Recombinant Mouse Dynamin-like 120 kDa protein, mitochondrial (Opa1), partial

1. Propose a novel function of OPA1 in mediating the CoQ10-responsive regulation of respiratory CIV activity in brain mitochondria from aging mice. PMID: 28890359
2. multiple OPA1 isoforms are required for mitochondrial dynamics, while any single isoform can support all other functions. PMID: 28636943
3. 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. PMID: 28552492
4. Mitochondrial dysfunction in an Opa1 mouse model of dominant optic atrophy results from Opa1 haploinsufficiency. PMID: 27468686
5. TNFR2 activation protects cardiac myocytes against stress by up-regulating OPA1 expression. PMID: 28637784
6. 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. PMID: 28607005
7. OPA1 modulates cristae morphology but is dispensable for cristae junction formation. Endogenous OPA1 and MIC60 show a physical interaction. PMID: 27587279
8. Opa1 deficiency was associated with increased sensitivity to Ischemia-Reperfusion Injuries, imbalance in dynamic mitochondrial Ca2+ uptake, and subsequent increase in NCX activity. PMID: 27723783
9. 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. PMID: 26024391
10. stress-induced OMA1 activation and guanosine triphosphatase OPA1 cleavage limit mitochondrial fusion and promote neuronal death PMID: 26783299
11. 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. PMID: 26393574
12. results indicate that the OPA1-dependent cristae remodeling pathway is a fundamental, targetable determinant of tissue damage in vivo. PMID: 26039448
13. cristae shape amelioration by controlled Opa1 overexpression improves two mouse models of mitochondrial disease. PMID: 26039449
14. 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. PMID: 26785494
15. 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] PMID: 26375863
16. Photoresponsive RGCs are protected against cell death due to the Opa1 mutation, but not by melanopsin expression itself. PMID: 26218912
17. 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. PMID: 25387754
18. Reactive oxygen species might affect MyHC content by modulating OPA1 cleavage in muscle degeneration. PMID: 25393477
19. mitochondria adapt to metabolic shifts through the parallel remodeling of the cristae and of the MERCs via a mechanism that degrades Opa1 in an Mfn2-dependent pathway. PMID: 25352671
20. a novel way in which OPA1 senses energy substrate availability, which modulates its function in the regulation of mitochondrial architecture in a SLC25A protein-dependent manner. PMID: 25298396
21. Proteolytic cleavage of Opa1 stimulates mitochondrial inner membrane fusion and couples fusion to oxidative phosphorylation. PMID: 24703695
22. OPA1 appears necessary for the normal adaptive response and mitochondrial biogenesis of skeletal muscle to training. PMID: 24042504
23. OMA1-mediated OPA1 proteolysis plays an important role in the disruption of mitochondrial dynamics in ischemic acute kidney injury. PMID: 24671334
24. findings show that transient matrix contraction is a novel cellular mechanism regulating mitochondrial activity through the function of the inner membrane dynamin OPA1 PMID: 24627489
25. Constitutive OPA1 cleavage by YME1L and OMA1 at two distinct sites leads to the accumulation of both long and short forms of OPA1 and maintains mitochondrial fusion. PMID: 24616225
26. OPA1 mutation leads to deficiency in antioxidant transcripts, increased reactive oxygen species, mitochondrial dysfunction, and late-onset cardiomyopathy. PMID: 23316298
27. the OPA1/PARL dependent pathway of cristae remodeling is implicated in heat shock. PMID: 22579715
28. Opa1-dependent inner membrane remodeling controls efficiency of steroidogenesis. PMID: 22658590
29. OPA1 plays an important role in mitochondrial morphology and mitochondrial permeability transition pore functioning. PMID: 22406748
30. This study showed that mitochondrial fission protein dynamin-related protein 1 (Drp1) and fusion protein optic atrophy 1 (Opa1) were both upregulated in the ischemic penumbra. PMID: 22345048
31. Opa1 is essential for retinal ganglion cell synaptic architecture and connectivity PMID: 22300878
32. Optic atrophy 1 is an A-kinase anchoring protein on lipid droplets that mediates adrenergic control of lipolysis. PMID: 21983901
33. Beta cells lacking Opa1 maintained normal copy numbers of mtDNA; however, the amount and activity of electron transport chain complex IV were significantly decreased PMID: 21551073
34. study provides the first evidence that homocysteine-induced ganglion cell loss involves the dysregulation of mitochondrial dynamics, both in vivo and in vitro. PMID: 21642619
35. Opa1 as a potential therapeutic target to promote neuronal survival following acute brain damage and neurodegenerative diseases. PMID: 21041314
36. Mitochondrial retention of Opa1 protein is essential for normal embryogenesis. PMID: 20652258
37. OPA1 can directly modulate retinal ganglion cell survival, and increasing OPA1 expression may protect against retinal ganglion cell death in glaucomatous optic neuropathy. PMID: 20664796
38. These results highlight the importance of normal mitochondrial fusion balance, as influenced by the OPA1 protein in maintaining the dendritic morphology of retinal ganglion cells. PMID: 20817698
39. OPA1 disease alleles associated with dominant optic atrophy display selective defects in several activities, including cardiolipin association, GTP hydrolysis and membrane tubulation. PMID: 20185555
40. Our results indicate an important role of OPA1 in mitochondrial dependent Ca(2+) homeostasis and cell survival in retinal ganglion cells. PMID: 20450306
41. A direct effect of loss of Omi/HtrA2 on mitochondrial morphology and a novel role of this mitochondrial serine protease in the modulation of OPA1. PMID: 20064504
42. This is the first electrophysiological demonstration of a visual function deficit in aged Opa1 mice. VEP measurements and retrograde labeling experiments show that the number of RGCs is reduced whereas the remaining RGCs and axons function normally. PMID: 19834041
43. Double Mfn-null cells show neither outer nor inner membrane fusion, while mitochondria in OPA1-null cells contain multiple matrix compartments bounded together by a single outer membrane, consistent with uncoupling of outer versus inner membrane fusion. PMID: 19477917
44. The data suggest an important and specific function of the OPA1 protein, not only in the optic nerve forming ganglion cells but also in the intrinsic signal processing of the inner retina. PMID: 15505078
45. OPA1 functionally requires mitofusin 1 to regulate mitochondrial fusion PMID: 15509649
46. OPA1, Mfn1 and Mfn2 have roles in mitochondrial fusion, cell growth, mitochondrial membrane potential, and cellular respiration PMID: 15899901
47. Thus, OPA1 has genetically and molecularly distinct functions in mitochondrial fusion and in cristae remodeling during apoptosis. PMID: 16839885
48. mitochondrial fragmentation correlates with processing of large isoforms of OPA1 PMID: 17003040
49. Manipulation of OPA1 isoform 1 levels in induces changes in the mitochondrial network in the cell; mutations of isoform 1 could lead to devastating effects on retinal ganglion cells. PMID: 18419770
50. IOP elevation may directly damage mitochondria in the ONH axons by promoting reduction of COX, mitochondrial fission and cristae depletion, alterations of OPA1 and Dnm1 expression, and induction of OPA1 release. PMID: 18469184

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KEGG: mmu:74143

STRING: 10090.ENSMUSP00000036993

UniGene: Mm.274285