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anti-Mouse (Murine) OPA1 Antikörper:
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Chicken Polyclonal OPA1 Primary Antibody für 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 für 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
Chinese Hamster Monoclonal OPA1 Primary Antibody für 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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Chicken Monoclonal OPA1 Primary Antibody für 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
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Human Polyclonal OPA1 Primary Antibody für 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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Human Polyclonal OPA1 Primary Antibody für 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 (zeige MED12 Antikörper) mouse model of dominant optic atrophy results from Opa1 (zeige MED12 Antikörper) haploinsufficiency.
TNFR2 (zeige TNFRSF1B Antikörper) activation protects cardiac myocytes against stress by up-regulating OPA1 (zeige MED12 Antikörper) expression.
OPA1 (zeige MED12 Antikörper) mutant mice are resistant to age- and diet-induced weight gain and insulin (zeige INS Antikörper) resistance, by mechanisms that involve activation of endoplasmic reticulum stress and secretion of fibroblast growth factor 21 (FGF21 (zeige FGF21 Antikörper)) from skeletal muscle, resulting in increased metabolic rates and improved whole-body insulin (zeige INS Antikörper) sensitivity.
OPA1 (zeige MED12 Antikörper) modulates cristae morphology but is dispensable for cristae junction formation. Endogenous OPA1 (zeige MED12 Antikörper) and MIC60 show a physical interaction.
Opa1 (zeige MED12 Antikörper) deficiency was associated with increased sensitivity to Ischemia-Reperfusion Injuries, imbalance in dynamic mitochondrial Ca2 (zeige CA2 Antikörper)+ uptake, and subsequent increase in NCX (zeige SLC8A1 Antikörper) activity.
Whereas Parkin (zeige PARK2 Antikörper) has been reported to positively regulate the expression of OPA1 (zeige MED12 Antikörper) through NEMO (zeige IKBKG Antikörper), herein we found that PARK2 (zeige PARK2 Antikörper) overexpression did not modify the expression of OPA1 (zeige MED12 Antikörper).
stress-induced OMA1 (zeige OMA1 Antikörper) activation and guanosine triphosphatase OPA1 (zeige MED12 Antikörper) 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 (zeige MED12 Antikörper) and Yme1L (zeige YME1L1 Antikörper), are altered; in vitro and in vivo, OPA1 (zeige MED12 Antikörper) is cleaved to shorter forms and Yme1L (zeige YME1L1 Antikörper) expression is reduced.
results indicate that the OPA1 (zeige MED12 Antikörper)-dependent cristae remodeling pathway is a fundamental, targetable determinant of tissue damage in vivo.
cristae shape amelioration by controlled Opa1 (zeige MED12 Antikörper) overexpression improves two mouse models of mitochondrial disease.
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 (zeige RACGAP1 Antikörper) 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.
contrary to conventional notion, S-OPA1 is fully competent for maintaining mitochondrial energetics and cristae structure
we analyzed ophthalmological data of a multicentre OPA1 patient cohort and found that women undergo more severe visual loss at adolescence and greater progressive thinning of the retinal nerve fibres than males. Thus, we disclosed a gender-dependent effect on ADOA severity, involving for the first time steroids and Muller glial cells, responsible for RGC degeneration.
The gene signature of OPA1, CTSA (zeige CTSA Antikörper), NDUFA1 (zeige NDUFA1 Antikörper), STK10 (zeige STK10 Antikörper) and PRDX1 (zeige PRDX1 Antikörper) was able to identify patients post-implant with a sensitivity of 91% and a specificity of 86% in discrimination between post-implant group and healthy controls.
The architecture of dendritic arborization in patients with OPA1 mutations is not known, but our data support the idea that loss of dendritic arborization may be involved in the pathogenesis of DOA rather than just population loss.
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