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Genetic analysis of a CLN4 Drosophila model suggests that the disease-causing alleles act as dominant gain of function mutations that cause CSPα oligomerization and impair secretory and prelysosomal trafficking.

In humans, specific sequence features can predict whether meiotic recombination occurs at sites bound by the protein PRDM9, whose DNA-binding zinc-finger domain can unexpectedly bind to gene promoters and to other copies of PRDM9.

Cell-type-specific molecular systems mapping reveals that striatal neuron degeneration in Huntington's disease is primarily driven by the loss of homeostatic responses.

Ceapins enable selective pharmacological inhibition of the cytoprotective transcriptional response to endoplasmic reticulum stress through ATF6α without affecting other branches of the unfolded protein response.

A multidisciplinary approach was used to translate the mathematical analysis of Dystrophin movements inside muscle cells into the biology of how Dystrophin interacts with the cell membrane.

The immune microenvironment has a pivotal role in hepatocellular carcinoma (HCC) progression and immune therapy resistance, and targeting this complex milieu holds great promise for improving therapeutic outcomes and patient prognoses in HCC management.

A network, composed of 22 relatives of the Beaten Path and Sidestep immunoglobulin superfamily cell surface proteins, also includes several neuronal Beaten Path subfamily receptors which interact selectively with Sidestep subfamily proteins expressed on peripheral tissues.

A perspective of the energy-sparing super-relaxed state of myosin and its evolutionary role in modulating skeletal and cardiac muscle power under different physiological and pathophysiological perturbations.