Affinage

ATL3

Atlastin-3 · UniProt Q6DD88

Length
541 aa
Mass
60.5 kDa
Annotated
2026-06-09
47 papers in source corpus 20 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATL3 is a dynamin-like GTPase of the tubular endoplasmic reticulum that drives homotypic ER membrane fusion to build and maintain the polygonal ER network, and additionally functions as a selective ER-phagy receptor (PMID:30773365, PMID:27669642). Loss of all three atlastins abolishes the formation of three-way ER tubule junctions, a defect rescuable by any single atlastin or distant orthologs, establishing ATL3 within a redundant machinery essential for the polygonal ER (PMID:27669642); crystallographic and biochemical analysis defines its catalytic cycle of nucleotide binding, dimerization, hydrolysis, and Mg2+ displacement to reset the enzyme, and an isoform-specific N-terminal hypervariable region subject to phospho-regulation (PMID:28602821, PMID:34546351). Its fusion activity is restrained downstream by Lunapark, which localizes to junctions in an ATL-dependent manner and inhibits further ATL-mediated fusion in vitro (PMID:30498943). As an ER-phagy receptor, ATL3 selectively binds GABARAP-subfamily Atg8 proteins (but not LC3) through two GABARAP-interaction motifs to target tubular ER for starvation-induced lysosomal degradation, with UVRAG promoting cargo-receptor oligomerization and Atg8 recruitment at ER-phagy sites (PMID:30773365, PMID:37902287); ATL3 acts in parallel with RTN3L to clear misfolded, aggregation-prone substrates and to sequester misassembled FG-nucleoporins as a form of ER quality control (PMID:38818751, PMID:40079246), and partners with RTN3L to form ER tubular bodies that mediate Golgi-independent unconventional secretion of transmembrane cargo (PMID:39919755). The HSAN I mutations Y192C and P338R abolish GABARAP binding and ER-phagy, mislocalize ATL3 from junctions, disrupt tubular ER and Golgi morphology, increase ER-mitochondria contacts, and impair axonal growth and mitochondrial transport, linking defective ER dynamics and ER-phagy to peripheral neuropathy (PMID:30773365, PMID:30680846, PMID:24459106, PMID:30666337, PMID:30339187). ATL3 is exploited by multiple pathogens: it is recruited to Zika virus replication complexes via NS2A/NS2B3 and to SV40 entry foci, supports Legionella-containing vacuole expansion through GTP-dependent membrane remodeling, and is sequestered by coronavirus ORF8/p62 condensates to suppress ER-phagy and promote viral double-membrane vesicle formation (PMID:31534046, PMID:28835546, PMID:36952345, PMID:37578227).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2011 Medium

    Early evidence connected ATL3 to maintenance of distinct ER subdomains by showing it associates with STAT5 and is required to maintain cystic ER boundaries, hinting at a structural ER-shaping role before its enzymology was defined.

    Evidence Cross-immunopanning and siRNA knockdown with fluorescence microscopy

    PMID:22159083 PMID:23151802

    Open questions at the time
    • Mechanistic link between STAT5 binding and ER morphology unresolved
    • Single immunopanning method without reciprocal biochemical validation of the interaction
  2. 2014 High

    Localization studies established ATL3 as a junction-enriched ER GTPase and showed the HSAN I mutation Y192C mislocalizes it and disrupts tubular ER, framing a dominant-negative morphological disease mechanism.

    Evidence Immunofluorescence of wild-type and mutant ATL3 in cells and patient samples

    PMID:24459106

    Open questions at the time
    • Did not define the catalytic basis of fusion
    • Did not establish whether the morphology defect is causal for neuropathy
  3. 2016 High

    CRISPR triple knockout of all atlastins resolved whether ATL3 is necessary for ER network architecture, showing atlastins are collectively required for three-way junction formation and functionally interchangeable with distant orthologs.

    Evidence Atl1/2/3 triple knockout NIH-3T3 cells with ortholog rescue and ER morphology imaging

    PMID:27669642

    Open questions at the time
    • Redundancy obscures ATL3-specific contributions
    • Did not address isoform-specific functions or regulation
  4. 2017 High

    Crystal structures of ATL3 captured discrete catalytic intermediates, establishing the molecular mechanism of its GTPase cycle including Mg2+ displacement to reset the enzyme for repeated fusion.

    Evidence X-ray crystallography with comparative ATL1/ATL3 GTPase biochemistry

    PMID:28602821

    Open questions at the time
    • Structures of full fusion intermediates on membranes not resolved
    • Functional difference between ATL1 and ATL3 isoforms not defined here
  5. 2017 High

    Work on Legionella showed ATL3/Sey1 is hijacked for pathogen vacuole biogenesis, with in vitro reconstitution demonstrating GTP-specific membrane aggregation, extending ATL3's fusion activity to a host-pathogen context.

    Evidence LCV proteomics, in vitro GTP/GDP aggregation assay, dominant-negative mutant and knockdown

    PMID:28835546

    Open questions at the time
    • Direct role in mammalian infection versus model amoeba not delineated
    • How the pathogen recruits ATL3 is unknown
  6. 2018 High

    Lunapark was placed downstream of ATL activity, showing ATL3 controls Lnp junction localization while Lnp in turn limits further ATL-mediated fusion, defining a feedback that stabilizes junctions.

    Evidence Mutation analysis, in vitro vesicle fusion with purified Lnp N-terminus, ATL KO rescue

    PMID:30498943

    Open questions at the time
    • Stoichiometry and dynamics of the ATL3-Lnp feedback in cells not quantified
  7. 2019 High

    ATL3 was identified as a selective tubular ER-phagy receptor binding GABARAP-subfamily proteins through two GIMs, defining a degradative function distinct from its fusion role and explaining starvation-induced ER turnover.

    Evidence Reciprocal Co-IP, GIM binding assays, starvation autophagy flux and microscopy

    PMID:30773365

    Open questions at the time
    • Selectivity for GABARAP over LC3 mechanism not fully resolved
    • Regulation of switching between fusion and ER-phagy functions unknown
  8. 2019 High

    The HSAN I mutations were mechanistically tied to ER-phagy and broad organelle dysfunction, showing Y192C and P338R abolish GABARAP binding, disrupt ER/Golgi/nuclear morphology, increase ER-mitochondria contacts, and impair axonal growth and mitochondrial transport.

    Evidence Mutant expression in cells and primary neurons, patient fibroblasts, EM of contact sites, Ca2+ imaging, autophagy and axon assays

    PMID:30339187 PMID:30666337 PMID:30680846 PMID:30773365

    Open questions at the time
    • Which downstream defect is the primary driver of neuropathy not established
    • Relative contributions of lost fusion versus lost ER-phagy not separated
  9. 2019 Medium

    ATL3 was shown to be co-opted by Zika virus, binding NS2A/NS2B3 and supporting replication, extending pathogen exploitation of ATL3 ER dynamics to a flavivirus.

    Evidence Co-IP with viral proteins, siRNA knockdown, colocalization at replication sites, viral titers

    PMID:31534046

    Open questions at the time
    • Whether fusion or ER-phagy activity is the relevant function for ZIKV unclear
    • Single lab without reciprocal interaction validation
  10. 2021 High

    Structures of both ATL1 and ATL3 defined the N-terminal hypervariable region as an isoform-specific, phospho-regulated element affecting membrane tethering, providing a basis for differential regulation of atlastin paralogs.

    Evidence X-ray crystallography of ATL1/ATL3, in vitro tethering assays, kinase screen and PTM mapping

    PMID:34546351

    Open questions at the time
    • Functional consequence of ATL3 HVR phosphorylation specifically not detailed
    • Physiological kinase for the site not validated
  11. 2023 Medium

    ATL3's ER-phagy receptor activity was shown to be a viral target, with coronavirus ORF8 sequestering ATL3 into p62 condensates to inhibit ER-phagy and promote double-membrane vesicle formation.

    Evidence Co-IP, condensate assays, ER-phagy flux, viral replication and DMV electron microscopy

    PMID:36952345

    Open questions at the time
    • Direct versus indirect ATL3-ORF8 binding within condensates not separated
    • Single lab
  12. 2023 Medium

    UVRAG was identified as a regulator of ER-phagy that interacts with ATL3 and promotes cargo-receptor oligomerization and Atg8 recruitment, placing ATL3 in a larger assembly mechanism for ER-phagy sites.

    Evidence Co-IP, oligomerization and ER-phagy flux assays, knockdown, microscopy

    PMID:37902287

    Open questions at the time
    • Whether UVRAG acts specifically on ATL3 versus multiple receptors not resolved
    • Single lab
  13. 2023 Medium

    ATL3's GTPase-dependent fusion was shown to build multi-tubular ER junctions at SV40 entry foci, demonstrating that a non-enveloped virus exploits ATL3 membrane remodeling for cell entry.

    Evidence Fluorescence and electron microscopy, knockdown, dominant-negative GTPase mutant, Co-IP with viral penetration complex

    PMID:37578227

    Open questions at the time
    • Mechanism by which ATL3 engages the penetration complex not defined
    • Single lab
  14. 2024 Medium

    ATL3 was shown to act with RTN3L at dedicated ER-phagy sites to clear aggregation-prone misfolded proteins, distinguishing parallel tubular ER-phagy pathways and defining ATL3 substrates.

    Evidence Colocalization microscopy, individual receptor knockdowns, autophagy flux with misfolded substrates

    PMID:38818751

    Open questions at the time
    • How substrate selectivity between parallel receptors is achieved unknown
    • Single lab
  15. 2025 High

    ATL3 was implicated in two further ER-shaping functions: with RTN3L it forms ER tubular bodies mediating Golgi-independent unconventional secretion, and with RTN3L/LNP it sequesters misassembled FG-nucleoporins as ER-based quality control.

    Evidence Correlative light-electron microscopy, knockdown/overexpression, UPS assays and nuclear transport assays

    PMID:39919755 PMID:40079246

    Open questions at the time
    • How ATL3 fusion activity is repurposed toward secretory tubular bodies versus degradation unclear
    • Mechanism of nucleoporin sequestration not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown how ATL3 is molecularly switched between its membrane-fusion, ER-phagy, unconventional-secretion, and quality-control roles, and which single downstream defect drives HSAN I pathology.
  • No defined regulatory mechanism partitioning ATL3 among its functions
  • Causal hierarchy of mutant phenotypes in neuropathy unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 5 GO:0060090 molecular adaptor activity 3 GO:0140657 ATP-dependent activity 2
Localization
GO:0005783 endoplasmic reticulum 4 GO:0005635 nuclear envelope 1
Pathway
R-HSA-1643685 Disease 4 R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-9612973 Autophagy 3 R-HSA-9609507 Protein localization 1
Partners
GABARAPLNPKRTN3LSTAT5ASTAT5BUVRAG

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2019 ATL3 functions as a receptor for tubular ER-phagy by specifically binding to GABARAP (but not LC3) subfamily proteins via two GABARAP interaction motifs (GIMs). This interaction is essential for ATL3-mediated selective autophagy of tubular ER upon starvation. Co-immunoprecipitation, binding assays, starvation-induced autophagy assays, fluorescence microscopy Current biology : CB High 30773365
2019 HSAN I-associated ATL3 mutations Y192C and P338R disrupt ATL3's association with GABARAP and impair ATL3's function in ER-phagy, linking defective ER-phagy to the disease mechanism. Co-immunoprecipitation with mutant constructs, autophagy flux assays in cells expressing disease mutants Current biology : CB High 30680846 30773365
2014 ATL3 is a dynamin-like GTPase enriched at three-way junctions of the tubular ER network. The disease-causing mutation p.Tyr192Cys causes mutant ATL3 to fail to localize to branch points and instead disrupts the tubular ER structure, suggesting a dominant-negative effect on ER morphology. Immunofluorescence microscopy of wild-type and mutant ATL3 localization in cells, patient-derived samples Brain : a journal of neurology High 24459106
2017 Crystal structure of ATL3 reveals discrete temporal steps in the GTPase catalytic cycle, including nucleotide binding, hydrolysis, ATL dimerization, and phosphate release. The structure suggests a mechanism for displacement of the catalytic Mg2+ ion following GTP hydrolysis to reset the cycle. X-ray crystallography, biochemical GTPase assays comparing ATL1 and ATL3 isoforms Structure (London, England : 1993) High 28602821
2016 Triple knockout of all three atlastins (Atl1/2/3) in mammalian NIH-3T3 cells using CRISPR/Cas9 markedly disrupts ER morphology, specifically impairing formation of three-way ER tubule junctions. This phenotype can be rescued by any single human atlastin or distant orthologs (Sey1p, RHD3), establishing atlastins as necessary for polygonal ER network formation. CRISPR/Cas9 knockout, rescue experiments with heterologous orthologs, fluorescence microscopy of ER morphology Experimental cell research High 27669642
2019 ATL3 mutation Y192C reduces the complexity of the tubular ER network, delays ER export by reducing the number of ER exit sites, reduces autophagy, fragments the Golgi, and causes nuclear malformation. In primary neurons, ATL3 Y192C does not localize to the growing axon, resulting in axon growth deficits. Expression of disease mutant in cultured cells and primary neurons, patient-derived fibroblasts, immunofluorescence, autophagosome quantification Cellular and molecular life sciences : CMLS High 30666337
2019 Disease-causing ATL3 mutations (Y192C and P338R) increase the number of ER-mitochondria contact sites in HeLa cells and patient-derived fibroblasts, reflected in higher phospholipid metabolism, upregulated autophagy, augmented Ca2+ crosstalk between ER and mitochondria, and decreased mitochondrial motility. Neurons expressing these mutations show strongly decreased numbers of axonal mitochondria. Electron microscopy of ER-mitochondria contacts, Ca2+ imaging, mitochondrial motility tracking, phospholipid analysis, patient-derived fibroblasts, neuronal culture Human molecular genetics High 30339187
2019 ATL3 interacts with Zika virus nonstructural proteins NS2A and NS2B3, is recruited to viral replication sites, and is required for efficient ZIKV replication. Depletion of ATL proteins significantly decreased intracellular viral protein levels and released virus. Co-immunoprecipitation of ATL3 with viral NS2A/NS2B3, siRNA knockdown, immunofluorescence colocalization at replication sites, viral titer measurements Journal of virology Medium 31534046
2017 Atlastin3 (Atl3/Sey1p) localizes to early Legionella-containing vacuoles (LCVs) and is critical for LCV expansion and pathogen replication. GTP (but not GDP) catalyzes Sey1-dependent aggregation of purified ER-positive LCVs in vitro. A catalytically inactive dominant-negative GTPase mutant or ATL3 depletion restricts replication and impairs LCV maturation. Proteomic analysis of purified LCVs, in vitro LCV aggregation assay with GTP/GDP, dominant-negative mutant expression, siRNA knockdown, fluorescence and electron microscopy EMBO reports High 28835546
2018 ATL3/Sey1 controls circumferential ER remodeling around the Legionella-containing vacuole. A dominant-negative Sey1_K154A mutant compromises ER accumulation on LCVs and causes aberrant ER morphology. Fluorescence microscopy and electron microscopy of infected D. discoideum, dominant-negative mutant expression Communicative & integrative biology Medium 30083282
2018 Lunapark (Lnp) localization to three-way ER junctions is dependent on ATL activity. Reintroduction of ATL1 R77A and ATL3 (which cluster at junctions) relocates Lnp to junctions, while wild-type ATL1 does not. Purified Lnp N-terminus inhibits ATL-mediated vesicle fusion in vitro, suggesting Lnp limits further ATL activity after junction formation. Deletion/mutation analysis, in vitro vesicle fusion assay with purified proteins, immunofluorescence, ATL KO cell rescue Protein & cell High 30498943
2021 Crystal structures of ATL1 and ATL3 reveal the N-terminal hypervariable region (HVR) as an isoform-specific structural feature. The HVR of ATL1 positively affects membrane tethering and cellular ATL1 function, and is post-translationally regulated through phosphorylation. A kinase screen identified candidates that specifically modify this HVR site. X-ray crystallography of ATL1 and ATL3, in vitro membrane tethering assays, kinase screen, phosphorylation site mapping in cells The Journal of cell biology High 34546351
2011 ATL3 physically associates with STAT5a and STAT5b in cross-immunopanning assays. Upon STAT5a/b knockdown, ATL3 accumulates at cyst-zone boundaries of cystic ER, and ATL3 siRNA leads to effacement of these cyst-zone boundaries, indicating ATL3 is required to maintain the boundaries of the cystic ER phenotype. Magnetic-bead cross-immunopanning, siRNA knockdown, immunofluorescence microscopy American journal of physiology. Cell physiology Medium 22159083 23151802
2023 Coronavirus ORF8 protein binds ATL3 (and FAM134B) and sequesters them into ORF8/p62 liquid droplets/condensates, inhibiting ER-phagy. This ER-phagy inhibition facilitates viral double-membrane vesicle (DMV) formation and activates ER stress. Co-immunoprecipitation, condensate/liquid droplet assays, ER-phagy flux assays, viral replication measurements, electron microscopy of DMVs Cell reports Medium 36952345
2023 UVRAG localizes to ER-phagy sites upon starvation and interacts with ER-phagy cargo receptors including ATL3. UVRAG regulates oligomerization of cargo receptors and facilitates recruitment of Atg8 family proteins, promoting efficient ER-phagy site assembly and ER turnover. Co-immunoprecipitation, fluorescence microscopy, oligomerization assays, ER-phagy flux assays, gene knockdown The EMBO journal Medium 37902287
2023 ATL3 is recruited to ER foci induced by simian virus 40 (SV40) during non-enveloped virus entry. ATL3 deploys its GTPase-dependent membrane fusion activity to promote formation of multi-tubular ER junctions within ER foci that serve as membrane penetration sites for SV40. ATL3 also engages the SV40-containing membrane penetration complex. Fluorescence and electron microscopy, ATL3 knockdown, dominant-negative GTPase mutant, co-immunoprecipitation with viral complex Journal of virology Medium 37578227
2025 ATL3, together with RTN3L, shapes an ER tubulovesicular structure called the ER tubular body (ER-TB) under cellular stress. ER-TB formation mediates Golgi-independent unconventional protein secretion (UPS) of transmembrane proteins such as ΔF508-CFTR and SARS-CoV-2 spike protein. Individual knockdown of ATL3 inhibits ER-TB formation and UPS; combined supplementation of ATL3 and RTN3L induces ER-TB formation. Correlative light-electron microscopy, gene knockdown, overexpression, UPS assays for ΔF508-CFTR and spike protein trafficking Developmental cell High 39919755
2024 RTN3L and ATL3 are both required for the formation of RTN3L-containing ER-phagy sites (ERPHS), while CALCOCO1 is not. ATL3 targets misfolded, aggregation-prone disease-causing proteins (same substrates as RTN3L) for autophagy, working in parallel with RTN3L and CALCOCO1 at different tubular ER sites. Colocalization microscopy, siRNA knockdown of individual receptors, autophagy flux assays with misfolded protein substrates Autophagy Medium 38818751
2025 ATL3, together with RTN3L and LNP (LNPK), is required for the formation of ER foci that sequester misassembled FG-rich nucleoporins (FG-Nups). Preventing this sequestration impairs NPC nucleo-cytoplasmic transport, suggesting ATL3 participates in an ER-based quality control mechanism for misassembled nuclear pore components. siRNA/shRNA knockdown of RTN3, ATL3, and LNP, immunofluorescence, nuclear transport assays Journal of cell science Medium 40079246

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 ATL3 Is a Tubular ER-Phagy Receptor for GABARAP-Mediated Selective Autophagy. Current biology : CB 251 30773365
2020 ATF4 links ER stress with reticulophagy in glioblastoma cells. Autophagy 123 33111629
2021 Therapeutic regulation of autophagy in hepatic metabolism. Acta pharmaceutica Sinica. B 121 35127371
2014 Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3. Brain : a journal of neurology 90 24459106
2017 ER remodeling by the large GTPase atlastin promotes vacuolar growth of Legionella pneumophila. EMBO reports 52 28835546
2023 Coronavirus subverts ER-phagy by hijacking FAM134B and ATL3 into p62 condensates to facilitate viral replication. Cell reports 50 36952345
2011 Nongenomic STAT5-dependent effects on Golgi apparatus and endoplasmic reticulum structure and function. American journal of physiology. Cell physiology 45 22159083
2019 Atlastin Endoplasmic Reticulum-Shaping Proteins Facilitate Zika Virus Replication. Journal of virology 43 31534046
2016 Mammalian knock out cells reveal prominent roles for atlastin GTPases in ER network morphology. Experimental cell research 42 27669642
2019 A disease causing ATLASTIN 3 mutation affects multiple endoplasmic reticulum-related pathways. Cellular and molecular life sciences : CMLS 37 30666337
2019 Sensory neuropathy-causing mutations in ATL3 affect ER-mitochondria contact sites and impair axonal mitochondrial distribution. Human molecular genetics 35 30339187
2020 Role of VAMP7-Dependent Secretion of Reticulon 3 in Neurite Growth. Cell reports 33 33357422
2019 TEX264 is a major receptor for mammalian reticulophagy. Autophagy 32 31362563
2024 USP20 deubiquitinates and stabilizes the reticulophagy receptor RETREG1/FAM134B to drive reticulophagy. Autophagy 30 38705724
2018 Reciprocal regulation between lunapark and atlastin facilitates ER three-way junction formation. Protein & cell 26 30498943
2017 Timing and Reset Mechanism of GTP Hydrolysis-Driven Conformational Changes of Atlastin. Structure (London, England : 1993) 26 28602821
2017 Drosophila Atlastin in motor neurons is required for locomotion and presynaptic function. Journal of cell science 25 28860117
2013 Non-genomic STAT5-dependent effects at the endoplasmic reticulum and Golgi apparatus and STAT6-GFP in mitochondria. JAK-STAT 23 24470974
2024 Reticulophagy and viral infection. Autophagy 20 39394962
2023 Genetic landscape of congenital insensitivity to pain and hereditary sensory and autonomic neuropathies. Brain : a journal of neurology 19 37769650
2019 ATL3, a cargo receptor for reticulophagy. Autophagy 19 31032711
2023 Inhibition of MiR-106b-5p mediated by exosomes mitigates acute kidney injury by modulating transmissible endoplasmic reticulum stress and M1 macrophage polarization. Journal of cellular and molecular medicine 18 37471571
2023 UVRAG cooperates with cargo receptors to assemble the ER-phagy site. The EMBO journal 17 37902287
2015 Deletion of STAT5a/b in vascular smooth muscle abrogates the male bias in hypoxic pulmonary hypertension in mice: implications in the human disease. Molecular medicine (Cambridge, Mass.) 16 25470773
2012 Definitive evidence using enucleated cytoplasts for a nongenomic basis for the cystic change in endoplasmic reticulum structure caused by STAT5a/b siRNAs. American journal of physiology. Cell physiology 14 23151802
2019 ATL3 gene mutation in a Chinese family with hereditary sensory neuropathy type 1F. Journal of the peripheral nervous system : JPNS 13 30680846
2024 Genetic overlap between ALS and other neurodegenerative or neuromuscular disorders. Amyotrophic lateral sclerosis & frontotemporal degeneration 12 37849306
2025 Tubular ER structures shaped by ER-phagy receptors engage in stress-induced Golgi bypass. Developmental cell 11 39919755
2024 Drp1 Aggravates Copper Nanoparticle-Induced ER-Phagy by Disturbing Mitochondria-Associated Membranes in Chicken Hepatocytes. Journal of agricultural and food chemistry 11 38986054
2022 Algorithmic reconstruction of glioblastoma network complexity. iScience 11 35479408
2023 A novel nonsense variant in the ATL3 gene is associated with disturbed pain sensitivity, numbness of distal limbs and muscle weakness. Annals of human genetics 9 36856139
2021 Rare mutations in ATL3, SPTLC2 and SCN9A explaining hereditary sensory neuropathy and congenital insensitivity to pain in a Brazilian cohort. Journal of the neurological sciences 8 34090020
2018 The large GTPase atlastin controls ER remodeling around a pathogen vacuole. Communicative & integrative biology 6 30083282
2024 RTN3L and CALCOCO1 function in parallel to maintain proteostasis in the endoplasmic reticulum. Autophagy 5 38818751
2021 The hypervariable region of atlastin-1 is a site for intrinsic and extrinsic regulation. The Journal of cell biology 5 34546351
2020 A novel reticulophagy receptor, Epr1: a bridge between the phagophore protein Atg8 and ER transmembrane VAP proteins. Autophagy 5 33121335
2025 RETREG1-mediated reticulophagy is activated by an ATF4-CEBPG/C/EBPγ heterodimer and confers protection against lipotoxicity. Autophagy 4 40437698
2023 The atlastin ER morphogenic proteins promote formation of a membrane penetration site during non-enveloped virus entry. Journal of virology 3 37578227
2025 ER tubular body: an ER-derived compartment for redirecting autophagy to secretory functions. Autophagy 2 40390263
2025 The impact of copper-induced oxidative damage on the endoplasmic reticulum quality control system in broiler kidneys. Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine 1 40404888
2023 The First Large Deletion of ATL3 Identified in a Patient Presenting with a Sensory Polyneuropathy. Biomedicines 1 37371660
2026 ER-phagy receptors: structural mechanisms in selective ER degradation and disease implications. Acta pharmacologica Sinica 0 41593210
2026 Subcellular Proteomic Analyses Reveal REEP5 Knockdown in the Mouse Heart Disrupts Mitochondrial Networks. Molecular & cellular proteomics : MCP 0 41672147
2026 Non-invasive profiling of exosomal miRNA and protein biomarkers from vaginal discharge for the early detection of preterm labor. Journal of nanobiotechnology 0 41928233
2026 Secretion of the HBV small surface antigen is driven by an ER autophagic pathway. Hepatology communications 0 42172500
2025 An ER-associated structure sequesters misassembled FG-rich nucleoporins to help maintain nuclear pore complex function. Journal of cell science 0 40079246
2025 Connecting tubules: mechanisms of endoplasmic reticulum membrane fusion. Biochemical Society transactions 0 40587263

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