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Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

Cognitively normal older adults show a positive relationship between neural activity during memory encoding and brain β-amyloid deposition rate over the subsequent 3-4 years, supporting preclinical data that associates neural activity with β-amyloid deposition.

A pentameric channel-receptor was studied by combining allosteric mutations, electrophysiology, fluorescent reporters and normal mode analysis, to dissect the long-range allosteric couplings specifically involved in its pre-activation and activation.

Mice with a mutation that disrupts the release of growth hormone show greatly increased lifespan, which can be further increased by caloric restriction.

Inhibition of serotonin transporter activity, by fluoxetine treatment, in early post-natal life induces persistent apnea in wild-type mice but restores normal breathing in Necdin-KO pups that reproduce breathing abnormalities observed in Prader-Willi syndrome.

A physiological mathematical model of chronic myeloid leukemia, validated by experiments in transgenic mice and clinical data, identifies mechanisms underlying the response to tyrosine kinase inhibitor therapy, predicts biomarkers of primary resistance, and suggests new strategies to improve treatment outcomes.

A new computational model explains how alternate rearing conditions affect the development of binocular vision.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

A cell-intrinsic surface area-dependent mechanism establishes centriole-cilia abundance in airway multiciliated cells.

Purinergic keratinocyte-to-sensory neuron signaling is a ubiquitous amplification mechanism that is required for normal mechanical, cold, and heat sensation in vivo.