OPA1 (D7C1A) Rabbit mAb #67589
- WB
- IP
- IF
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 80-100 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
| Immunofluorescence (Immunocytochemistry) | 1:800 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
OPA1, or Optic Atrophy 1, was originally identified as a genetic cause for Autosomal Dominant Optic Atrophy, a neuropathy resulting in progressive visual loss (2,3). OPA1 is a widely expressed protein localized to the inner mitochondrial membrane, which regulates mitochondrial fusion and cristae morphology and protects against apoptosis (4-6). OPA1 activity is tightly regulated through alternative splicing and post-translational modifications including complex proteolytic processing by multiple proteases (7-12). In addition, OPA1 expression can be induced under conditions of metabolic demand through a pathway involving Parkin induced NF-κB activation (13).
- Kasahara, A. and Scorrano, L. (2014) Trends Cell Biol 24, 761-70.
- Delettre, C. et al. (2000) Nat Genet 26, 207-10.
- Alexander, C. et al. (2000) Nat Genet 26, 211-5.
- Frezza, C. et al. (2006) Cell 126, 177-89.
- Olichon, A. et al. (2003) J Biol Chem 278, 7743-6.
- Griparic, L. et al. (2004) J Biol Chem 279, 18792-8.
- Delettre, C. et al. (2001) Hum Genet 109, 584-91.
- Olichon, A. et al. (2007) Cell Death Differ 14, 682-92.
- Ishihara, N. et al. (2006) EMBO J 25, 2966-77.
- Cipolat, S. et al. (2006) Cell 126, 163-75.
- Griparic, L. et al. (2007) J Cell Biol 178, 757-64.
- Merkwirth, C. et al. (2008) Genes Dev 22, 476-88.
- Müller-Rischart, A.K. et al. (2013) Mol Cell 49, 908-21.
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