| pubmed-article:21526220 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21526220 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:21526220 | lifeskim:mentions | umls-concept:C0010531 | lld:lifeskim |
| pubmed-article:21526220 | lifeskim:mentions | umls-concept:C1412311 | lld:lifeskim |
| pubmed-article:21526220 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:21526220 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:21526220 | pubmed:dateCreated | 2011-4-28 | lld:pubmed |
| pubmed-article:21526220 | pubmed:abstractText | Mitochondrial shape is determined by fission and fusion reactions catalyzed by large GTPases of the dynamin family, mutation of which can cause neurological dysfunction. While fission-inducing protein phosphatases have been identified, the identity of opposing kinase signaling complexes has remained elusive. We report here that in both neurons and non-neuronal cells, cAMP elevation and expression of an outer-mitochondrial membrane (OMM) targeted form of the protein kinase A (PKA) catalytic subunit reshapes mitochondria into an interconnected network. Conversely, OMM-targeting of the PKA inhibitor PKI promotes mitochondrial fragmentation upstream of neuronal death. RNAi and overexpression approaches identify mitochondria-localized A kinase anchoring protein 1 (AKAP1) as a neuroprotective and mitochondria-stabilizing factor in vitro and in vivo. According to epistasis studies with phosphorylation site-mutant dynamin-related protein 1 (Drp1), inhibition of the mitochondrial fission enzyme through a conserved PKA site is the principal mechanism by which cAMP and PKA/AKAP1 promote both mitochondrial elongation and neuronal survival. Phenocopied by a mutation that slows GTP hydrolysis, Drp1 phosphorylation inhibits the disassembly step of its catalytic cycle, accumulating large, slowly recycling Drp1 oligomers at the OMM. Unopposed fusion then promotes formation of a mitochondrial reticulum, which protects neurons from diverse insults. | lld:pubmed |
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| pubmed-article:21526220 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21526220 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21526220 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:21526220 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21526220 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:21526220 | pubmed:issn | 1545-7885 | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:UsachevYuriy... | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:StrackStefanS | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:DagdaRuben... | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:CribbsJ... | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:GreenSteven... | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:MerrillRonald... | lld:pubmed |
| pubmed-article:21526220 | pubmed:author | pubmed-author:DickeyAudrey... | lld:pubmed |
| pubmed-article:21526220 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21526220 | pubmed:volume | 9 | lld:pubmed |
| pubmed-article:21526220 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21526220 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21526220 | pubmed:pagination | e1000612 | lld:pubmed |
| pubmed-article:21526220 | pubmed:meshHeading | pubmed-meshheading:21526220... | lld:pubmed |
