputs. New insights for capability of protein computation + implications for new opto and thermo probes

www.biorxiv.org/content/10.1...

Check out the 🧵 from first author Dennis Huang:

and the second
www.sciencedirect.com/science/arti...