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Claire Bar on Muck Rack

Claire Bar

As seen in: Wiley Online Library, BioRxiv
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Articles

kcnb1 loss of function in zebrafish causes neurodevelopmental and epileptic disorders associated with γ‐aminobutyric acid dysregulation

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By Lauralee Robichon, Institut Imagine, Claire Bar
| Wiley Online Library Verified
kcnb1 is expressed in specific cell subtypes and in various regions of the central nervous system in WT larval zebrafish. Brain anatomy and neuronal circuits are not disrupted in the kcnb1 lossoffunction zebrafish model. Loss of kcnb1 leads to altered behavioral phenotype, and light- and sound-induced locomotor impairments. kcnb1 knockout zebrafish larvae exhibit elevated locomotor sensitivity to PTZ and increased expression of epileptogenesis-related genes.
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kcnb1 loss-of-function in zebrafish causes neurodevelopmental and epileptic disorders associated with GABA dysregulation

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By Lauralee Robichon, Claire Bar, Anca Marian, Lisa Lehmann
| BioRxiv
Abstract Objective: KCNB1 encodes an α-subunit of the delayed-rectifier voltage-dependent potassium channel Kv2.1. De novo pathogenic variants of KCNB1 have been linked to developmental and epileptic encephalopathies (DEE), diagnosed in early childhood and sharing limited treatment options. Loss-of-function (LOF) of KCNB1 with dominant negative effects has been proposed as the pathogenic mechanism in these disorders.
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Functional assessment of a kcnb1 knock-out zebrafish to model KCNB1-related neurodevelopmental and epileptic disorders

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By Lauralee Robichon, Claire Bar, Anca Marian, Lisa Lehmann
| BioRxiv
Abstract KCNB1 encodes the Kv2.1 potassium channel alpha subunit. De novo pathogenic variants of KCNB1 with loss-of-function (LOF) properties have been associated with neurodevelopmental and epileptic disorders (DEE) diagnosed in early childhood. The study aims to characterize a knock-out (KO) zebrafish line targeting kcnb1 (kcnb1+/- and kcnb1-/-).
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