| http://purl.uniprot.org/citations/21212236 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21212236 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21212236 | http://www.w3.org/2000/01/rdf-schema#comment | "Cells and organisms face anoxia in a wide variety of contexts, including ischemia and hibernation. Cells respond to anoxic conditions through multiple signaling pathways. We report that NSY-1, the Caenorhabditis elegans ortholog of mammalian apoptosis signal-regulating kinase (ASK) family of MAP kinase (MAPK) kinase kinases (MAP3Ks), regulates viability of animals in anoxia. Loss-of-function mutations of nsy-1 increased survival under anoxic conditions, and increased survival was also observed in animals with mutations in tir-1 and the MAPK kinase (MAP2K) sek-1, which are upstream and downstream factors of NSY-1, respectively. Consistent with these findings, anoxia was found to activate the p38 MAPK ortholog PMK-1, and this was suppressed in nsy-1 and tir-1 mutant animals. Furthermore, double-mutant analysis showed that the insulin-signaling pathway, which also regulates viability in anoxia, functioned in parallel to NSY-1. These results suggest that the TIR-1-NSY-1-SEK-1-PMK-1 pathway plays important roles in the reponse to anoxia in C. elegans."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.org/dc/terms/identifier | "doi:10.1534/genetics.110.124883"xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.org/dc/terms/identifier | "doi:10.1534/genetics.110.124883"xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Hayakawa T."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Hayakawa T."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Kato K."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Kato K."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Matsumoto K."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Matsumoto K."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Takeda K."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Takeda K."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Ichijo H."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Ichijo H."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Hisamoto N."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Hisamoto N."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Hayakawa R."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/author | "Hayakawa R."xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/name | "Genetics"xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/name | "Genetics"xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/pages | "785-792"xsd:string |
| http://purl.uniprot.org/citations/21212236 | http://purl.uniprot.org/core/pages | "785-792"xsd:string |