salubrinal and Stroke

salubrinal has been researched along with Stroke* in 2 studies

Other Studies

2 other study(ies) available for salubrinal and Stroke

Article	Year
PERK (Protein Kinase RNA-Like ER Kinase) Branch of the Unfolded Protein Response Confers Neuroprotection in Ischemic Stroke by Suppressing Protein Synthesis. Stroke, 2020, Volume: 51, Issue:5 Background and Purpose- Ischemic stroke impairs endoplasmic reticulum (ER) function, causes ER stress, and activates the unfolded protein response. The unfolded protein response consists of 3 branches controlled by ER stress sensor proteins, which include PERK (protein kinase RNA-like ER kinase). Activated PERK phosphorylates eIF2α (eukaryotic initiation factor 2 alpha), resulting in inhibition of global protein synthesis. Here, we aimed to clarify the role of the PERK unfolded protein response branch in stroke. Methods- Neuron-specific and tamoxifen-inducible PERK conditional knockout (cKO) mice were generated by cross-breeding Camk2a-CreERT2 with Topics: Animals; Brain Ischemia; Cinnamates; eIF-2 Kinase; Endoplasmic Reticulum Stress; Eukaryotic Initiation Factor-2; Infarction, Middle Cerebral Artery; Mice; Mice, Knockout; Neurons; Neuroprotection; Phosphorylation; Protein Biosynthesis; Stroke; Thiourea; Unfolded Protein Response	2020
Small molecule SUMOylation activators are novel neuroprotective agents. Bioorganic & medicinal chemistry letters, 2018, 02-01, Volume: 28, Issue:3 Neuronal loss characterizes many of the most intractable nervous system diseases that deprive our ageing population of their quality of life. Neuroprotective pharmacological modalities are urgently needed to address this burgeoning population. Small ubiquitin-like modifier (SUMO) conjugation has been established as an endogenous neuroprotective response, and we have discovered several classes of small molecules that enhance SUMO conjugation. Herein we describe the hit to lead campaign that enabled the discovery of 3 diverse classes of drug-like SUMOylation activators. Optimized compounds were ultimately validated in cell-based models of neuronal loss and provide a foundation for establishing systemically active SUMO activators to treat degenerative diseases such as Parkinson's disease, Alzheimer's disease, and stroke. Topics: Alzheimer Disease; Benzothiazoles; Dose-Response Relationship, Drug; HEK293 Cells; Humans; Molecular Structure; Neuroprotective Agents; Parkinson Disease; Quinolines; Small Molecule Libraries; Small Ubiquitin-Related Modifier Proteins; Stroke; Structure-Activity Relationship; Sumoylation; Thiazoles	2018

Article

Year

PERK (Protein Kinase RNA-Like ER Kinase) Branch of the Unfolded Protein Response Confers Neuroprotection in Ischemic Stroke by Suppressing Protein Synthesis.

Stroke, 2020, Volume: 51, Issue:5

Background and Purpose- Ischemic stroke impairs endoplasmic reticulum (ER) function, causes ER stress, and activates the unfolded protein response. The unfolded protein response consists of 3 branches controlled by ER stress sensor proteins, which include PERK (protein kinase RNA-like ER kinase). Activated PERK phosphorylates eIF2α (eukaryotic initiation factor 2 alpha), resulting in inhibition of global protein synthesis. Here, we aimed to clarify the role of the PERK unfolded protein response branch in stroke. Methods- Neuron-specific and tamoxifen-inducible PERK conditional knockout (cKO) mice were generated by cross-breeding Camk2a-CreERT2 with

Topics: Animals; Brain Ischemia; Cinnamates; eIF-2 Kinase; Endoplasmic Reticulum Stress; Eukaryotic Initiation Factor-2; Infarction, Middle Cerebral Artery; Mice; Mice, Knockout; Neurons; Neuroprotection; Phosphorylation; Protein Biosynthesis; Stroke; Thiourea; Unfolded Protein Response

2020

Small molecule SUMOylation activators are novel neuroprotective agents.

Bioorganic & medicinal chemistry letters, 2018, 02-01, Volume: 28, Issue:3

Neuronal loss characterizes many of the most intractable nervous system diseases that deprive our ageing population of their quality of life. Neuroprotective pharmacological modalities are urgently needed to address this burgeoning population. Small ubiquitin-like modifier (SUMO) conjugation has been established as an endogenous neuroprotective response, and we have discovered several classes of small molecules that enhance SUMO conjugation. Herein we describe the hit to lead campaign that enabled the discovery of 3 diverse classes of drug-like SUMOylation activators. Optimized compounds were ultimately validated in cell-based models of neuronal loss and provide a foundation for establishing systemically active SUMO activators to treat degenerative diseases such as Parkinson's disease, Alzheimer's disease, and stroke.

Topics: Alzheimer Disease; Benzothiazoles; Dose-Response Relationship, Drug; HEK293 Cells; Humans; Molecular Structure; Neuroprotective Agents; Parkinson Disease; Quinolines; Small Molecule Libraries; Small Ubiquitin-Related Modifier Proteins; Stroke; Structure-Activity Relationship; Sumoylation; Thiazoles

2018