Genetic disruption of sodium-hydrogen exchanger 6 (NHE6) reduces amyloid plaques in humanized Alzheimer's disease mouse models and restores normal synaptic responses to neuromodulatory input in humanized ApoE4-expressing animals.
Combining cerebral organoid technology with cryo-correlative microscopy reveals the organization of cytoskeleton, membrane compartments, and protein synthesis machinery contributing to the rapid expansion of developing human axons.
Alternative splicing and the endoplasmic reticulum (ER)-associated protein degradation (ERAD) system represent essential, fat depot-specific components of the adipogenesis that are altered in preadipocytes from obese individuals with metabolic disease.
The current findings address the redox regulation of hypoxia inducible factor 1α (HIF1α) stability in hypoxia by showing that cytosolic, mitochondrial or lipid ROS are not necessary for HIF1α stabilization in hypoxia.
Lineage tracing and genetic experiments resolve a long-standing controversy by showing that retinoic acid signaling is active in cardiomyocytes, both during development and after myocardial infarction, and protects damaged hearts from apoptosis.
Myogenin promotes centrosome attenuation and establishes the nuclear envelope as the dominant microtubule organization center via the scaffold protein AKAP6, which is required for the recruitment of centrosomal proteins.
A combination of spatial proteomic and autophagic flux approaches was used to reveal the landscape of turnover of damaged lysosomes, demonstrating a key role for the autophagy receptor TAX1BP1 and its associated kinase TBK1 in both HeLa cells and iNeurons.