OMA1 antibody - middle region
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB |
---|---|
Primary Accession | Q96E52 |
Other Accession | NM_145243, NP_660286 |
Reactivity | Human, Zebrafish, Pig |
Host | Rabbit |
Clonality | Polyclonal |
Calculated MW | 60 KDa |
Gene ID | 115209 |
---|---|
Alias Symbol | 2010001O09Rik, DAB1, FLJ33782, MPRP-1, YKR087C, ZMPOMA1 |
Other Names | Metalloendopeptidase OMA1, mitochondrial, 3.4.24.-, Metalloprotease-related protein 1, MPRP-1, Overlapping with the m-AAA protease 1 homolog, OMA1, MPRP1 |
Format | Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose. |
Reconstitution & Storage | Add 50 ul of distilled water. Final anti-OMA1 antibody concentration is 1 mg/ml in PBS buffer with 2% sucrose. For longer periods of storage, store at 20°C. Avoid repeat freeze-thaw cycles. |
Precautions | OMA1 antibody - middle region is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | OMA1 {ECO:0000303|PubMed:20038677, ECO:0000312|HGNC:HGNC:29661} |
---|---|
Function | Metalloprotease that is part of the quality control system in the inner membrane of mitochondria (PubMed:20038677, PubMed:25605331, PubMed:32132706, PubMed:32132707). Activated in response to various mitochondrial stress, leading to the proteolytic cleavage of target proteins, such as OPA1, UQCC3 and DELE1 (PubMed:20038677, PubMed:25275009, PubMed:32132706, PubMed:32132707). Following stress conditions that induce loss of mitochondrial membrane potential, mediates cleavage of OPA1 at S1 position, leading to OPA1 inactivation and negative regulation of mitochondrial fusion (PubMed:20038677, PubMed:25275009). Also acts as a regulator of apoptosis: upon BAK and BAX aggregation, mediates cleavage of OPA1, leading to the remodeling of mitochondrial cristae and allowing the release of cytochrome c from mitochondrial cristae (PubMed:25275009). In depolarized mitochondria, may also act as a backup protease for PINK1 by mediating PINK1 cleavage and promoting its subsequent degradation by the proteasome (PubMed:30733118). May also cleave UQCC3 in response to mitochondrial depolarization (PubMed:25605331). Also acts as an activator of the integrated stress response (ISR): in response to mitochondrial stress, mediates cleavage of DELE1 to generate the processed form of DELE1 (S- DELE1), which translocates to the cytosol and activates EIF2AK1/HRI to trigger the ISR (PubMed:32132706, PubMed:32132707). Its role in mitochondrial quality control is essential for regulating lipid metabolism as well as to maintain body temperature and energy expenditure under cold-stress conditions (By similarity). Binds cardiolipin, possibly regulating its protein turnover (By similarity). Required for the stability of the respiratory supercomplexes (By similarity). |
Cellular Location | Mitochondrion inner membrane; Single-pass membrane protein {ECO:0000250|UniProtKB:Q9D8H7} |
Tissue Location | Widely expressed, with strong expression in the heart, skeletal muscle, kidney and liver |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
info@abcepta.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
References
Bao Y.-C.,et al.DNA Res. 10:123-128(2003).
Gregory S.G.,et al.Nature 441:315-321(2006).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Head B.,et al.J. Cell Biol. 187:959-966(2009).
If you have used an Abcepta product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at tech@abcepta.com.