| http://purl.uniprot.org/citations/21856340 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21856340 | http://www.w3.org/2000/01/rdf-schema#comment | "Higd-1a (hypoxia induced gene domain family-1a) is a mitochondrial inner membrane protein with a conformation of N-terminal outside-C-terminal outside and loop inside. There are four Higd genes, Higd-1a, -1b, -1c and -2a, in the mouse. Higd-1a and -2a are expressed primarily in the brain, heart, kidney and leukocytes. HIF (hypoxia-inducible factor) overexpression induced the endogenous expression and promoter activity of Higd-1a. Mutation of the HRE (hypoxia-response element) site at -32bp in the Higd-1a promoter reduced the promoter activity, suggesting that transcription of Higd-1a is regulated by binding of the transcription factor HIF to the HRE. Higd-1a promoted cell survival under hypoxia. RAW264.7 cells stably transfected with Higd-1a underwent less apoptosis than control cells in a hypoxic condition, and hypoxia-induced apoptosis was strongly enhanced when endogenous Higd-1a was silenced by siRNA. The survival effect of Higd-1a was completely abolished by deletion of the 26 N-terminal amino acids, and we showed that Higd-1a increased survival by inhibiting cytochrome C release and reducing the activities of caspases. However, expression of Bcl-2, Bax, Bad, and BNIP3 and translocation of AIF were unaffected under the same conditions. Higd-2a also enhanced cell survival under hypoxia. Cells transfected with Higd-2a underwent less apoptosis than control cells in hypoxic conditions, and hypoxia-induced apoptosis increased when endogenous Higd-2a was depleted. Together these observations indicate that Higd-1a is induced by hypoxia in a HIF-dependent manner and its anti-apoptotic effect results from inhibiting cytochrome C release and reducing caspase activities."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbamcr.2011.07.017"xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "Kim Y.J."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "Lee H."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "Shin H."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "An H.J."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "Lee J.O."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "Paik S.G."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/author | "Jo S.G."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/name | "Biochim Biophys Acta"xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/pages | "2088-2098"xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/title | "The survival effect of mitochondrial Higd-1a is associated with suppression of cytochrome C release and prevention of caspase activation."xsd:string |
| http://purl.uniprot.org/citations/21856340 | http://purl.uniprot.org/core/volume | "1813"xsd:string |
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