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http://purl.uniprot.org/citations/22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22552281http://www.w3.org/2000/01/rdf-schema#comment"Ca²⁺ transfer from endoplasmic reticulum (ER) to mitochondria can trigger apoptotic pathways by inducing release of mitochondrial pro-apoptotic factors. Three different types of inositol 1,4,5-trisphosphate receptor (IP₃R) serve to discharge Ca²⁺ from ER, but possess some peculiarities, especially in apoptosis induction. The anti-apoptotic protein Akt can phosphorylate all IP₃R isoforms and protect cells from apoptosis, reducing ER Ca²⁺ release. However, it has not been elucidated which IP₃R subtypes mediate these effects. Here, we show that Akt activation in COS7 cells, which lack of IP₃R I, strongly suppresses IP₃-mediated Ca²⁺ release and apoptosis. Conversely, in SH-SY 5Y cells, which are type III-deficient, Akt is unable to modulate ER Ca²⁺ flux, losing its anti-apoptotic activity. In SH-SY 5Y-expressing subtype III, Akt recovers its protective function on cell death, by reduction of Ca²⁺ release. Moreover, regulating Ca²⁺ flux to mitochondria, Akt maintains the mitochondrial integrity and delays the trigger of apoptosis, in a type III-dependent mechanism. These results demonstrate a specific activity of Akt on IP₃R III, leading to diminished Ca²⁺ transfer to mitochondria and protection from apoptosis, suggesting an additional level of cell death regulation mediated by Akt."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.org/dc/terms/identifier"doi:10.1038/cddis.2012.45"xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Giorgi C."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Marchi S."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Pinton P."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Rimessi A."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Bonora M."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Bononi A."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/author"Marinello M."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/name"Cell Death Dis"xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/pages"e304"xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/title"Selective modulation of subtype III IP(3)R by Akt regulates ER Ca^2⁺ release and apoptosis."xsd:string
http://purl.uniprot.org/citations/22552281http://purl.uniprot.org/core/volume"3"xsd:string
http://purl.uniprot.org/citations/22552281http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22552281
http://purl.uniprot.org/citations/22552281http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22552281
http://purl.uniprot.org/uniprot/#_B3KVH4-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_A0A0S2Z3D6-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_A0A142IKA9-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_A6H8K3-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_B0LPE5-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_P31749-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_Q59ES2-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281
http://purl.uniprot.org/uniprot/#_Q14573-mappedCitation-22552281http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22552281