Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Nuclear gene OPA1, encoding a mitochondrial dynamin-related protein, is mutated in dominant optic atrophy.
OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28.
Primary structure of a dynamin-related mouse mitochondrial GTPase and its distribution in brain, subcellular localization, and effect on mitochondrial morphology.
Differential sublocalization of the dynamin-related protein OPA1 isoforms in mitochondria.
Loss of OPA1 perturbates the mitochondrial inner membrane structure and integrity, leading to cytochrome c release and apoptosis.
Regulation of mitochondrial morphology through proteolytic cleavage of OPA1.
Mitochondrial functions and estrogen receptor-dependent nuclear translocation of pleiotropic human prohibitin 2.
Mitochondrial fission and fusion mediators, hFis1 and OPA1, modulate cellular senescence.
OPA1 mutations induce mitochondrial DNA instability and optic atrophy 'plus' phenotypes.
Defining the membrane proteome of NK cells.
OPA1 disease alleles causing dominant optic atrophy have defects in cardiolipin-stimulated GTP hydrolysis and membrane tubulation.
The BH3-only Bnip3 binds to the dynamin Opa1 to promote mitochondrial fragmentation and apoptosis by distinct mechanisms.
OPA1 links human mitochondrial genome maintenance to mtDNA replication and distribution.
ChChd3, an inner mitochondrial membrane protein, is essential for maintaining crista integrity and mitochondrial function.
Mff is an essential factor for mitochondrial recruitment of Drp1 during mitochondrial fission in mammalian cells.
Vital function of PRELI and essential requirement of its LEA motif.
The E3 ligase parkin maintains mitochondrial integrity by increasing linear ubiquitination of NEMO.
Functional interaction of Parkinson's disease-associated LRRK2 with members of the dynamin GTPase superfamily.
SIRT3 deacetylates and activates OPA1 to regulate mitochondrial dynamics during stress.
A Genome-wide CRISPR Death Screen Identifies Genes Essential for Oxidative Phosphorylation.
Molecular basis of selective mitochondrial fusion by heterotypic action between OPA1 and cardiolipin.
WBSCR16 Is a Guanine Nucleotide Exchange Factor Important for Mitochondrial Fusion.
Parkinson's disease-associated LRRK2-G2019S mutant acts through regulation of SERCA activity to control ER stress in astrocytes.
Two forms of Opa1 cooperate to complete fusion of the mitochondrial inner-membrane.
Cryo-EM structures of S-OPA1 reveal its interactions with membrane and changes upon nucleotide binding.
The short variant of optic atrophy 1 (OPA1) improves cell survival under oxidative stress.
Structural insights into G domain dimerization and pathogenic mutation of OPA1.
MICOS assembly controls mitochondrial inner membrane remodeling and crista junction redistribution to mediate cristae formation.
OPA1 and MICOS Regulate mitochondrial crista dynamics and formation.
Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.
Structural mechanism of mitochondrial membrane remodelling by human OPA1.
OPA1 helical structures give perspective to mitochondrial dysfunction.