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
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Atlastin GTPases are required for Golgi apparatus and ER morphogenesis.
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ATL2 and ATL3 localize to the ER and atlastin GTPase-defective mutants disrupt ER reticularization, while general ER-to-Golgi trafficking remains essentially normal.
"atlastin-2 and -3 are localized to the endoplasmic reticulum (ER)"
A class of dynamin-like GTPases involved in the generation of the tubular ER network.
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Mammalian atlastins are dynamin-like integral membrane GTPases that localize to tubular ER and support formation of the tubular ER network.
"mammalian atlastins, which are dynamin-like, integral membrane GTPases, interact with the tubule-shaping proteins"
Defining the membrane proteome of NK cells.
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A broad high-throughput membrane proteomics study identified membrane-associated proteins; this supports only a generic membrane annotation for ATL3.
"The present study was initiated to define the composition of the membrane proteome of the Natural Killer (NK) like cell line YTS."
Protrudin binds atlastins and endoplasmic reticulum-shaping proteins and regulates network formation.
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Protrudin/ZFYVE27 binds atlastins and other tubular ER network proteins, supporting an interaction annotation but not a specific molecular activity for ATL3.
"Protrudin binds atlastins and endoplasmic reticulum-shaping proteins and regulates network formation."
Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3.
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ATL3 is an ER-shaping GTPase enriched at three-way junctions, and the HSN1F variant disrupts tubular ER structure.
"ATL3 proteins are enriched in three-way junctions, branch points of the endoplasmic reticulum that connect membranous tubules to a continuous network."
Lunapark stabilizes nascent three-way junctions in the endoplasmic reticulum.
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Lunapark work supports the three-way-junction context of the ER tubular network, but the accessible cached abstract is not ATL3-specific.
"The endoplasmic reticulum (ER) consists of a polygonal network of sheets and tubules interconnected by three-way junctions."
Cooperation of the ER-shaping proteins atlastin, lunapark, and reticulons to generate a tubular membrane network.
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ATL proteins, including ATL3 in mammalian cells, are needed for formation and maintenance of the tubular ER network.
"ATL is needed to not only form, but also maintain, the ER network."
Timing and Reset Mechanism of GTP Hydrolysis-Driven Conformational Changes of Atlastin.
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Structural and kinetic work on ATL1 and ATL3 supports ATL3 GTPase activity and nucleotide-dependent dimerization during the atlastin catalytic cycle.
"we identify discrete temporal steps in the catalytic cycle for the two most dissimilar isoforms, ATL1 and ATL3"
REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects.
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REEP5 work places atlastin-mediated membrane fusion in the SR/ER network organization context and supports an ATL3-REEP5 interaction annotation only as a generic protein interaction.
"ER tubules are also stabilized by forming a characteristic polygonal network through membrane fusion mediated by the atlastin family of dynamin-related GTPases"
The hypervariable region of atlastin-1 is a site for intrinsic and extrinsic regulation.
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Atlastin proteins catalyze homotypic peripheral ER tubule fusion, and the study includes ATL3 structural/biochemical comparisons.
"Atlastin (ATL) GTPases catalyze homotypic membrane fusion of the peripheral endoplasmic reticulum (ER)."
Human atlastin-3 is a constitutive ER membrane fusion catalyst.
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Purified human ATL3 directly catalyzes GTP-dependent membrane fusion and can sustain ER network structure in ATL knockout cells.
"purified human ATL3 catalyzes efficient membrane fusion in vitro and is sufficient to sustain the ER network in triple knockout cells."
ATL3 review notes for Proteostasis PN batch
Falcon deep research report on ATL3
Proteostasis Network projected annotations report