G Guidotti, L Brambilla, D Rossi - Trends in pharmacological sciences, 2017 - cell.com
The presence of cell and tissue barriers together with the low biomembrane permeability of various therapeutics often hampers systemic drug distribution; thus, most of the available …
S Wang, T Dai, Z Qin, T Pan, F Chu, L Lou, L Zhang… - Nature Cell …, 2021 - nature.com
Patients with Coronavirus disease 2019 exhibit low expression of interferon-stimulated genes, contributing to a limited antiviral response. Uncovering the underlying mechanism of …
The accumulation of irreparable cellular damage restricts healthspan after acute stress or natural aging. Senescent cells are thought to impair tissue function, and their genetic …
A Zeke, M Misheva, A Reményi… - … and Molecular Biology …, 2016 - Am Soc Microbiol
The c-Jun N-terminal kinases (JNKs), as members of the mitogen-activated protein kinase (MAPK) family, mediate eukaryotic cell responses to a wide range of abiotic and biotic stress …
Excitotoxicity is classically defined as the neuronal damage caused by the excessive release of glutamate, and subsequent activation of excitatory plasma membrane receptors …
QJ Wu, M Tymianski - Molecular brain, 2018 - Springer
Abstract NMDA (N-methyl-d-aspartate) receptors (NMDARs) play a central role in excitotoxic neuronal death caused by ischemic stroke, but NMDAR channel blockers have failed to be …
Excitotoxicity, the specific type of neurotoxicity mediated by glutamate, may be the missing link between ischemia and neuronal death, and intervening the mechanistic steps that lead …
R Yarza, S Vela, M Solas, MJ Ramirez - Frontiers in pharmacology, 2016 - frontiersin.org
c-Jun N-terminal kinases (JNKs) are a family of protein kinases that play a central role in stress signaling pathways implicated in gene expression, neuronal plasticity, regeneration …
Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members function in a cell context-specific and cell type-specific manner to integrate signals …