A5101553260- Biotin and Related Studies
- Neuroscience and Neuropharmacology Research
- Advanced Biosensing Techniques and Applications
- Bioinformatics and Genomic Networks
- Alzheimer's disease research and treatments
- Epigenetics and DNA Methylation
- Mitochondrial Function and Pathology
- RNA modifications and cancer
- Photoreceptor and optogenetics research
- Cancer-related gene regulation
- Neural dynamics and brain function
- Ion channel regulation and function
University of Colorado Anschutz Medical Campus
2019-2020
University of Colorado Denver
2018-2020
DAPK1 binding to GluN2B was prominently reported mediate ischemic cell death in vivo. and CaMKII bind the same region, their is mutually exclusive. Here, we show that mutating region on (L1298A/R1300Q) protected against neuronal induced by cardiac arrest followed resuscitation. Importantly, mutation selectively abolished only CaMKII, but not DAPK1, binding. During or excitotoxic insults, further accumulated at excitatory synapses, this accumulation mediated Interestingly, extra-synaptic...
Highlights•FingR intrabodies enabled simultaneous live imaging of three endogenous proteins•Aβ inhibits CaMKII trafficking after LTP-, but not LTD-inducing, stimuli•The Aβ-induced block requires activity•Aβ induced internalization the extrasynaptic, synaptic, NMDA receptorSummaryCaMKIIα is a central mediator bidirectional synaptic plasticity, including long-term potentiation (LTP) and depression (LTD). To study how CaMKIIα movement during plasticity affected by soluble amyloid-β peptide...
Presynaptic α-neurexins are highly expressed and more frequently linked to neuropsychiatric neurodevelopmental disorders than β-neurexins. However, how extracellular sequences specific enable synaptic transmission is poorly understood. We identified a mutation in an region of neurexin-3α (A687T), located conserved among throughout vertebrate evolution, patient diagnosed with profound intellectual disability epilepsy. systematically interrogated this using knockdown-replacement approach,...
Protein interactions at cellular interfaces dictate a multitude of biological outcomes ranging from tissue development and cancer progression to synapse formation maintenance. Many these fundamental occur in trans are typically induced by heterophilic or homophilic between cells expressing membrane anchored binding pairs. Elucidating how disease relevant mutations disrupt protein can provide insight into myriad cell biology fields. protein-protein interaction assays do not disambiguate cis...
Protein interactions at cellular interfaces dictate a multitude of biological outcomes ranging from tissue development and cancer progression to synapse formation maintenance. Many these fundamental occur in trans are typically induced by heterophilic or homophilic between cells expressing membrane anchored binding pairs. Elucidating how disease relevant mutations disrupt protein can provide insight into myriad cell biology fields. protein-protein interaction assays do not disambiguate cis...