IndraLab

Statements

REST inhibits HCN1. 7 / 7
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"This phenomenon might be partly due to REST mediated transcriptional repression of Hcn1 56."
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"While in simple neural culture systems this may be the case, in animal models where REST/NRSF expression varies by age, brain region, and cell type, the role of REST/NRSF in the pathology of seizures and epilepsy becomes more complex, as demonstrated in studies where seizure-induced REST activation triggers a reduction in HCN1 channels that is associated with the generation of unprovoked seizures and memory defects in animal models of epilepsy."
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"Indeed, a common regulatory mechanism consisting of an increase in the expression of the repressor NRSF and REST (Neuron Restrictive Silencer Factor), that potently represses HCN1 and other key neuronal genes, might exist in these scenarios."
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"Further studies showed that if the combination of REST and HCN1 promoter was blocked, which prevented inhibition of HCN1 by REST, the excitability of dendrites can be maintained at normal levels [24,25]."
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"This hypothesis may also explain the clinical phenomenon that among drug-resistant mesial temporal lobe epilepsy patients, hippocampal REST/NRSF level is proportional to seizure frequency, where epilepsy-inducing insults may precipitate seizures as REST/NRSF, at a higher level, represses hcn1 to a larger extent (Navarrete-Modesto et al., 2019)."
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"NRSF dependent downregulation of HCN1 in vitro."
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"NRSF can also repress the genes HCN1 and KCC2, which can regulate neural activity through ion channels."
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