Deciphering cellular and molecular mechanisms of synaptic function and impact on neuronal circuit output. Viral vector development and CNS gene therapy.
Iowa City, IA
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Amazing findings !!
Congrats you and the team
Delighted to share our new Nature paper: rdcu.be/dNlMQ
This works shows a surprising off-target effect of glutamate on another cell death channel, acid sensing ion channels (ASICs). It turns out that glutamate directly binds to ASICs as a positive allosteric modulator
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Love cellular and molecular neuro. We are hiring a staff scientist interested in building framework of molecular principles for accurate sound information encoding and contribution to auditory deficits.
unc.peopleadmin.com/hr/posti…
Must have background in patch clamp
DM or email
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Big news. We are moving.
I have officially started as the Director of the Gene Therapy Center, and as a Professor of Pediatrics and Professor of Pharmacology at UNC-Chapel Hill. I am returning “home” to lead the Center where I earned my PhD.
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I will always treasure my time in the Department and at the U. Amazing colleagues and research environment. It is extremely difficult to say goodbye. Once a Hawkeye always a Hawkeye.
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Finally, I want to thank Dr. Emre Kul, Uchechi Okorafor @MissSafie and the rest of the team for taking on this immense challenge to solve a fundamental problem in the gene therapy field.
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We thank @FamilieSCN2A @scn2agene @cacna1a @ncats_nih_gov @NIH_NINDS @NIDCD @uihealthcare @uiowaOUR funding this research We thank @UIowaACB @UIowaNeuro @UIowaResearch for creating an amazing environment for carrying out high risk high reward research
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Since Ad vector transduction properties are dependent on their capsid proteins, these chimeric 1st generation Ad vectors open new avenues for high capacity helper-dependent adenovirus (HdAd) gene therapy approaches for cerebellar disorders and multiple neurological disorders.
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Using a “humanized” hCD46 mouse model, we demonstrate these Ad vectors transduce cerebellar cell-types, including Purkinje cells, that are refractory to Ad5 transduction.
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Therefore, to overcome the current limitations of Ad vectors to treat CNS disorders, we created chimeric 1st generation Ad vectors that utilize the hCD46 receptor.
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However, these Ad5 vectors are unable to transduce many neuronal cell types that are dysfunctional in many CNS disorders. The human CD46 (hCD46) receptor is widely expressed throughout the human CNS and is the primary attachment receptor for many Ad serotypes.
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Adenoviral vectors (Ad) have tremendous potential for CNS gene therapy approaches. Currently, the most common vectors utilize the Group C Ad5 serotype capsid proteins, which rely on the Coxsackievirus-Adenovirus receptor (CAR) to infect cells.
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Viral vector gene therapy has immense promise for treating central nervous system (CNS) disorders. Although adeno-associated virus vectors (AAV) have had success, their small packaging capacity limit their utility to treat the root cause of many CNS disorders.
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For ~25 years Ad vectors had little to no ability to transduce Purkinje cells, until now! Excited to announce our paper in MTMCD @MolTherapy on the development of Ad vectors that transduce Purkinje cells in a humanized mouse model shorturl.at/wyBW5
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We are cranking away to get at this code that determine tpresynaptic Cav2 subtype specificity as it is a the keystone that determines how neuronal circuits transmit information in health and disease
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The CaV2 α1 subunit motifs determining the presynaptic CaV2 preference are distinct from abundance.
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The CaV2.3 α1 subunit cytoplasmic C-terminus negatively regulates presynaptic CaV2 subtype abundance but not preference, whereas the CaV2.2 α1 subunit cytoplasmic C-terminus is not a key regulator of presynaptic CaV2 subtype abundance or preference.
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