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- Publisher Website: 10.1074/jbc.M405747200
- Scopus: eid_2-s2.0-4544368511
- PMID: 15262985
- WOS: WOS:000223791500091
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Article: Induced inhibition of ischemic/hypoxic injury by APIP, a novel Apaf-1-interacting protein
Title | Induced inhibition of ischemic/hypoxic injury by APIP, a novel Apaf-1-interacting protein |
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Authors | |
Issue Date | 2004 |
Citation | Journal of Biological Chemistry, 2004, v. 279, n. 38, p. 39942-39950 How to Cite? |
Abstract | We describe the isolation and characterization of a new agaf-1-interacting protein (APIP) as a negative regulator of ischemic injury. APIP is highly expressed in skeletal muscle and heart and binds to the CARD of Apaf-1 in competition with caspase-9. Exogenous APIP inhibits cytochrome c-induced activation of caspase-3 and caspase-9, and suppresses cell death triggered by mitochondrial apoptotic stimuli through inhibiting the downstream activity of cytochrome c released from mitochondria. Conversely, reduction of APIP expression potentiates mitochondrial apoptosis. APIP expression is highly induced in mouse muscle affected by ischemia produced by interruption of the artery in the hindlimb and in C2C12 myotubes created by hypoxia in vitro, and the blockade of APIP up-regulation results in TUNEL-positive ischemic damage. Furthermore, forced expression of APIP suppresses ischemia/hypoxia-induced death of skeletal muscle cells. Taken together, these results suggest that APIP functions to inhibit muscle ischemic damage by binding to Apaf-1 in the Apaf-1/caspase-9 apoptosis pathway. |
Persistent Identifier | http://hdl.handle.net/10722/291832 |
ISSN | 2020 Impact Factor: 5.157 2023 SCImago Journal Rankings: 1.766 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Cho, Dong Hyung | - |
dc.contributor.author | Hong, Yeon Mi | - |
dc.contributor.author | Lee, Ho June | - |
dc.contributor.author | Woo, Ha Na | - |
dc.contributor.author | Pyo, Jong Ok | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Jung, Yong Keun | - |
dc.date.accessioned | 2020-11-17T14:55:12Z | - |
dc.date.available | 2020-11-17T14:55:12Z | - |
dc.date.issued | 2004 | - |
dc.identifier.citation | Journal of Biological Chemistry, 2004, v. 279, n. 38, p. 39942-39950 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291832 | - |
dc.description.abstract | We describe the isolation and characterization of a new agaf-1-interacting protein (APIP) as a negative regulator of ischemic injury. APIP is highly expressed in skeletal muscle and heart and binds to the CARD of Apaf-1 in competition with caspase-9. Exogenous APIP inhibits cytochrome c-induced activation of caspase-3 and caspase-9, and suppresses cell death triggered by mitochondrial apoptotic stimuli through inhibiting the downstream activity of cytochrome c released from mitochondria. Conversely, reduction of APIP expression potentiates mitochondrial apoptosis. APIP expression is highly induced in mouse muscle affected by ischemia produced by interruption of the artery in the hindlimb and in C2C12 myotubes created by hypoxia in vitro, and the blockade of APIP up-regulation results in TUNEL-positive ischemic damage. Furthermore, forced expression of APIP suppresses ischemia/hypoxia-induced death of skeletal muscle cells. Taken together, these results suggest that APIP functions to inhibit muscle ischemic damage by binding to Apaf-1 in the Apaf-1/caspase-9 apoptosis pathway. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Biological Chemistry | - |
dc.title | Induced inhibition of ischemic/hypoxic injury by APIP, a novel Apaf-1-interacting protein | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1074/jbc.M405747200 | - |
dc.identifier.pmid | 15262985 | - |
dc.identifier.scopus | eid_2-s2.0-4544368511 | - |
dc.identifier.volume | 279 | - |
dc.identifier.issue | 38 | - |
dc.identifier.spage | 39942 | - |
dc.identifier.epage | 39950 | - |
dc.identifier.isi | WOS:000223791500091 | - |
dc.identifier.issnl | 0021-9258 | - |