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anti-Mouse (Murine) OPA1 Antibodies:
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Chicken Polyclonal OPA1 Primary Antibody for IHC, IHC (p) - ABIN258401
Dai, Hsieh, Liu, Chen, Beyer, Chin, MacCoss, Rabinovitch: Mitochondrial proteome remodelling in pressure overload-induced heart failure: the role of mitochondrial oxidative stress. in Cardiovascular research 2011
Show all 14 Pubmed References
Chicken Monoclonal OPA1 Primary Antibody for IF, WB - ABIN968891
Alexander, Votruba, Pesch, Thiselton, Mayer, Moore, Rodriguez, Kellner, Leo-Kottler, Auburger, Bhattacharya, Wissinger: OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28. in Nature genetics 2000
Show all 3 Pubmed References
Chicken Monoclonal OPA1 Primary Antibody for IF, WB - ABIN968892
Delettre, Lenaers, Griffoin, Gigarel, Lorenzo, Belenguer, Pelloquin, Grosgeorge, Turc-Carel, Perret, Astarie-Dequeker, Lasquellec, Arnaud, Ducommun, Kaplan, Hamel: Nuclear gene OPA1, encoding a mitochondrial dynamin-related protein, is mutated in dominant optic atrophy. in Nature genetics 2000
Show all 3 Pubmed References
Human Polyclonal OPA1 Primary Antibody for IF (p), IHC (p) - ABIN1387244
Ku, Ji, Zhang, Li, Sang: PM2.5, SO2 and NO2 co-exposure impairs neurobehavior and induces mitochondrial injuries in the mouse brain. in Chemosphere 2016
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Chinese Hamster Monoclonal OPA1 Primary Antibody for ICC, IF - ABIN4341456
Montaigne, Marechal, Coisne, Debry, Modine, Fayad, Potelle, El Arid, Mouton, Sebti, Duez, Preau, Remy-Jouet, Zerimech, Koussa, Richard, Neviere, Edme, Lefebvre, Staels: Myocardial contractile dysfunction is associated with impaired mitochondrial function and dynamics in type 2 diabetic but not in obese patients. in Circulation 2014
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Human Polyclonal OPA1 Primary Antibody for ELISA - ABIN562069
Yarosh, Monserrate, Tong, Tse, Le, Nguyen, Brachmann, Wallace, Huang: The molecular mechanisms of OPA1-mediated optic atrophy in Drosophila model and prospects for antioxidant treatment. in PLoS genetics 2008
Mitochondrial dysfunction in an Opa1 (show MED12 Antibodies) mouse model of dominant optic atrophy results from Opa1 (show MED12 Antibodies) haploinsufficiency.
TNFR2 (show TNFRSF1B Antibodies) activation protects cardiac myocytes against stress by up-regulating OPA1 (show MED12 Antibodies) expression.
OPA1 (show MED12 Antibodies) mutant mice are resistant to age- and diet-induced weight gain and insulin (show INS Antibodies) resistance, by mechanisms that involve activation of endoplasmic reticulum stress and secretion of fibroblast growth factor 21 (FGF21 (show FGF21 Antibodies)) from skeletal muscle, resulting in increased metabolic rates and improved whole-body insulin (show INS Antibodies) sensitivity.
OPA1 (show MED12 Antibodies) modulates cristae morphology but is dispensable for cristae junction formation. Endogenous OPA1 (show MED12 Antibodies) and MIC60 show a physical interaction.
Opa1 (show MED12 Antibodies) deficiency was associated with increased sensitivity to Ischemia-Reperfusion Injuries, imbalance in dynamic mitochondrial Ca2 (show CA2 Antibodies)+ uptake, and subsequent increase in NCX (show SLC8A1 Antibodies) activity.
Whereas Parkin (show PARK2 Antibodies) has been reported to positively regulate the expression of OPA1 (show MED12 Antibodies) through NEMO (show IKBKG Antibodies), herein we found that PARK2 (show PARK2 Antibodies) overexpression did not modify the expression of OPA1 (show MED12 Antibodies).
stress-induced OMA1 (show OMA1 Antibodies) activation and guanosine triphosphatase OPA1 (show MED12 Antibodies) cleavage limit mitochondrial fusion and promote neuronal death
Data suggest that in a mouse model of neonatal hypoxic-ischemic brain injury, the expression of mitochondrial shaping proteins, such as OPA1 (show MED12 Antibodies) and Yme1L (show YME1L1 Antibodies), are altered; in vitro and in vivo, OPA1 (show MED12 Antibodies) is cleaved to shorter forms and Yme1L (show YME1L1 Antibodies) expression is reduced.
results indicate that the OPA1 (show MED12 Antibodies)-dependent cristae remodeling pathway is a fundamental, targetable determinant of tissue damage in vivo.
cristae shape amelioration by controlled Opa1 (show MED12 Antibodies) overexpression improves two mouse models of mitochondrial disease.
Identification of genomic rearrangements or pathogenic variants of OPA1 is meaningful for disease prognosis and proper genetic counseling in DOA consultation.
In brown adipocytes indirect evidence support the notion that OPA1 regulation of fission serves to increase thermogenesis, which thereby contributes to dissipation of energy.
Stabilization of OPA1 impedes cristae remodeling.
Our combination of proteomics, biochemistry, genetics, and electron tomography provides a unifying model for mammalian cristae biogenesis by OPA1 and MICOS.
The splice site mutation (c.985G>T) identified in the present study led to exon 10 skipping (c.985_1065del, p.V329_D355del), suggesting loss-of-function of the GTPase (show RACGAP1 Antibodies) domain of the OPA1 protein, which is likely to cause haplo-insufficiency, a major disease mechanism in DOA.
study identifies a novel pathogenic OPA1 mutation and shows that it is located in the transcript region not prone for NMD activation
OPA1 gene screening in patients with bilateral optic atrophy is an important part of clinical evaluation as it may establish correct clinical diagnosis
OPA1 and cardiolipin cooperate in heterotypic mitochondrial inner membrane fusion.
We propose that OPA1 stabilizes respiratory chain supercomplexes in a conformation that enables respiring mitochondria to compensate a drop in Deltapsim by an explosive matrix pH flash.
We report the first cases of genetically confirmed OPA1-related autosomal-dominant optic atrophy from Singapore, including a novel mutation causing 'ADOA plus' syndrome.
Opa1 is required for proper mitochondrial metabolism in early development
This gene product is a nuclear-encoded mitochondrial protein with similarity to dynamin-related GTPases. It is a component of the mitochondrial network. Mutations in this gene have been associated with optic atrophy type 1, which is a dominantly inherited optic neuropathy resulting in progressive loss of visual acuity, leading in many cases to legal blindness. Multiple transcript variants encoding different isoforms have been found for this gene.
dynamin-like 120 kDa protein, mitochondrial
, large GTP-binding protein
, optic atrophy 1 homolog
, optic atrophy protein 1 homolog
, RN protein
, optic atrophy 1 (autosomal dominant)
, optic atrophy 1-like protein
, dynamin-like guanosine triphosphatase
, mitochondrial dynamin-like GTPase
, optic atrophy protein 1