scholarly article | Q13442814 |
P50 | author | Donald D Newmeyer | Q82635337 |
Marcela Votruba | Q56469509 | ||
Alexander Y. Andreyev | Q58048217 | ||
P2093 | author name string | T Kuwana | |
Y Seong | |||
W B Kiosses | |||
Y Kushnareva | |||
P2860 | cites work | The effect of OPA1 on mitochondrial Ca²⁺ signaling | Q21135012 |
OPA1 mutations induce mitochondrial DNA instability and optic atrophy 'plus' phenotypes | Q24304868 | ||
Loss of OPA1 perturbates the mitochondrial inner membrane structure and integrity, leading to cytochrome c release and apoptosis | Q24338169 | ||
Opa1 deficiency in a mouse model of autosomal dominant optic atrophy impairs mitochondrial morphology, optic nerve structure and visual function | Q80146686 | ||
Preparation, culture, and immortalization of mouse embryonic fibroblasts | Q80674195 | ||
Defective mitochondrial fusion, altered respiratory function, and distorted cristae structure in skin fibroblasts with heterozygous OPA1 mutations | Q84577155 | ||
Characterization of Ca2+ signalling in postnatal mouse retinal ganglion cells: involvement of OPA1 in Ca2+ clearance | Q43070109 | ||
Mitochondrial shape governs BAX-induced membrane permeabilization and apoptosis. | Q43099640 | ||
Loss of the intermembrane space protein Mgm1/OPA1 induces swelling and localized constrictions along the lengths of mitochondria | Q44768454 | ||
OPA1 deficiency associated with increased autophagy in retinal ganglion cells in a murine model of dominant optic atrophy. | Q46113788 | ||
OPA1 mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion | Q46789094 | ||
The human OPA1delTTAG mutation induces premature age-related systemic neurodegeneration in mouse. | Q48248957 | ||
Opa1 is essential for retinal ganglion cell synaptic architecture and connectivity. | Q48679280 | ||
Endoplasmic reticulum stress-induced apoptosis requires bax for commitment and Apaf-1 for execution in primary neurons. | Q50913051 | ||
OPA1 mutations in patients with autosomal dominant optic atrophy and evidence for semi-dominant inheritance | Q74147611 | ||
Effects of OPA1 mutations on mitochondrial morphology and apoptosis: relevance to ADOA pathogenesis | Q79432048 | ||
Roles of the mammalian mitochondrial fission and fusion mediators Fis1, Drp1, and Opa1 in apoptosis | Q24562044 | ||
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy | Q24652230 | ||
Deletion of the OPA1 gene in a dominant optic atrophy family: evidence that haploinsufficiency is the cause of disease | Q24679112 | ||
Endoplasmic reticulum stress induces calcium-dependent permeability transition, mitochondrial outer membrane permeabilization and apoptosis | Q28240946 | ||
OPA1-dependent cristae modulation is essential for cellular adaptation to metabolic demand | Q28249429 | ||
OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion | Q28251846 | ||
A novel deletion in the GTPase domain of OPA1 causes defects in mitochondrial morphology and distribution, but not in function | Q28289677 | ||
Bax activation initiates the assembly of a multimeric catalyst that facilitates Bax pore formation in mitochondrial outer membranes | Q28483986 | ||
Mfn2 modulates the UPR and mitochondrial function via repression of PERK | Q28589398 | ||
Disruption of fusion results in mitochondrial heterogeneity and dysfunction | Q29616566 | ||
Nonsense-mediated mRNA decay in health and disease | Q29619553 | ||
Dominant optic atrophy. | Q30459784 | ||
Opa1-mediated cristae opening is Bax/Bak and BH3 dependent, required for apoptosis, and independent of Bak oligomerization | Q30485835 | ||
Loss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity | Q30532888 | ||
OPA1 mutations cause cytochrome c oxidase deficiency due to loss of wild-type mtDNA molecules | Q33980340 | ||
Increased optic atrophy type 1 expression protects retinal ganglion cells in a mouse model of glaucoma | Q34001754 | ||
Mitochondrial optic neuropathies - disease mechanisms and therapeutic strategies | Q34152110 | ||
Higd-1a interacts with Opa1 and is required for the morphological and functional integrity of mitochondria | Q34359338 | ||
Activation of mitochondrial protease OMA1 by Bax and Bak promotes cytochrome c release during apoptosis | Q34384160 | ||
The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells | Q35083432 | ||
A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics | Q35657086 | ||
The impact of the unfolded protein response on human disease | Q36062081 | ||
OPA1 mutation and late-onset cardiomyopathy: mitochondrial dysfunction and mtDNA instability | Q36522684 | ||
Mitochondrial cristae shape determines respiratory chain supercomplexes assembly and respiratory efficiency | Q37215027 | ||
Caspase-independent mitochondrial cell death results from loss of respiration, not cytotoxic protein release. | Q37448270 | ||
OPA1 functions in mitochondria and dysfunctions in optic nerve. | Q37457225 | ||
OPA1-associated disorders: phenotypes and pathophysiology. | Q37457238 | ||
Bioenergetics and cell death. | Q37774677 | ||
Mouse models of dominant optic atrophy: what do they tell us about the pathophysiology of visual loss? | Q37783778 | ||
Mitochondrial Cristae: Where Beauty Meets Functionality. | Q38726665 | ||
The antiapoptotic OPA1/Parl couple participates in mitochondrial adaptation to heat shock | Q39349684 | ||
Secondary mtDNA defects do not cause optic nerve dysfunction in a mouse model of dominant optic atrophy | Q39951945 | ||
A splice site mutation in the murine Opa1 gene features pathology of autosomal dominant optic atrophy. | Q40240586 | ||
Low reserve of cytochrome c oxidase capacity in vivo in the respiratory chain of a variety of human cell types. | Q40993797 | ||
P275 | copyright license | Creative Commons Attribution 4.0 International | Q20007257 |
P6216 | copyright status | copyrighted | Q50423863 |
P921 | main subject | haploinsufficiency | Q852654 |
optic atrophy | Q3629049 | ||
P304 | page(s) | e2309 | |
P577 | publication date | 2016-07-28 | |
P1433 | published in | Cell Death and Disease | Q2197222 |
P1476 | title | Mitochondrial dysfunction in an Opa1(Q285STOP) mouse model of dominant optic atrophy results from Opa1 haploinsufficiency | |
P478 | volume | 7 |
Q41825073 | Autophagy controls the pathogenicity of OPA1 mutations in dominant optic atrophy |
Q89295264 | Mitochondrial dynamics in adaptive and maladaptive cellular stress responses |
Q57490178 | Overexpression of Optic Atrophy Type 1 Protects Retinal Ganglion Cells and Upregulates Parkin Expression in Experimental Glaucoma |
Q92632027 | Phenotypic selection with an intrabody library reveals an anti-apoptotic function of PKM2 requiring Mitofusin-1 |
Q89558188 | Targeted next-generation sequencing extends the mutational spectrums for OPA1 mutations in Chinese families with optic atrophy |