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PARL Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF, ICC, E |
|---|---|
| Primary Accession | Q9H300 |
| Other Accession | Q9H300, 143811433 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 42190 Da |
| Application Notes | PARL antibody can be used for detection of PARL by Western blot at 1 - 2 µg/mL. Despite its predicted molecular weight of ~42kDa, PARL is observed at a higher molecular weight in SDS-PAGE. Antibody can also be used for immunocytochemistry starting at 2.5 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 55486 |
|---|---|
| Target/Specificity | PARL; |
| Reconstitution & Storage | PARL antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | PARL Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | PARL |
|---|---|
| Synonyms | PSARL |
| Function | Required for the control of apoptosis during postnatal growth. Essential for proteolytic processing of an antiapoptotic form of OPA1 which prevents the release of mitochondrial cytochrome c in response to intrinsic apoptotic signals (By similarity). Required for the maturation of PINK1 into its 52kDa mature form after its cleavage by mitochondrial-processing peptidase (MPP) (PubMed:22354088). Promotes cleavage of serine/threonine-protein phosphatase PGAM5 in damaged mitochondria in response to loss of mitochondrial membrane potential (PubMed:22915595). Mediates differential cleavage of PINK1 and PGAM5 depending on the health status of mitochondria, disassociating from PINK1 and associating with PGAM5 in response to mitochondrial membrane potential loss (PubMed:22915595). Required for processing of CLPB into a form with higher protein disaggregase activity by removing an autoinhibitory N-terminal peptide (PubMed:28288130, PubMed:32573439). Promotes processing of DIABLO/SMAC in the mitochondrion which is required for DIABLO apoptotic activity (PubMed:28288130). Also required for cleavage of STARD7 and TTC19 (PubMed:28288130). Promotes changes in mitochondria morphology regulated by phosphorylation of P-beta domain (PubMed:14732705, PubMed:17116872). |
| Cellular Location | Mitochondrion inner membrane; Multi-pass membrane protein |
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.
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Provided below are standard protocols that you may find useful for product applications.
Background
PARL Antibody: PARL is a mitochondrial integral membrane protein and a member of the highly conserved rhomboid superfamily of membrane proteins. PARL is required for the control of apoptosis during postnatal growth and is required for the processing of OPA1, a protein that prevents the release of cytochrome C from the mitochondria in response to apoptotic signals. In lymphocytes and neurons, PARL's association with other proteins, such as the Bcl-2 family-related protein Hax1 and Omi can lead to the proteolytic processing of Omi by PARL, preventing the accumulation of Bax, thereby suppressing apoptosis. Variations in this gene have been associated with increased risk for type 2 diabetes. PARL may also play a role in the progression of Alzheimer's disease through its associations with presenilin-1 and -2. Multiple isoforms of PARL are known to exist.
References
Pellegrini L, Passer BJ, Canelles M, et al. PAMP and PARL, two novel putative metalloproteases interacting with the COOH-terminus of Presenilin-1 and -2. J. Alzheimers Dis.2001; 3:181-90.
Cipolat S, Rudka T, Hartmann D, et al. Mitochondrial rhomboid PARL regulates cytochrome c release during apoptosis via OPA1-dependent cristae remodeling. Cell2006; 126:163-75.
Chao JR, Parganas E, Boyd K, et al. Hax1-mediated processing of HtrA2 by PARL allows survival of lymphocytes and neurons. Nature2008; 452:98-102.
Walder K, Kerr-Bayles L, Civitarese A, et al. The mitochondrial rhomboid protease PSARL is a new candidate gene for type 2 diabetes. Diabetologia2005; 48:459-68.
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