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OPA1 product is a nuclear-encoded mitochondrial protein with similarity to dynamin-related GTPases. Additionally we are shipping OPA1 Antibodies (61) and many more products for this protein.
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Whereas Parkin (show PARK2 Proteins) has been reported to positively regulate the expression of OPA1 through NEMO (show IKBKG Proteins), herein we found that PARK2 (show PARK2 Proteins) overexpression did not modify the expression of OPA1.
stress-induced OMA1 (show OMA1 Proteins) 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 (show YME1L1 Proteins), are altered; in vitro and in vivo, OPA1 is cleaved to shorter forms and Yme1L (show YME1L1 Proteins) 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 (show OMA1 Proteins) 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 (show DNM1L Proteins)), and Mfn1 (show MFN1 Proteins)/2 (mitofusin 1 (show MFN1 Proteins) and 2). [REVIEW]
Photoresponsive RGCs are protected against cell death due to the Opa1 mutation, but not by melanopsin (show OPN4 Proteins) expression itself.
Results suggest that Mfn2 (show MFN2 Proteins) and OPA1 are upregulated during bone marrow progenitor differentiation and promote the migration of immature dendritic cells by regulating the expression of CCR7 (show CCR7 Proteins).
Reactive oxygen species might affect MyHC content by modulating OPA1 cleavage in muscle degeneration.
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 Proteins) and middle domains of OPA1, respectively, were identified in two patients.These two different conformational changes might result in decreased GTPase (show RACGAP1 Proteins) 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 Proteins) 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
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