CO) announced on Wednesday that a manuscript reporting the Phase II trial results for arimoclomol in patients with
SOD1 Amyotrophic Lateral Sclerosis (ALS) was published in the peer-reviewed clinical journal Neurology.
We have come a long way since the first ALS pathogenic gene
SOD1 was discovered 20 years ago.
A copper or zinc deficiency reduces the function and activity of the
SOD1 enzyme.
Rheumatoid arthritis, rs2070424,
SOD1 A/G polymorphism, Metals, Minerals.
Therefore, the amounts of caspase-3, PARP-1, APP, BACE, ADAM-10,
SOD1, CAT, GR and GPx transcripts in the other samples (from quercetin- or rutin-treated cells) were assigned dimensionless numbers relative to the levels in the calibrator sample.
Nrf2 as a basic leucine zipper transcription factor protects the cell against oxidative stress through antioxidant response elements-mediated induction of several phase 2 detoxifying and anti-oxidant enzymes, including the HO-1, GPX1, and
SOD1 (Cho et al.
In this study we characterized the complete sequence of the
SOD1 gene from an animal representing the Murrah breed of the river buffalo (Bubalus bubalis) and we compared its coding sequence and the amino acid sequence with its homologous from others mammals.
Modeling ALS with iPSCs Reveals that Mutant
SOD1 Misregulates Neurofilament Balance in Motor Neurons.
These inclusions generally contain ubiquitin, and often incorporate one of the ALS-associated proteins such as
SOD1, TAR DNA binding protein (TDP-43, or TARDBP) or FUS.
The big problem in ALS is that there are more than a hundred mutations in dozens of genes that all cause the disease, but almost all of the therapeutics that have gone forward in the clinic have done so for just one of those mutations,
SOD1, which almost everyone studies in mice," said Eggan.
Interestingly, MARCH5 could only interact with mSOD1 not wild type
SOD1, and this interaction led to enhanced ubiquitination of mSOD1, in a manner that depended on the E3 ubiquitin ligase activity of MARCH5.
TDP-43 immunoreactivity in neuronal inclusions in familial amyotrophic lateral sclerosis with or without
SOD1 gene mutation.
ALS - thickening of tissue in the motor tracts of the lateral columns and anterior horns of the spinal cord; results in progressive muscle atrophy that starts in the limbs