Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
The layered structure of human mitochondrial DNA nucleoids.
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ATAD3 is associated with native nucleoids but does not cross-link to mtDNA, supporting a peripheral/layered nucleoid interpretation.
"Several other metabolic proteins and chaperones identified in native nucleoids, including ATAD3, were not observed to cross-link to mtDNA"
The AAA+ ATPase ATAD3A controls mitochondrial dynamics at the interface of the inner and outer membranes.
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ATAD3A spans mitochondrial membrane interfaces with an N-terminal outer-membrane-facing region, inner-membrane anchoring segment, and matrix-facing AAA+ ATPase domain.
"The N-terminal domain interacts with the OM"
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ATAD3A regulates mitochondrial inner/outer membrane interactions and mitochondrial dynamics.
"ATAD3A regulates dynamic interactions between the mitochondrial OM and IM sensed by the cell fission machinery."
ATPase family AAA domain-containing 3A is a novel anti-apoptotic factor in lung adenocarcinoma cells.
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ATAD3A is experimentally detected in lung adenocarcinoma and supports survival/drug-response phenotypes.
"Expression of ATAD3A was detected by reverse transcription-polymerase chain reaction, immunoblotting, immunohistochemistry and confocal immunofluorescent microscopy."
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ATAD3A silencing increases mitochondrial fragmentation and cisplatin sensitivity in lung adenocarcinoma cells.
"Silencing of ATAD3A expression increased mitochondrial fragmentation and cisplatin sensitivity."
Topological analysis of ATAD3A insertion in purified human mitochondria.
ATAD3B is a human embryonic stem cell specific mitochondrial protein, re-expressed in cancer cells, that functions as dominant negative for the ubiquitous ATAD3A.
ATAD3A oligomerization causes neurodegeneration by coupling mitochondrial fragmentation and bioenergetics defects.
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ATAD3A interacts with Drp1 and links mitochondrial fragmentation to mtDNA damage and bioenergetic defects in neurodegeneration models.
"ATAD3A plays a key role in neurodegeneration by linking Drp1-induced mitochondrial fragmentation to defective mtDNA maintenance"
Structural Basis of Mitochondrial Scaffolds by Prohibitin Complexes: Insight into a Role of the Coiled-Coil Region.
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ATAD3A participates in a mitochondrial CLPB/PHB/MAVS scaffold required for antiviral innate immune signaling.
"CLPB bridges PHB complexes (IMM) and MAVS (OMM) with the assistance of AKAP1 and ATAD3A at the IMS and invokes an immune response from the mitochondrial signalosome"
Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.
Mitochondrial DNA breaks activate an integrated stress response to reestablish homeostasis.
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ATAD3A participates in mitochondrial DNA break-triggered ISR signaling from damaged genomes to the inner membrane.
"we identified ATAD3A-a membrane-bound protein interacting with nucleoids-as potentially pivotal in relaying signals from impaired genomes to the inner mitochondrial membrane."
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Mitochondrial DNA breaks activate integrated stress response signaling.
"mtDSBs triggered the integrated stress response (ISR)"
PERK-ATAD3A interaction provides a subcellular safe haven for protein synthesis during ER stress.
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ATAD3A binds PERK during ER stress and forms mitochondria-ER contact sites.
"PERK-ATAD3A interactions increased during ER stress, forming mitochondria-ER contact sites."
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ATAD3A attenuates local PERK signaling and helps preserve mitochondrial protein synthesis during ER stress.
"ATAD3A binding attenuated local PERK signaling and rescued the expression of some mitochondrial proteins."
The AAA+ protein ATAD3 has displacement loop binding properties and is involved in mitochondrial nucleoid organization.
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ATAD3 is a mitochondrial nucleoid-associated AAA+ protein with D-loop binding properties.
"human ATAD3 is a component of many, but not all, mitochondrial nucleoids"
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ATAD3 depletion alters mitochondrial nucleoid structure and affects protein-bound D-loop-containing mtDNA fragments.
"altered the structure of mitochondrial nucleoids and led to the dissociation of mitochondrial DNA fragments held together by protein, specifically, ones containing the D-loop region"
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ATAD3 has functional ATPase activity.
"The ATPase of ATAD3 is functional"
Mitochondrial nucleoid interacting proteins support mitochondrial protein synthesis.
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ATAD3 supports mitochondrial protein synthesis and binds mitochondrial ribosomes.
"Both proteins are demonstrated to be required for mitochondrial protein synthesis in human cultured cells, and the major binding partner of ATAD3 is the mitochondrial ribosome."
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Altered ATAD3 expression perturbs mtDNA maintenance and replication.
"Altered ATAD3 expression also perturbs mtDNA maintenance and replication."
Manual deep research synthesis for ATAD3A
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Provider-backed deep research was unavailable, so this review used a manual synthesis.
"Falcon deep research was requested but timed out after 600 seconds, and the configured Perplexity fallback failed with an insufficient-quota 401 error."
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The PN mitophagy projection was not propagated for ATAD3A.
"Manual synthesis decision: ATAD3A is not currently supported as a direct mitophagy cargo-marking or PINK/PRKN pathway factor."
Curator notes for ATAD3A PN review
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The Proteostasis PN mitophagy projection was evaluated conservatively and not added.
"I did not add GO:0000423 mitophagy."
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Generic protein binding annotations were marked as over-annotations.
"Marked generic protein binding annotations as over-annotated."