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OPA1 product is a nuclear-encoded mitochondrial protein with similarity to dynamin-related GTPases. Additionally we are shipping OPA1 Proteins (9) and many more products for this protein.
Showing 10 out of 63 products:
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 13 references for ABIN258401
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 references for ABIN968891
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
Show all 2 references for ABIN4341456
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
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
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.
unprocessed OPA1 (show MED12 Antibodies) is sufficient to maintain heart function, OMA1 (show OMA1 Antibodies) is a critical regulator of cardiomyocyte survival, and mitochondrial morphology and cardiac metabolism are intimately linked.
Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: OPA1 (show MED12 Antibodies), Drp1 (dynamin 1-like protein (show DNM1L Antibodies)), and Mfn1 (show MFN1 Antibodies)/2 (mitofusin 1 (show MFN1 Antibodies) and 2). [REVIEW]
Photoresponsive RGCs are protected against cell death due to the Opa1 (show MED12 Antibodies) mutation, but not by melanopsin (show OPN4 Antibodies) expression itself.
The present study identified novel compound heterozygous OPA1 mutations in a patient with recessive optic atrophy, sensorimotor neuropathy and congenital cataracts, indicating an expansion of the clinical spectrum of pathologies associated with OPA1 mutations.
Optic atrophy type 1, caused by mutations in the OPA1 gene is believed to be the most common hereditary optic neuropathy, and most patients inherit a mutation from an affected parent. In this study we used whole-exome sequencing to investigate the genetic aetiology in a patient affected with isolated optic atrophy. Exome results identified a novel de novo OPA1 mutation.
Findings show a new mode of regulation of the mitochondrial fusion proteins, Mfns degradation or OPA1 processing, in response to mitochondrial morphology.
Loss of OPA1 protein function by pathogenic OPA1 gene mutation induces increased mitochondrial fragmentation that promotes instability of the mitochondrial respiratory chain complexes.
Two heterozygous mutations, p.T414P (c.1240A>C) and p.T540P (c.1618A>C), located in the GTPase (show RACGAP1 Antibodies) and middle domains of OPA1, respectively, were identified in two patients.These two different conformational changes might result in decreased GTPase (show RACGAP1 Antibodies) activities that trigger autosomal dominant optic atrophy associated with auditory neuropathy spectrum disorder
A causal link between a pathogenic homozygous OPA1 mutation and hypertrophic cardiomyopathy with optic atrophy was established.It emphasise the vital role played by OPA1 in mitochondrial biogenesis and mtDNA maintenance.
OPA1 variants confer risk of leprosy in Chinese Han population and may affect OPA1 expression, mitochondrial function and antimicrobial pathways.
Genotype-phenotype heterogeneity in OPA1 autosomal-dominant optic atrophy (ADOA). is evident when inner retinal atrophy is examined as a function of age.
Heterozygous mutation in OPA1 disrupts the GTPase (show RACGAP1 Antibodies) domain of OPA1 and is associated with phenotypically variable ADOA Plus.
Identification of copy number variation in the gene for autosomal dominant optic atrophy, OPA1, in a Chinese pedigree
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