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Fernandez, R. A.

Publications and source records attributed to Fernandez, R. A..

2 recordsLinked to original sources

Systematic molecular glue drug discovery with a high-throughput effector protein remodeling platform

Realising the promise of new medicines that operate through a targeted molecular glue-induced degradation mechanism requires systematic tools that can uncover the relevant principles of neomorphic protein-protein interactions. Whilst some monovalent glue degraders have been found through serendipity, the rules for small molecule attributes and the pairs or complexes of proteins that are amenable to drug-induced proximity control remain poorly articulated. Here we introduce a new approach to address this by using programmed libraries of intramolecularly edited proteins to expand protein surface landscapes and trigger new druggable interactions. We show that effector proteins, such as the E3 ligase Cereblon, can be engineered to provoke neomorphic activity by inducing the degradation of new client proteins and that these de novo interactions provide a blueprint from which new small molecule degraders can be built. As a demonstration of the approach, we use the platform to identify new non-IMiD molecular glue degraders of the oncology target GSPT1. SUMMARYO_LIMolecular glues are a highly important and promising new form of therapeutic agent, but rationalising their discovery has so far been impossible C_LIO_LIGlueSEEKER screening enables prospective monovalent drug discovery by using high-throughput deep mutational scanning to re-engineer the function of effector proteins like E3 ligases C_LIO_LIWe used this approach to enable the computational discovery of small molecule glues which degrade the oncology target GSPT1 and show how the technology can be used across new targets C_LI

bioengineering↗

Early exercise disrupts a pro-repair extracellular matrix program during zebrafish fin regeneration

Mechanical stimulation effects on cell behaviors that restore organ form and function during tissue repair are unresolved. We applied swim flume-mediated exercise during zebrafish caudal fin regeneration to explore mechanical loading impacts on a robust model of organ regeneration. Exercise initiated during but not after blastema establishment compromised fin regeneration, including outgrowth and skeletal pattern. Long-term tracking of fluorescently labeled fibroblasts showed exercise loading disrupted blastemal mesenchyme formation. Transcriptomic profiling and section staining indicated loading reduced an extracellular matrix (ECM) gene expression program, including for hyaluronic acid (HA) synthesis. As with exercise loading, HA synthesis inhibition or blastemal HA depletion impaired blastema formation. We considered if injury-upregulated HA establishes a pro-regenerative environment facilitating mechanotransduction. HA density across the blastema correlated with nuclear localization of the mechanotransducer Yes-associated protein (Yap). Exercise loading or HA depletion decreased nuclear Yap, and culturing primary fin fibroblasts on HA-coated surfaces induced Yap nuclear localization. We conclude early exercise during fin regeneration disrupts expression of an HA-rich ECM supporting Yap-promoted blastema expansion. These findings reveal that fin regeneration is acutely sensitive to the timing and intensity of mechanical loading, underscoring how biomechanical forces integrate with regenerative programs to guide robust tissue repair.

developmental biology↗