epilepsy/protease

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Activation of CPP-32 protease in hippocampal neurons following ischemia and epilepsy.

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Recent in vitro studies indicate an involvement of members of the interleukin-1beta converting enzyme (ICE) family of proteases in programmed neuronal cell death. Cell death of hippocampal neurons in animal models of cerebral ischemia and epilepsy shows morphological features of apoptosis and can be

The epilepsy, the protease inhibitor and the dodecamer: progressive myoclonus epilepsy, cystatin b and a 12-mer repeat expansion.

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Progressive myoclonus epilepsy 1 (EPM1) or Unverricht-Lundborg disease is a human autosomal recessive neurodegenerative disorder caused by mutations in cystatin B (CSTB). The CSTB gene maps to human chromosome 21 and encodes an inhibitor of lysosomal cysteine proteases. Five point mutations have

Extracellular proteases in epilepsy.

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During the last decade, multiple data have been obtained, pointing to an involvement of extracellular, including extrasynaptic, proteolysis in epilepsy pathogenesis. The most productive avenues of investigations have been analyses of seizure-evoked gene and protein expression patterns, both

The serine protease subtilisin suppresses epileptiform activity in rat hippocampal slices and neocortex in vivo.

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Serine proteases of the S8A family and those belonging to the subtilase group generate a long-lasting inhibition of hippocampal evoked potentials, which shows little recovery and resembles long-term depression. The present work investigates the effects of subtilisin A on epileptiform activity

Post Stroke Seizures and Epilepsy: From Proteases to Maladaptive Plasticity.

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Post stroke epilepsy (PSE) is the most common cause of seizures in the elderly, yet its underlying mechanism is poorly understood. The classification of PSE is confusing, and there is neither a clear agreement on its incidence and prognosis nor a consensus about specific treatments. The diagnosis of

Cystatin C, a cysteine protease inhibitor, is persistently up-regulated in neurons and glia in a rat model for mesial temporal lobe epilepsy.

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Cystatin C (CSTC), a cysteine protease inhibitor, has been implicated in the processes of neuronal degeneration and repair of the nervous system. Using serial analysis of gene expression (SAGE), we recently identified CSTC as one of the genes that are overexpressed after electrically induced status

Blockade of neuropsin, a serine protease, ameliorates kindling epilepsy.

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The behavioural and electrographical abnormalities associated with seizures in epileptic (kindled) mice correspond with those of human epilepsy. In kindled mice, neuropsin was markedly increased in the hippocampus and cerebral cortices. A single intraventricular injection of monoclonal antibodies

Degrading epilepsy: the role of extracellular proteases and the extracellular matrix.

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Epilepsy. Protease inhibitor implicated.

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Impact of protease inhibitor substitution with efavirenz in HIV-infected children: results of the First Pediatric Switch Study.

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OBJECTIVE Simplification of antiretroviral regimen in human immunodeficiency virus (HIV)-infected children has not yet been investigated. In general, children have a more difficult time maintaining viral suppression because of many factors, including frequent nonadherence and less availability of

Anti-HIV-1 activity, protease inhibition and safety profile of extracts prepared from Rhus parviflora.

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BACKGROUND In the present study, extracts prepared from the leaves of Rhus parviflora Roxb. (Anacardiaceae) were evaluated for their anti-HIV activity, which have been traditionally used for the treatment of neurological disorders such as anxiety, insomnia and epilepsy. METHODS Aqueous and 50%

Three-dimensional reconstruction of the S885A mutant of human mitochondrial Lon protease.

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The Lon protein is a protease belonging to the superfamily of ATPases associated with diverse cellular activities (AAA+). Its main function is the control of protein quality and the maintenance of proteostasis by degradation of misfolded and damaged proteins, which occur in response to numerous

[Kallikrein-family serine protease in the central nervous system].

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Serine proteases exert a variety of functions under physiological and pathological conditions. Tissue plasminogen activator (tPA) is expressed widely in the central nervous system (CNS) and play important roles in development, synaptic plasticity and neuronal cell death. In addition to this

New insights into the molecular basis of progressive myoclonus epilepsy: a multiprotein complex with cystatin B.

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Cystatin B is an anti-proteolytic polypeptide implicated in progressive myoclonus epilepsy (EPM1), a degenerative disease of the central nervous system. The knock-out mouse model of the disease shows apoptosis of the cerebellar granule cells. We have identified five recombinant proteins interacting

Nuclear localization of cystatin B, the cathepsin inhibitor implicated in myoclonus epilepsy (EPM1).

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Cystatin B is an anti-protease implicated in myoclonus epilepsy, a degenerative disease of the central nervous system. In vitro, cystatin B interacts with and inhibits proteases of the cathepsin family. Confocal microscopy analysis of the subcellular localization of cystatin B and cathepsin B shows

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