Browse the latest research summaries in the field of genetics for spinal cord injury patients and caregivers.
Showing 1,451-1,460 of 1,773 results
CHANNELS, 2018 • May 22, 2018
This study investigates the role of a conserved negatively charged residue (D4) in the voltage-sensing domain IV (VSD IV) of CaV1.2 and CaV1.3 calcium channels, focusing on its impact on channel gatin...
KEY FINDING: In both CaV1.3 and CaV1.2 channels, a mutation neutralizing the D4 charge (D4N) in voltage-sensing domain IV (VSD IV) resulted in a right-shift of the voltage-dependence of activation by approximately 5 mV.
Nature, 2018 • August 1, 2018
This study elucidates a unifying mechanism for small-molecule enhancers of oligodendrocyte formation: the elevation of 8,9-unsaturated sterol intermediate levels via inhibition of cholesterol biosynth...
KEY FINDING: A broad range of pro-myelinating small molecules function by directly inhibiting CYP51, TM7SF2, or EBP, enzymes within the cholesterol biosynthesis pathway.
Nat Cell Biol, 2018 • August 1, 2018
This study reveals a previously unappreciated function of FAPs as a source of pro-atrophic and pro-fibrotic signals in denervated muscles, particularly due to the aberrant activation of IL6-STAT3 sign...
KEY FINDING: Denervation leads to the accumulation of FAPs in skeletal muscles, without a corresponding increase in macrophages or muscle stem cells.
The Journal of Neuroscience, 2018 • August 29, 2018
The study identifies PRMT8 as a key regulator of stress tolerance in spinal cord motoneurons. PRMT8 maintains ADMA levels, protecting against age-related DNA damage and promoting cell survival. Loss o...
KEY FINDING: Spinal cord motoneurons exhibit high levels of asymmetric dimethyl arginines (ADMAs), providing protection against environmental stress.
Mol Cell Neurosci, 2018 • October 1, 2018
This study investigates the genomic locations bound by Jun in DRG neurons following a peripheral axotomy, observing that the majority of Jun’s injury-responsive binding sites are on putative enhancer ...
KEY FINDING: The majority of Jun's injury-responsive changes in DNA binding occur at putative enhancer elements, not proximal to transcription start sites.
MethodsX, 2018 • March 14, 2018
The presented method combines genotyping and phenotype analyses of mutant zebrafish larvae from heterozygous incrosses. The procedure involves genotyping the larval tail after transection and performin...
KEY FINDING: The method allows for both genotyping and phenotype analyses of mutant zebrafish larvae from heterozygous zebrafish incrosses.
British Journal of Dermatology, 2019 • January 1, 2019
This study presents an ex vivo RNA trans-splicing-based therapeutic approach to correct the phenotype of generalized severe epidermolysis bullosa simplex (EBS-gen sev). The researchers stably transduc...
KEY FINDING: Transplanted skin equivalents generated from trans-splicing-corrected patient keratinocytes showed a stable and blister-free epidermis.
PNAS, 2018 • August 13, 2018
This study investigates the divergent tail regeneration outcomes in lizards and salamanders, focusing on the role of neural stem cells (NSCs) in the spinal cords of regenerated tails. The research rev...
KEY FINDING: Salamander NSCs can differentiate into multiple neural lineages, while lizard NSCs are restricted and primarily form astrocytes.
Neural Regeneration Research, 2018 • August 1, 2018
This study examined the impact of matrix metalloproteinase (MMP) inhibition on macrophage migration and spinal function recovery in rats with completely transected spinal cords treated with fibroblast...
KEY FINDING: MMP-9, but not MMP-2, was upregulated in the graft area of rats treated with fibroblast growth factor-1 and peripheral nerve grafts, suggesting a role in the regenerative process.
Neural Regen Res, 2018 • June 1, 2018
This study investigates the analgesic effect of AG490 on oxaliplatin-induced acute neuropathic pain in rats. The findings demonstrate that AG490 attenuates oxaliplatin-induced acute neuropathic pain b...
KEY FINDING: AG490 treatment significantly increased paw withdrawal threshold and tail withdrawal latency in rats with oxaliplatin-induced neuropathic pain, indicating reduced sensitivity to mechanical and cold stimuli.