CWRU the daily: Findings may lead to clues for possible treatments for autism spectrum disorders and schizophrenia
Congratulations to Xinrui Zhang from Deneris lab on her NIH NRSA F30 Predoctoral Fellowship!
Recessive loss of function mutations in the FEV (Pet1) gene discovered in autism spectrum disorder cases.
Congratulations to Polyxeni Philippidou for her new NIH R01 Award!
Our Own Heather Broihier Earns the National Institutes of Health Landis Award for Outstanding Mentorship!
Dr. Peng Zhang will join us as a new Assistant Professor in April 2020!
Dr. Masashi Tabuchi will join us as a new Assistant Professor in January 2020!
Todd Pressler, PhD
Thursday, January 23, 2020, 12:10 pm, BRB 105
Lecture Title: "Synaptic organization of inhibitory circuits in the olfactory bulb"
Spencer, Clay, PhD
Thursday, January 30, 2020, 12:10 pm, BRB 105
Lecture Title: "Functional genomic analysis of Serotonin neuron maturation"
Sujata Rao, PhD
Thursday, February 6, 2020, 12:10 pm, BRB 105
Lecture Title: "Functional genomic analysis of Serotonin neuron maturation"
It has long been known that proteins are important in maintaining synapses, but the mechanism by which they do so has remained elusive. In a study in Drosophila neuromuscular junction the laboratory of Dr. Heather Broihier has found that α2δ-3 protein provides an extracellular scaffold for an autocrine Bone Morphogenetic Protein signal that can help to maintain synaptic density, structure and function.
Nature Communications,10, 5575 (2019)
Everyone hates taking out the trash, but we do it because we can’t function properly if we don't. It turns out that the same is true of the brain. Cullin 3 is a core component of an E3 ubiquitin ligase responsible for clearance of a cell's proteins. Mutations in the gene that encodes for it, CUL3, have been associated with Autism Spectrum Disorders (ASD), and Schizophrenia (SCZ), but the mechanism of CUL3 mutation has been elusive. Researchers in the Mei lab have just elucidated the mechanism of the CUL3 mutation, and shown the impact it has on social interactions.
Neuromuscular junction is a synapse between motoneurons and skeletal muscles to control muscle contraction. Underlying mechanisms of NMJ formation was not well understood. Through studying mutant gene, Rapsyn, implicated in congenital myasthenic syndrome (CMS), the Mei lab uncovered a novel signaling pathway by which Agrin-LRP4-MuSK induces tyrosine phosphorylation of Rapsyn, which is required for its self-association and E3 ligase activity.
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