Other
13 Authors
- Kwak S,
- Khatri RG,
- Cheng A,
- Gonzales C,
- Xin O,
- Liu D,
- Mark RJ,
- Mustafa K,
- Guo Z,
- Mattson MP,
- Ling HP,
- Jo DG,
- Arumugam TV
| First Author | Cheng A | Year | 2007 |
| Journal | J Neurosci | Volume | 27 |
| Issue | 7 | Pages | 1519-28 |
| PubMed ID | 17301160 | Mgi Jnum | J:118333 |
| Mgi Id | MGI:3699446 | Doi | 10.1523/JNEUROSCI.5154-06.2007 |
| Citation | Cheng A, et al. (2007) Pancortin-2 interacts with WAVE1 and Bcl-xL in a mitochondria-associated protein complex that mediates ischemic neuronal death. J Neurosci 27(7):1519-28 |
| abstractText | The actin-modulating protein Wiskott-Aldrich syndrome protein verprolin homologous-1 (WAVE1) and a novel CNS-specific protein, pancortin, are highly enriched in adult cerebral cortex, but their functions are unknown. Here we show that WAVE1 and pancortin-2 interact in a novel cell death cascade in adult, but not embryonic, cerebral cortical neurons. Focal ischemic stroke induces the formation of a protein complex that includes pancortin-2, WAVE1, and the anti-apoptotic protein Bcl-xL. The three-protein complex is associated with mitochondria resulting in increased association of Bax with mitochondria, cytochrome c release, and neuronal apoptosis. In pancortin null mice generated using a Cre-loxP system, ischemia-induced WAVE1-Bcl-xL interaction is diminished, and cortical neurons in these mice are protected against ischemic injury. Thus, pancortin-2 is a mediator of ischemia-induced apoptosis of neurons in the adult cerebral cortex and functions in a novel mitochondrial/actin-associated protein complex that sequesters Bcl-xL. |
