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Improperly folded proteins are targeted for destruction through the endoplasmic-reticulum-associated degradation pathway (ERAD). Kopito and colleagues present a high-resolution interaction analysis of the ERAD system in combination with functional genomics, and identify new ERAD components.
Bershadsky and colleagues show that fibroblast polarization depends on matrix rigidity and focal adhesion mechanosensing. They target protein tyrosine kinases through RNAi to identify signalling molecules that regulate traction force generation, focal adhesion assembly and mechanosensitivity.
