Matthew C. Weston
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View article: Decomposing SV2A Function and Dysfunction one Neuron at a Time
Decomposing SV2A Function and Dysfunction one Neuron at a Time Open
Synaptic Vesicle Glycoprotein 2A Knockout in Parvalbumin and Somatostatin Interneurons Drives Seizures in the Postnatal Mouse Brain Bartholome O, Neirinckx V, De La Brassinne O, Desloovere J, Van Den Ackerveken P, Raedt R, Rogister B. J Ne…
View article: KCN Channels “Cue” Up GABA Release from Astrocytes
KCN Channels “Cue” Up GABA Release from Astrocytes Open
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View article: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on somatostatin- and parvalbumin-expressing cortical GABAergic neurons
Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on somatostatin- and parvalbumin-expressing cortical GABAergic neurons Open
More than 20 recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (K Na ) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which a…
View article: Author response: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on somatostatin- and parvalbumin-expressing cortical GABAergic neurons
Author response: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on somatostatin- and parvalbumin-expressing cortical GABAergic neurons Open
View article: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons
Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons Open
More than twenty recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (KNa) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which…
View article: Author response: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons
Author response: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons Open
More than twenty recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (KNa) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which…
View article: Effective knockdown-replace gene therapy in a novel mouse model of DNM1 developmental and epileptic encephalopathy
Effective knockdown-replace gene therapy in a novel mouse model of DNM1 developmental and epileptic encephalopathy Open
View article: Author response: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons
Author response: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons Open
More than twenty recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (KNa) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which…
View article: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons
Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons Open
More than twenty recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (KNa) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which…
View article: Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss
Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN , PIK3CA , an…
View article: Author Response: Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss
Author Response: Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss Open
View article: Reviewer #3 (Public Review): Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss
Reviewer #3 (Public Review): Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIK3CA, and …
View article: Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss
Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIK3CA, and …
View article: Reviewer #2 (Public Review): Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss
Reviewer #2 (Public Review): Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIK3CA, and …
View article: Author Response: Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss
Author Response: Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIK3CA, and …
View article: Reviewer #1 (Public Review): Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss
Reviewer #1 (Public Review): Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIK3CA, and …
View article: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on somatostatin- and parvalbumin-expressing cortical GABAergic neurons
Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on somatostatin- and parvalbumin-expressing cortical GABAergic neurons Open
More than 20 recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (K Na ) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which a…
View article: Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons
Heterozygous expression of a Kcnt1 gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons Open
More than twenty recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (KNa) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of which…
View article: Author Response: Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss
Author Response: Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIC3CA, and …
View article: Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss
Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN , PIK3CA , an…
View article: Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss
Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIC3CA, and …
View article: Reviewer #1 (Public Review): Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss
Reviewer #1 (Public Review): Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIC3CA, and …
View article: Reviewer #2 (Public Review): Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss
Reviewer #2 (Public Review): Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIC3CA, and …
View article: Reviewer #3 (Public Review): Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss
Reviewer #3 (Public Review): Hyperactivity of mTORC1 or mTORC2-dependent signaling causes epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN, PIC3CA, and …
View article: Heterozygous expression of a <i>Kcnt1</i> gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons
Heterozygous expression of a <i>Kcnt1</i> gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neurons Open
More than twenty recurrent missense gain-of-function (GOF) mutations have been identified in the sodium-activated potassium (K Na ) channel gene KCNT1 in patients with severe developmental and epileptic encephalopathies (DEEs), most of whi…
View article: Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss
Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss Open
Gene variants that hyperactivate PI3K-mTOR signaling in the brain lead to epilepsy and cortical malformations in humans. Some gene variants associated with these pathologies only hyperactivate mTORC1, but others, such as PTEN , PIK3CA , an…
View article: Distinct Features of Interictal Activity Predict Seizure Localization and Burden in a Mouse Model of Childhood Epilepsy
Distinct Features of Interictal Activity Predict Seizure Localization and Burden in a Mouse Model of Childhood Epilepsy Open
The epileptic brain is distinguished by spontaneous seizures and interictal epileptiform discharges (IEDs). Basic patterns of mesoscale brain activity outside of seizures and IEDs are also frequently disrupted in the epileptic brain and li…
View article: mTORC2 Inhibition Improves Morphological Effects of PTEN Loss, But Does Not Correct Synaptic Dysfunction or Prevent Seizures
mTORC2 Inhibition Improves Morphological Effects of PTEN Loss, But Does Not Correct Synaptic Dysfunction or Prevent Seizures Open
Hyperactivation of PI3K/PTEN-mTOR signaling during neural development is associated with focal cortical dysplasia (FCD), autism, and epilepsy. mTOR can signal through two major hubs, mTORC1 and mTORC2, both of which are hyperactive followi…
View article: Disruption of mTORC1 rescues neuronal overgrowth and synapse function dysregulated by Pten loss
Disruption of mTORC1 rescues neuronal overgrowth and synapse function dysregulated by Pten loss Open
View article: Excess interictal activity marks seizure prone cortical areas and mice in a genetic epilepsy model
Excess interictal activity marks seizure prone cortical areas and mice in a genetic epilepsy model Open
Genetic epilepsies are often caused by variants in widely expressed genes, potentially impacting numerous brain regions and functions. For instance, gain-of-function (GOF) variants in the widely expressed Na + -activated K + channel gene K…