O-linked β-N-acetylglucosamine modification of proteins is activated in post-ischemic brains of young but not aged mice: Implications for impaired functional recovery from ischemic stress

Small Ubiquitin-Like Modifier 3–Modified Proteome Regulated by Brain Ischemia in Novel Small Ubiquitin-Like Modifier Transgenic Mice

(2014) Wei Yang et al.   STROKE

Characterization of the Ubiquitin-Modified Proteome Regulated by Transient Forebrain Ischemia

(2013) Masahiro Iwabuchi et al.   JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM

Perfusion of Ischemic Brain in Young and Aged Animals

(2013) Bharti Manwani et al.   STROKE

Reperfusion Rather than Ischemia Drives the Formation of Ubiquitin Aggregates After Middle Cerebral Artery Occlusion

(2012) Karin Hochrainer et al.   STROKE

SUMO2/3 Conjugation is an Endogenous Neuroprotective Mechanism

(2011) Anna Lena Datwyler et al.   JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM

Elevated Global SUMOylation in Ubc9 Transgenic Mice Protects Their Brains against Focal Cerebral Ischemic Damage

(2011) Yang-ja Lee et al.   PLoS One

The role of protein O-linked β-N-acetylglucosamine in mediating cardiac stress responses

(2009) John C. Chatham et al.   BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS

In VivoModulation ofO-GlcNAc Levels Regulates Hippocampal Synaptic Plasticity through Interplay with Phosphorylation

(2008) Melanie K. Tallent et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

New Insights into Metabolic Signaling and Cell Survival: The Role of  -O-Linkage of N-Acetylglucosamine

(2008) G. A. Ngoh et al.   JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS

Stroke Incidence and Survival in the Beginning of the 21st Century in Southern Sweden

(2007) Björn Hallström et al.   STROKE