Eukaryotic translation elongation factor 1A1 controls the process of heat shock response, from transcriptional activation of the HSP70 gene, to HSP70 mRNA stabilization, nuclear export, and translation.
Electrophysiological and simulation approaches show that a chloride-related longer relaxation of the inhibitory synaptic events partially compensates the early defect in the chloride homeostasis detected in fetal SOD spinal motoneurons.
In neuronal mitophagy, Parkin and OPTN induce efficient sequestration of damaged somal mitochondria into autophagosomes, but slow turnover via lysosomal acidification may be a point of vulnerability for the cell.
Text mining of complete EHRs for 14,017 diabetes patients and subsequent clustering led to phenotypically deep clusters, showing distinct glycemic profiles, comorbidities, and SNP association patterns.
Impaired lysosomal acidification results in retention of iron inside lysosomes, triggering functional iron deficiency, dysfunctional mitochondria (especially mtDNA loss), and inflammation in vivo in a mouse model of lysosomal disease.
Directly targeting the ribosome to attenuate translation partly mimics the integrated stress response, increasing lifespan and preserving protein folding capacity even in older individuals with dysfunctional stress response signaling.
The amount of secreted Pgk1 is sharply decreased in Rtn4al/NogoA-overexpressed muscle cells, leading to various manifestations of neurodegenerative disease, including denervated neuromuscular junction and failed neurite outgrowth of motoneurons.