Biological Trace Element Research, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 30, 2024
Language: Английский
Biological Trace Element Research, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 30, 2024
Language: Английский
Measurement Food, Journal Year: 2024, Volume and Issue: 15, P. 100195 - 100195
Published: Aug. 28, 2024
Language: Английский
Citations
13Neurochemical Research, Journal Year: 2025, Volume and Issue: 50(2)
Published: Feb. 10, 2025
Language: Английский
Citations
1Cytokine & Growth Factor Reviews, Journal Year: 2025, Volume and Issue: unknown
Published: March 1, 2025
Language: Английский
Citations
1Trends in Neurosciences, Journal Year: 2024, Volume and Issue: 47(9), P. 677 - 692
Published: Aug. 10, 2024
Traumatic brain injury (TBI) is a complex condition that can resolve over time but all too often leads to persistent symptoms, and the risk of poor patient outcomes increases with aging. TBI damages neurons long axons within white matter tracts are critical for communication between regions; this causes slowed information processing neuronal circuit dysfunction. This review focuses on after multifactorial processes underlie damage, potential recovery, progression degeneration. A multiscale perspective across clinical preclinical advances presented encourage interdisciplinary insights from whole-brain neuroimaging down cellular molecular responses axons, myelin, glial cells tissue.
Language: Английский
Citations
5Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown
Published: Dec. 23, 2024
Language: Английский
Citations
4bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 13, 2025
Abstract N-methyl-D-aspartate receptors (NMDARs) are essential for excitatory neurotransmission and their pathogenic variants can lead to proteostasis defects thus neurological diseases. However, how the network degrades is not well understood. Here, we demonstrated that R519Q GluN2B variant retained in endoplasmic reticulum (ER) fails traffic surface form functional NMDARs. Pharmacological genetic inhibition of autophagy results accumulation this variant, indicating it degraded by autophagy-lysosomal proteolysis pathway. Since has a cytosolic LIR motif, which interact with machinery, disrupting motif impairs autophagic clearance variant. Additionally, recognized ER-phagy receptors, including CCPG1 RTN3L. Our result provides molecular mechanism degradation NMDAR identifies pathway targeted therapeutic intervention disorders dysfunctional Summary NMDA Benske et al. report predispose subunits
Language: Английский
Citations
0Biomolecules and Biomedicine, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 21, 2025
HEK293T cells are extensively utilized for therapeutic protein production due to their human origin, which enables accurate post-translational modifications. This study aimed enhance membrane in by knocking out the ATF4 gene using CRISPR-Cas9 technology. The was edited infecting with a lentivirus carrying optimized single-guide RNA (ATF4-KO-3) and Cas9 genes. Comparative evaluations were conducted all-in-one two-vector systems. Genome sequencing productivity of ATF4-knockout (KO) compared wild-type (WT) next-generation (NGS) isolation kit, respectively. Single-cell analysis confirmed editing patterns, NGS verifying intended deletions. Membrane also assessed indirectly via flow cytometry, analyzing expressing Membrane-GFP. Compared WT cells, ATF4-KO exhibited significant increase production, 52.2 ± 19.0% improvement. Gene efficiency between two delivery systems, system demonstrating higher based on T7 endonuclease I assays. Western blot suppression increased expression proteins, including E-cadherin CD63. Quantitative PAGE revealed 77.2 30.6% purified yields, consistent observed enhancements. Flow cytometry Membrane-GFP further demonstrated 22.9 9.7% productivity. In summary, knockout significantly enhances offering potential improvements biopharmaceutical manufacturing enabling more efficient synthesis.
Language: Английский
Citations
0International Immunopharmacology, Journal Year: 2025, Volume and Issue: 149, P. 114150 - 114150
Published: Feb. 3, 2025
Language: Английский
Citations
0Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 20, 2025
Language: Английский
Citations
0NeuroToxicology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
0