T. Hark

发表

Pulse-Chase Proteomics of the App Knockin Mouse Models of Alzheimer's Disease Reveals that Synaptic Dysfunction Originates in Presynaptic Terminals.

E. O'Toole, M. Stowell, Charlotte Castillon, 2020, Cell systems.

NAAG peptidase inhibitors block cognitive deficit induced by MK-801 and motor activation induced by d-amphetamine in animal models of schizophrenia

J. Neale, T. Bzdȩga, C. Profaci, 2012, Translational Psychiatry.

Long-lived mitochondrial cristae proteins in mouse heart and brain

J. Savas, Ewa Bomba-Warczak, S. Edassery, 2021, The Journal of cell biology.

Using stable isotope labeling to advance our understanding of Alzheimer’s disease etiology and pathology

J. Savas, T. Hark, 2021, Journal of neurochemistry.

Sex-Dependent Effects of Chronic Microdrive Implantation on Acquisition of Trace Eyeblink Conditioning

J. Disterhoft, J. Power, J. Savas, 2021, Neurobiology of Learning and Memory.

NAAG Peptidase Inhibitors Act via mGluR3: Animal Models of Memory, Alzheimer’s, and Ethanol Intoxication

J. Neale, T. Bzdȩga, C. Moussa, 2017, Neurochemical Research.

Amyloid accumulation drives proteome-wide alterations in mouse models of Alzheimer’s disease like pathology

Daniel B. McClatchy, J. Yates, Anirvan Ghosh, 2017, bioRxiv.

Analysis of proteome-wide degradation dynamics in ALS SOD1 iPSC-derived patient neurons reveals disrupted VCP homeostasis

E. Kiskinis, J. Gilthorpe, S. Edassery, 2023, Cell reports.

Pulse-chase proteomics of the App Knock-In mouse models of Alzheimer’s disease reveals synaptic dysfunction originates in presynaptic terminals

Charlotte Castillon, M. Steinhauser, Samuel N. Smukowski, 2021 .