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http://purl.uniprot.org/citations/16524385http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16524385http://www.w3.org/2000/01/rdf-schema#comment"Calpains represent a superfamily of Ca2+-activated cysteine-proteases, which are important mediators of apoptosis and necrosis. In the brain, m-calpain and micro-calpain, the two ubiquitous calpain-isoforms, are strongly activated in neurones after an excitotoxic Ca2+ influx occurring, for example, during cerebral ischemia. Because oestrogen and its receptors (ERalpha/ERbeta) can exert neuroprotective activity, we investigated their influence on expression of calpains and their endogenous inhibitor, calpastatin. We found that ectopic expression of ERalpha in human neuroblastoma SK-N-MC cells led to a ligand-independent constitutive down-regulation of m-calpain accompanied by an up-regulation of micro-calpain expression. Up-regulation of micro-calpain was reversed in the presence of oestrogen, which, in turn, could be blocked by co-treatment with the oestrogen-receptor antagonist ICI 182,780. Expression of calpastatin was not altered, either in the absence or in the presence of oestrogen. Additional studies revealed that ERalpha-expressing cells exhibited decreased calpain enzymatic activity and increased survival when cells were exposed to the Ca2+ ionophore, ionomycin. Since all investigated effects could be observed exclusively in the presence of ERalpha, but not ERbeta, and since the effects are reduced when ERalpha and ERbeta are co-expressed, our data suggest a novel ER subtype-specific neuroprotective action by repressing calpain expression and calpain activity under conditions of a massive Ca2+ influx."xsd:string
http://purl.uniprot.org/citations/16524385http://purl.org/dc/terms/identifier"doi:10.1111/j.1471-4159.2006.03675.x"xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/author"Behl C."xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/author"Manthey D."xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/author"Gamerdinger M."xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/name"J Neurochem"xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/pages"57-68"xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/title"Oestrogen receptor subtype-specific repression of calpain expression and calpain enzymatic activity in neuronal cells--implications for neuroprotection against Ca-mediated excitotoxicity."xsd:string
http://purl.uniprot.org/citations/16524385http://purl.uniprot.org/core/volume"97"xsd:string
http://purl.uniprot.org/citations/16524385http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16524385
http://purl.uniprot.org/citations/16524385http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16524385
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http://purl.uniprot.org/uniprot/#_A0A125SXW2-mappedCitation-16524385http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16524385
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http://purl.uniprot.org/uniprot/#_A0A125SXV7-mappedCitation-16524385http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16524385