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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 17 Pubmed References
Human Monoclonal OPA1 Primary Antibody for WB - ABIN5529589
Ruegsegger, Manjunatha, Summer, Gopala, Zabeilski, Dasari, Vanderboom, Lanza, Klaus, Nair: Insulin deficiency and intranasal insulin alter brain mitochondrial function: a potential factor for dementia in diabetes. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2019
Show all 2 Pubmed References
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 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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Human Polyclonal OPA1 Primary Antibody for WB - ABIN6145031
Shao, Zhao, Wang, Liu, Zong, Xing: Copper-Mediated Mitochondrial Fission/Fusion Is Associated with Intrinsic Apoptosis and Autophagy in the Testis Tissues of Chicken. in Biological trace element research 2018
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
These findings show that the disruption of OPA1 leads to a remodelling of bioenergetic pathways with the central role being played by aspartate and related metabolites.
Opa1 ablation causes inflammatory myopathy.
Propose a novel function of OPA1 in mediating the CoQ10-responsive regulation of respiratory CIV activity in brain mitochondria from aging mice.
multiple OPA1 isoforms are required for mitochondrial dynamics, while any single isoform can support all other functions.
Mechanistically, the ablation of Opa1 leads to ER stress, which signals via the unfolded protein response (UPR) and FoxOs, inducing a catabolic program of muscle loss and systemic aging.
Mitochondrial dysfunction in an Opa1 mouse model of dominant optic atrophy results from Opa1 haploinsufficiency.
TNFR2 activation protects cardiac myocytes against stress by up-regulating OPA1 expression.
OPA1 mutant mice are resistant to age- and diet-induced weight gain and insulin resistance, by mechanisms that involve activation of endoplasmic reticulum stress and secretion of fibroblast growth factor 21 (FGF21) from skeletal muscle, resulting in increased metabolic rates and improved whole-body insulin sensitivity.
OPA1 modulates cristae morphology but is dispensable for cristae junction formation. Endogenous OPA1 and MIC60 show a physical interaction.
Opa1 deficiency was associated with increased sensitivity to Ischemia-Reperfusion Injuries, imbalance in dynamic mitochondrial Ca2+ uptake, and subsequent increase in NCX activity.
Whereas Parkin has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that PARK2 overexpression did not modify the expression of OPA1.
stress-induced OMA1 activation and guanosine triphosphatase OPA1 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 and Yme1L, are altered; in vitro and in vivo, OPA1 is cleaved to shorter forms and Yme1L expression is reduced.
results indicate that the OPA1-dependent cristae remodeling pathway is a fundamental, targetable determinant of tissue damage in vivo.
cristae shape amelioration by controlled Opa1 overexpression improves two mouse models of mitochondrial disease.
unprocessed OPA1 is sufficient to maintain heart function, OMA1 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, Drp1 (dynamin 1-like protein), and Mfn1/2 (mitofusin 1 and 2). [REVIEW]
Photoresponsive RGCs are protected against cell death due to the Opa1 mutation, but not by melanopsin expression itself.
Results suggest that Mfn2 and OPA1 are upregulated during bone marrow progenitor differentiation and promote the migration of immature dendritic cells by regulating the expression of CCR7.
Reactive oxygen species might affect MyHC content by modulating OPA1 cleavage in muscle degeneration.
Diminished OPA1 expression and impaired mitochondrial morphology and homeostasis in APTX-deficient cells have been reported.
therefore identified a pivotal leptin/OPA1/SGLT1 signaling pathway for mitochondrial dynamicmediated glycolysis, which may optimize the therapeutic efficiency of MSCs.
leptin targeting the GSK3/OMA1/OPA1 signaling pathway can optimize hMSCs therapy for cardiovascular diseases such
we identify AFG3L2 [matrix (m)-AAA complex] as the major protease mediating this event, which acts by maturing the 60 kDa pre-pro-OMA1 to the 40 kDa pro-OMA1 form by severing the N-terminal portion without recognizing a specific consensus sequence.
Study reveals a crucial role for OPA1 processing in the pathogenesis of neurodegenerative disease caused by m-AAA defects.
Classic ADOA groups were more likely to have mutations in exon 8 and 9, while ADOA 'plus' groups (patients with extra-ocular manifestations) were more likely to have mutations in exons 14, 15 and 17.
OPA1 levels maintain oxidative phosphorylation in iPSC-derived neurons, at least in part, by regulating the stability of complex I
A functional characterization using lymphoblostoid cell lines derived from affected members of a large Han Chinese family with autosomal dominant optic atrophy (ADOA) and control subjects provided the direct evidence for c.1198C > G mutation leading to ADOA.
Two models of Dominant Optic Atrophy were generated: the MGM1/OPA1 chimera yeast model and the Opa1-/- mouse embryonic fibroblasts model expressing the mutated human OPA1 isoform 1. The two models proved to be valuable tools to functionally assess and define the deleterious mechanism and the pathogenicity of novel OPA1 mutations.
OPA1 pathogenic variants are associated with autosomal-dominant optic atrophy.
OPA1 mediates adrenergic control of lipolysis in human adipocytes by regulating phosphorylation of perilipin 1.
clarify the role of Opa-1 and Drp-1 in mitochondrial dynamics and cell survival, a controversial alpha-synuclein research issue
This review presents an overview of all recent findings on OPA1 protein functions, on its dysfunction and related clinical phenotypes, focusing on the current therapeutic options and future perspectives to treat dominant optic atrophy and the other associated neurological disorders due to OPA1 mutations. [review]
Our data indicate that the LEU396ARG mutation in OPA1 is associated with severe dominant optic atrophy.
OPA1 gene therapy prevents retinal ganglion cell loss in a dominant optic atrophy mouse model.
We have generated a human iPSC line IISHDOi003-A from fibroblasts of a patient with a dominant optic atrophy 'plus' phenotype, harbouring a heterozygous mutation, c.1635C>A; p.Ser545Arg, in the OPA1 gene.
OPA1 is a dynamin-related GTPase that controls mitochondrial dynamics, cristae integrity, energetics and mitochondrial DNA maintenance, with eight isoforms being characterized. (Review)
Reports an assessment of the afferent visual system and OCT examination in an Italian cohort of fifty-two fully penetrant probands affected by Autosomal Dominant Optic Atrophy (ADOA) with OPA1 mutations and eight asymptomatic carriers of OPA1 mutations. Visual acuity and OCT data in missense mutations were compared with those associated with mutations inducing haploinsufficiency, and correlated with age in both groups.
we propose that the SIRT4-OPA1 axis is causally linked to mitochondrial dysfunction and altered mitochondrial dynamics that translates into aging-associated decreased mitophagy based on an unbalanced mitochondrial fusion/fission cycle.
Data indicate genotype-phenotype correlations between various types of optic Atrophy 1 (OPA1) mutation and mitophagy.
To our knowledge, our study is the first composite analysis of sirtuins in adult zebrafish retina and provides sufficient evidence that resveratrol, as an activator of SIRT1, protects NMDA-induced zebrafish retinal damage by potentially mediating mitochondrial sirtuins and OPA1 genes.
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