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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 59 products:
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
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
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.
Results suggest that Mfn2 (show MFN2 Antibodies) and OPA1 (show MED12 Antibodies) are upregulated during bone marrow progenitor differentiation and promote the migration of immature dendritic cells by regulating the expression of CCR7 (show CCR7 Antibodies).
Reactive oxygen species might affect MyHC (show MYH13 Antibodies) content by modulating OPA1 (show MED12 Antibodies) cleavage in muscle degeneration.
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
Data show that OPA1 physiological levels are important in cardiovascular health by maintaining mitochondrial shape and respiratory function, while its down-regulation is associated with cardiovascular disease. [review]
increased percentage of apoptotic cells in autosomal dominant optic atrophy patients compared to controls; suggests susceptibility of ADOA cells to oxidative stress and correlation between OPA1 protein dysfunctions and morphological-functional alterations to mitochondria; also results imply sensitivity of mutated protein to free radical damage
Distributed abnormalities of diffusivity indexes might reflect abnormal intracellular mitochondrial morphology as well as alteration of protein levels due to OPA1 mutations.
A recurrent deletion mutation in OPA1 causes autosomal dominant optic atrophy in a Chinese family.
Two heterozygous OPA1 missense mutations affecting highly conserved amino acid positions (p.G488R, p.A495V) were associated with chronic progressive external ophthalmoplegia, parkinsonism, and dementia in two Italian families.
OPA1 mutations induced mitochondrial fragmentation, uncoupled mitochondrial respiration, and elicited dysfunctional bioenergetics.
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