A5059199301- RNA modifications and cancer
- Advanced Sensor and Energy Harvesting Materials
- RNA and protein synthesis mechanisms
- Autophagy in Disease and Therapy
- Neuroscience and Neuropharmacology Research
- Ubiquitin and proteasome pathways
- Memory and Neural Mechanisms
- Cancer-related molecular mechanisms research
- Corneal Surgery and Treatments
- Cholinesterase and Neurodegenerative Diseases
- Amyotrophic Lateral Sclerosis Research
- Mitochondrial Function and Pathology
- Epigenetics and DNA Methylation
- Neuroendocrine regulation and behavior
- NF-κB Signaling Pathways
- Conducting polymers and applications
- Neuroscience and Neural Engineering
- Cancer-related gene regulation
- Receptor Mechanisms and Signaling
- Alzheimer's disease research and treatments
SUNY Upstate Medical University
2019-2025
Neurological Surgery
2015
Cleveland Clinic
2015
The Neurological Institute
2015
Abstract Epitranscriptomic mechanisms linking tRNA function and the brain proteome to cognition complex behaviors are not well described. Here, we report bi-directional changes in depression-related after genetic disruption of neuronal cytosine methylation, including conditional ablation transgene-derived overexpression Nsun2 mouse prefrontal cortex (PFC). Neuronal Nsun2-deficiency was associated with a decrease m 5 C levels, resulting deficits expression 70% Gly isodecoders. Altogether,...
The infralimbic (IL) subregion of the prefrontal cortex (PFC), via its descending projection to nucleus accumbens (NAc), inhibits cue-induced drug seeking and reinstatement, but underlying mechanisms are not fully understood. Here we show that intrinsic membrane excitability IL layer 5 pyramidal neurons projecting NAc shell (IL-NAcSh neurons) suppresses cocaine-associated memories. Following repeated cocaine exposures in a conditioned place preference paradigm, IL-NAcSh anatomically traced...
ABSTRACT The lysine-63 deubiquitinase cylindromatosis (CYLD) is long recognized as a tumor suppressor in immunity and inflammation its loss-of-function mutations lead to familial cylindromatosis. However, recent studies reveal that CYLD enriched mammalian brain postsynaptic densities, gain-of-function mutation causes frontotemporal dementia (FTD), suggesting critical roles at excitatory synapses. Here we report drives synapse elimination weakening by acting on the Akt-mTOR-autophagy axis....