Training enables adult humans to rapidly adapt their sound localization abilities to unilateral hearing loss by combining different strategies that rely on partially distinct neurophysiological substrates.

Short linear motifs throughout the intrinsically disordered proteome use sequence context in diverse ways to target actin remodeler ENAH.

Short peptides that bind tightly to anti-apoptotic protein Bfl-1 but not other Bcl-2 family members provide a tool for diagnosing cancer cell survival mechanisms and a lead for developing new therapeutics.

Deep neural network modeling of auditory processing identifies distorted cross-frequency interactions as the key problem for the processing of speech in noise after hearing loss.

A peptide from PCARE achieves >100-fold binding specificity for the EVH1 domain of ENAH, a protein important for metastasis, using a conformational shift mechanism unavailable to ENAH's closely related paralogs VASP and EVL.

Two myosin 15 isoforms are required separately for the development and long-term maintenance of hearing.

Mitogen-activated protein kinase phosphatase 1 (DUSP1) deficiency causes early redox imbalance and increased inflammatory response in the cochlea, leading to cell loss and progressive neurosensory hearing loss.

Piezo1 activity within keratinocytes slows healing of wounded skin via dynamic channel enrichment at regions of the wound edge, causing localized retraction and thus hindering keratinocyte migration during wound healing.

Cancer-directed treatment using Tumor-Treating Fields spatially modulates the tumor microenvironment at the cellular and molecular levels, decreasing nanotube-based cellular networks of communication while creating a microenvironment more susceptible to immunotherapeutic strategies.

A comprehensive microRNA expression and function landscape of human wounds unraveled miRNAs highly relevant to venous ulcer pathology.