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Oxidative stress leads to the translocation of Rab5 from endosome to mitochondria, regulated by ALS/Alsin, a component associated with amyotrophic lateral sclerosis, leading to mitochondrial-endosomal physical contacts and a cytoprotective response.

The projections from discrete areas to motor cortex increase over disease course in motoneuron disease model with selective spatial and temporal patterns.

The AAA-ATPase VCP sustains sarcoplasmic proteostasis, in part, by controlling autophagosome-lysosome fusion and the integrity of a dynamic tubular lysosomal network.

In the SOD1^G93A mouse model of amyotrophic lateral sclerosis (ALS), expression of transmembrane signaling molecule ephrinB2 in spinal cord astrocytes contributes to motor neuron damage and loss of diaphragm function.

SERBP1 is associate with protein complexes regulating splicing, cell division, and ribosomal biogenesis that likely depend on G quadruplex (G4) binding and polyADP-ribosylation (PARylation) for their assembly and function.

microRNA-1 plays an essential role in the development and functioning of the heart by ensuring that genes for striated, rather than smooth, muscle are expressed there.

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.

How do the metal cofactors present in the protein SOD1 collaborate with the interacting membrane to define the role of this protein in the disease ALS?

Protein aggregates resulting from mutations in C9orf72 impair different aspects of cellular quality control in the cytosol and the nucleus, but mRNA-mediated effects contribute more strongly to toxicity.

An easy-to-implement antibody validation pipeline addresses the reproducibility crisis resulting from the use of non-specific antibodies.