Affinage

ATL2

Atlastin-2 · UniProt Q8NHH9

Round 2 corrected
Length
583 aa
Mass
66.2 kDa
Annotated
2026-04-28
90 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATL2 is a dynamin-related integral membrane GTPase that drives homotypic ER membrane tethering and fusion to generate and maintain the polygonal tubular ER network through three-way junction formation (PMID:19665976, PMID:18270207, PMID:27619977). Its GTPase activity is essential for tubule interconnection, and its function is regulated by Lunapark-mediated ubiquitination at specific lysine residues (K56, K57, K282, K302), which is required for proper junction formation (PMID:35894092). ATL2 interacts physically with reticulons, TMCC3, and protrudin to coordinate ER shape, and its ER-shaping activity underpins diverse downstream processes including intracellular Ca²⁺ signaling dynamics in neurons, autophagosome initiation site assembly, lipid synthesis and membrane homeostasis, and viral replication organelle organization (PMID:31696206, PMID:23969831, PMID:33812310, PMID:36198318, PMID:30879769). ATL2-knockout mice are embryonic lethal with compromised cerebellar development, reduced phosphatidylcholine and cholesterol synthesis, and defective synaptic function, establishing ATL2 as essential for neural development and membrane biogenesis in vivo (PMID:27669642).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2008 High

    The first question was whether atlastin GTPase activity is required for ER tubule network architecture: dominant-negative and knockdown experiments demonstrated that ATL2 localizes to the ER in non-neuronal cells and that its GTPase activity is essential for three-way junction formation and ER reticularization.

    Evidence siRNA knockdown and dominant-negative overexpression with ER morphology imaging in HeLa cells

    PMID:18270207

    Open questions at the time
    • Mechanism of membrane fusion was not resolved
    • No biochemical reconstitution of ATL2-mediated fusion
    • Functional redundancy among atlastin isoforms not addressed
  2. 2009 High

    The mechanistic basis of atlastin function was established: ATL2 and family members mediate homotypic ER membrane fusion through dynamin-like GTPase activity, functionally conserved from yeast (Sey1p) to mammals, and their activity is balanced against tubule-shaping reticulons.

    Evidence In vitro ER network reconstitution, genetic epistasis with reticulons/Yop1p in yeast, co-immunoprecipitation, live-cell imaging

    PMID:19665976

    Open questions at the time
    • Post-translational regulation of ATL2 at junctions unknown
    • Relative contributions of individual atlastin isoforms not separated
  3. 2013 Medium

    The physical interaction network of ATL2 was expanded by showing that protrudin (SPG33 protein) binds ATL2 via intramembrane hairpin domains and participates in ER sheet-to-tubule balance, linking ATL2 to the hereditary spastic paraplegia protein network.

    Evidence Co-immunoprecipitation, yeast two-hybrid, ER morphology assays upon overexpression/knockdown

    PMID:23969831

    Open questions at the time
    • Structural basis of ATL2–protrudin interaction not resolved
    • Single-lab finding without independent replication
  4. 2016 High

    Complete genetic removal of all three mammalian atlastins confirmed functional redundancy and established that atlastin-mediated ER fusion is essential for junction maintenance, BMP signaling, stress responses, and differentiation; separately, the dynamic interplay between ATL, reticulons, and lunapark at junctions was elucidated, revealing that ATL transiently occupies nascent junctions before lunapark replacement.

    Evidence CRISPR/Cas9 triple knockout with cross-species rescue in NIH-3T3; quantitative live-cell imaging of junction dynamics with lunapark phospho-mutants

    PMID:27619977 PMID:27669642

    Open questions at the time
    • Molecular mechanism by which lunapark regulates ATL2 turnover at junctions not known
    • Tissue-specific contributions of ATL2 versus ATL1/3 in vivo not resolved
  5. 2017 High

    Using the Drosophila single atlastin ortholog, the requirement for atlastin-mediated ER shaping in presynaptic function was demonstrated: loss disrupts synaptic vesicle pools, axonal organelle distribution, and locomotor behavior.

    Evidence Tissue-specific RNAi and overexpression in Drosophila motor neurons, electrophysiology, behavioral assays, electron microscopy

    PMID:28860117

    Open questions at the time
    • Cannot separate ATL2-specific from ATL1/3 roles due to single ortholog
    • Direct lipid synthesis consequences not measured
  6. 2019 Medium

    ATL2 was functionally distinguished from ATL3: ATL2 primarily drives ER fusion and morphology, whereas ATL3 serves as an ER-phagy receptor; additionally, TMCC3 was identified as a direct ATL2-binding partner at three-way junctions that acts upstream of atlastin to promote junction formation.

    Evidence Comparative siRNA knockdown with ER morphology and autophagy readouts; co-IP and rescue experiments for TMCC3–ATL2 epistasis

    PMID:30773365 PMID:31696206

    Open questions at the time
    • ATL2-specific contribution to ER-phagy not fully excluded
    • TMCC3–ATL2 interaction not validated by structural methods
  7. 2019 Medium

    ATL2 was linked to lipid droplet biogenesis and ER integrity in a physiological secretory tissue: miR-30b-5p-mediated downregulation of ATL2 in mammary epithelial cells caused ER fragmentation, enlarged lipid droplets, and altered milk fatty acid composition.

    Evidence Transgenic miR-30b-5p mouse, EM of ER morphology, miRNA target validation, lipidomic analysis of milk

    PMID:30879769

    Open questions at the time
    • Direct enzymatic role of ATL2 in lipid metabolism not shown
    • miRNA-mediated knockdown may affect additional targets
  8. 2021 Medium

    ATL2's GTPase activity was shown to regulate intracellular Ca²⁺ signaling: GTPase-deficient ATL2 mutants in hippocampal neurons altered ER morphology, redistributed IP3R1 and RyR2 channels, and delayed IP3-evoked Ca²⁺ transients, establishing a functional link between ER shape and Ca²⁺ dynamics.

    Evidence Expression of GTPase-deficient ATL2 mutants in primary hippocampal neurons, live Ca²⁺ imaging, confocal imaging of ER and Ca²⁺ channel distribution

    PMID:33812310

    Open questions at the time
    • Whether ATL2's Ca²⁺ signaling role is independent of general ER morphology disruption not established
    • In vivo neuronal Ca²⁺ phenotype not confirmed
  9. 2022 High

    The post-translational regulation of ATL2 was resolved: Lunapark ubiquitinates ATL2 at K56/K57/K282/K302 at three-way junctions, and this ubiquitination is required for proper tubular ER network formation, as shown by failure of ubiquitination-deficient ATL2 to rescue junction loss.

    Evidence In vitro ubiquitination assay, site-directed mutagenesis (K→R), siRNA knockdown with rescue, ER morphology imaging

    PMID:35894092

    Open questions at the time
    • Fate of ubiquitinated ATL2 (degradation vs. non-degradative signaling) unknown
    • Structural basis of Lnp–ATL2 recognition not determined
  10. 2022 Medium

    ATL2 was connected to autophagosome biogenesis: ER-localized Ca²⁺ transients trigger FIP200 phase separation into autophagosome initiation sites on the ER in a manner dependent on ATL2/3 and VAPA/B, establishing that ER tubule architecture specified by atlastins scaffolds autophagosome assembly.

    Evidence Live-cell Ca²⁺ and SIM imaging, siRNA knockdown of ATL2/3 and VAPA/B, LLPS assays for FIP200

    PMID:36198318

    Open questions at the time
    • ATL2-specific versus ATL3-specific contribution to autophagosome initiation not separated
    • Direct physical interaction between ATL2 and FIP200 not shown
  11. 2024 Medium

    Drosophila studies revealed that atlastin is required in muscle for autophagy and proteostasis: atlastin-null muscle accumulates poly-ubiquitin aggregates, and neuronal excitability exacerbates this phenotype, revealing a non-cell-autonomous axis of atlastin-dependent protein quality control.

    Evidence Drosophila atl-null mutant, tissue-specific TrpA1 activation, poly-ubiquitin immunofluorescence, viability assays

    PMID:38166124

    Open questions at the time
    • Mechanism by which neuronal excitability modulates muscle proteostasis is unclear
    • Direct autophagy flux measurements not shown
  12. 2025 Medium

    Two preprints extended ATL2 biology: (1) ATL2-knockout mice are embryonic lethal with compromised cerebellar development, reduced phosphatidylcholine/cholesterol synthesis, diminished presynaptic vesicle pools, and deafness, directly linking ER fusion to lipid synthesis and membrane homeostasis; (2) ATL2 membrane tethering (not fusion) activity is the critical function for flavivirus replication organelle biogenesis, as shown by tethering-competent/fusion-defective mutant rescue.

    Evidence (preprint) Conditional ATL2 KO mice with lipidomics, electrophysiology, cerebellar histology; ATL2 KO and mutant rescue in DENV/ZIKV infection models with EM and viral titer assays

    PMID:41394679 PMID:bio_10.1101_2025.04.12.648519

    Open questions at the time
    • Both findings are preprints awaiting peer review
    • Mechanistic link between ATL2-mediated tethering and vRO assembly not molecularly resolved
    • Whether lipid synthesis defects are direct or secondary to ER morphology disruption not determined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis of ATL2 regulation by ubiquitination and the fate of ubiquitinated ATL2; how ATL2-dependent ER morphology is sensed by downstream processes (Ca²⁺ signaling, lipid synthesis, autophagy); and the tissue-specific division of labor among ATL1, ATL2, and ATL3 in vivo.
  • No high-resolution structure of full-length ATL2 in a membrane context
  • Isoform-specific knockout phenotypes in mammals incompletely characterized
  • Whether ATL2 ubiquitination leads to proteasomal degradation or serves as a non-degradative signal is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 6 GO:0140657 ATP-dependent activity 2
Localization
GO:0005783 endoplasmic reticulum 7
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 6 R-HSA-9612973 Autophagy 2 R-HSA-382551 Transport of small molecules 1
Partners
LNPNOMO1RTN4TMCC3VAPAZFYVE27

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Mammalian atlastins (including ATL2) are dynamin-like integral membrane GTPases that localize to ER tubules and are required for the formation of the tubular ER network by mediating tubule interconnections and three-way junctions. Depletion or dominant-negative forms of atlastins inhibit tubule fusion; the yeast ortholog Sey1p shares the same signature motifs, membrane topology, and genetic interactions with tubule-shaping proteins (reticulons/DP1/Yop1p). siRNA knockdown, dominant-negative overexpression, in vitro ER network reconstitution, genetic epistasis in yeast, live-cell imaging, co-immunoprecipitation Cell High 19665976
2008 ATL2 and ATL3 localize to the ER (not cis-Golgi like ATL1) in non-neuronal tissues. siRNA knockdown of ATL2 and ATL3 in HeLa cells disrupts Golgi morphology (while the Golgi remains brefeldin A-sensitive), and dominant-negative atlastin proteins lacking GTPase activity prominently inhibit ER reticularization, demonstrating a role for atlastin GTPase activity in forming three-way junctions in the ER. Secretory pathway trafficking (assessed by VSVG-GFP) is largely unaffected. siRNA knockdown, dominant-negative overexpression, immunofluorescence, brefeldin A treatment, VSVG-GFP trafficking assay Human molecular genetics High 18270207
2016 Triple knockout of all three mammalian atlastins (Atl1/2/3) in NIH-3T3 cells using CRISPR/Cas9 markedly disrupts ER morphology with prominent impairment in three-way ER tubule junction formation. This phenotype is rescued by expression of distant orthologs (yeast Sey1p, Arabidopsis RHD3) or any single human atlastin isoform, establishing functional redundancy. Triple KO cells also show altered BMP signaling, increased ER stress sensitivity, and impaired adipocyte-like differentiation. CRISPR/Cas9 triple knockout, rescue by heterologous expression, live-cell imaging, ER morphology quantification, BMP signaling assay Experimental cell research High 27669642
2016 ATL (atlastin) mediates both formation and maintenance of the tubular ER network through GTPase-dependent membrane fusion. ATL activity must be balanced against reticulon (Rtn) levels: insufficient ATL or excess Rtn4a causes ER fragmentation. ATL transiently occupies newly formed three-way junctions, after which lunapark (Lnp) moves into junctional sheets and oligomerizes. Lnp inactivation by mitotic phosphorylation contributes to tubule-to-sheet ER conversion during mitosis. siRNA knockdown, dominant-negative overexpression, GTPase activity assays, quantitative live-cell imaging, phospho-mutant analysis eLife High 27619977
2013 Protrudin (SPG33 protein) physically interacts with atlastin-2 (and other tubular ER proteins including reticulons and REEPs) via its hydrophobic intramembrane hairpin domains, and functions in ER morphogenesis by regulating the sheet-to-tubule balance and tubule interconnection density. Co-immunoprecipitation, yeast two-hybrid, overexpression/knockdown with ER morphology imaging Proceedings of the National Academy of Sciences of the United States of America Medium 23969831
2019 ATL2 primarily promotes ER fusion and affects ER morphology, whereas ATL3 (but not ATL2) functions as an ER-phagy receptor by binding GABARAP subfamily proteins via GABARAP-interaction motifs (GIMs). ATL2 depletion causes detectable ER morphology changes while ATL3 depletion does not, distinguishing their cellular roles. siRNA knockdown, live-cell fluorescence imaging of ER morphology, autophagy flux assays, co-IP Current biology : CB Medium 30773365
2019 TMCC3 (a TEX28-family ER membrane protein) localizes to ER three-way junctions and binds directly to atlastins (including ATL2) through its C-terminal transmembrane domains. TMCC3 knockdown decreases three-way junction number and expands ER sheets; this phenotype is partially rescued by ATL2 overexpression, placing TMCC3 upstream of atlastin activity at junctions. Co-immunoprecipitation, siRNA knockdown, rescue by ATL2 overexpression, fluorescence microscopy of ER morphology The Biochemical journal Medium 31696206
2021 ATL2 GTPase activity is required for proper IP3-induced Ca2+ signal dynamics in hippocampal neuron dendrites. GTPase-deficient ATL2 mutants induce specific ER morphological alterations, delay the onset and increase the rising time of IP3-evoked Ca2+ signals, and cause aggregation and redistribution of RyR2 and IP3R1 ER Ca2+ channels. This links ATL2-mediated ER shaping to regulation of intracellular Ca2+ signaling. Expression of GTPase-deficient ATL2 mutants in primary hippocampal neurons, live Ca2+ imaging, confocal imaging of ER morphology, immunofluorescence of Ca2+ channel distribution Cell calcium Medium 33812310
2021 ATL2 expression is upregulated by the familial Alzheimer's disease-associated PS1 M146V mutation and increases ER-mitochondria contacts (MAM formation). Downregulation of ATL2 after PS1 mutant induction rescues the abnormally elevated ER-mitochondria interactions back to normal levels, establishing ATL2 as a downstream effector of PS1-driven MAM dysregulation. Comparative hippocampal gene expression profiling in PS1M146V knock-in mice, ATL2 siRNA knockdown, fluorescence microscopy of ER-mitochondria contacts, quantification of MAM markers Theranostics Medium 34522215
2021 NOMO1 (nodal modulator) functions in the ER-shaping protein network; genetic epistasis analysis including atlastin-2 (ATL2) and Climp63 places NOMO1 in the functional network of ER-shaping proteins, where it regulates ER intermembrane luminal distance through immunoglobulin-like domain stacking. Genetic epistasis (double depletion of NOMO + ATL2), ER morphology imaging, in vitro reconstitution of NOMO1 structure, insertion of Ig folds to alter ER luminal spacing The Journal of biological chemistry Medium 34224731
2022 Lunapark (Lnp) ubiquitinates ATL2 at ER three-way junctions; the E3 ubiquitin ligase activity of Lnp's N-terminal cytoplasmic domain targets ATL2 at lysine residues K56, K57, K282, and K302. Lnp localization at three-way junctions is required for ATL2 ubiquitination. An ATL2 mutant in which these lysines are substituted with arginine fails to rescue the reduction in three-way junctions caused by ATL2 knockdown, demonstrating that ubiquitination of ATL2 by Lnp is required for proper tubular ER network formation. In vitro ubiquitination assay, site-directed mutagenesis of ATL2 ubiquitination sites, co-immunoprecipitation, siRNA knockdown, rescue experiments, fluorescence microscopy of ER morphology Journal of biochemistry High 35894092
2022 Ca2+ transients on the cytosolic ER surface trigger liquid-liquid phase separation of FIP200 autophagosome initiation complexes. Multiple FIP200 puncta on the ER assemble into autophagosome formation sites in a manner dependent on ER proteins VAPA/B and ATL2/3, linking ATL2's ER-shaping function to autophagosome initiation site specification. Live-cell Ca2+ imaging, multi-modal SIM microscopy, siRNA knockdown of ATL2/3 and VAPA/B, LLPS assays for FIP200 Cell Medium 36198318
2023 ATL2 supports reticular ER morphology critical for the integrity of an ATL3-dependent membrane penetration complex used by the non-enveloped polyomavirus SV40. During ER-to-cytosol membrane penetration, ATL3 (but not ATL2) mobilizes to viral ER-foci and uses GTPase-dependent membrane fusion to form multi-tubular junctions; ATL2 does not relocalize to foci but its ER-shaping activity is required to maintain the reticular ER context supporting the ATL3-dependent complex. siRNA knockdown of ATL2 and ATL3, viral infectivity assays, confocal immunofluorescence of ATL2/ATL3 localization during infection, dominant-negative GTPase mutants Journal of virology Medium 37578227
2019 miR-30b-5p overexpression in mouse mammary epithelial cells directly downregulates ATL2 expression (confirmed as a miRNA target), leading to fragmented and discontinuous tubular ER network and increased lipid droplet size during lactation, with altered milk fatty acid composition. This establishes ATL2 as a regulator of lipid droplet formation and ER morphology in mammary epithelial cells. Transgenic mouse overexpressing miR-30b-5p, electron microscopy of ER morphology, miRNA target validation, Western blot and qPCR for ATL2, milk fatty acid analysis Biochemical and biophysical research communications Medium 30879769
2022 miR-30e-5p negatively regulates ATL2 expression in fibroblast-like synoviocytes (FLS); ATL2 knockdown exerts a pro-inflammatory effect on RA-FLS, and ATL2 knockdown rescues the inhibitory effect of miR-30e-5p silencing on proliferation and inflammatory response. This places ATL2 downstream of miR-30e-5p as an anti-inflammatory effector in rheumatoid arthritis synoviocytes. Luciferase reporter assay (miR-30e-5p→ATL2 targeting), siRNA knockdown of ATL2, ELISA for cytokines, Western blot, EdU proliferation assay, mouse RA model Archives of rheumatology Low 37235116
2017 Drosophila Atlastin (the single ortholog of human ATL1-3) is required in motor neurons for normal locomotion and presynaptic function. Downregulation or overexpression in motor neurons reduces larval crawling speed and adult climbing ability. Both spontaneous synaptic vesicle release and the reserve pool of vesicles are reduced. Axonal secretory organelles are abnormally distributed, and presynaptic proteins accumulate in distal axons (possibly in lysosomes), suggesting that atlastin-mediated ER shaping is critical for presynaptic protein trafficking. Tissue-specific RNAi knockdown and overexpression in Drosophila motor neurons, behavioral assays (crawling, climbing), electrophysiology (mEJP/EJP), immunofluorescence of synaptic markers, electron microscopy Journal of cell science High 28860117
2024 In Drosophila, loss of atlastin (atl) from muscle (but not neuron) causes defective autophagy and accumulation of ubiquitin-positive protein aggregates (poly-UB aggregates). Activation of neuronal TrpA1 excitability channel enhances poly-UB aggregate accumulation specifically in atl-null muscle but not wild-type muscle, and also worsens pupal size and viability phenotypes of muscle atl loss. This establishes that atlastin in muscle is required for autophagy and proteostasis, and that neuronal excitability modulates the severity of muscle atlastin loss-of-function. Drosophila genetic null mutant (atl2), tissue-specific TrpA1 activation, immunofluorescence for poly-ubiquitin aggregates, viability and pupal size assays PloS one Medium 38166124
2025 ATL2-knockout mice are embryonic lethal and display compromised cerebellar development; ATL2 is highly expressed in neuroglia. Loss of ATL2 disorganizes Bergmann glia positioning, which interferes with granule cell migration. ATL2-deficient cells show significant shrinkage of intracellular membrane area associated with decreased phosphatidylcholine and cholesterol synthesis. In calyx-type synapses of ATL-deleted mice, reduced membrane reservoir (fewer presynaptic vesicles) causes defective synaptic function and deafness, linking atlastin-mediated ER fusion to lipid synthesis and membrane homeostasis. Conditional and full ATL2 knockout mice, cerebellar histology, glial cell positioning analysis, lipidomics (phosphatidylcholine, cholesterol), electrophysiology of calyx-type synapses, auditory function testing bioRxivpreprint Medium bio_10.1101_2025.04.12.648519
2025 ATL2 plays a conserved role in flavivirus (dengue, Zika) replication by organizing viral replication organelle (vRO) spatial distribution within infected cells. ATL2 depletion reduces vRO spatial distribution, decreases virus production, and induces innate immune responses. A tethering-competent but fusion-defective ATL2 mutant rescues DENV and ZIKV replication in ATL2-knockout cells, demonstrating that membrane tethering (not fusion) activity of ATL2 is the critical function for flavivirus vRO biogenesis. ATL2 accumulates in areas of vRO formation during infection. ATL2 siRNA knockdown and CRISPR knockout, confocal and electron microscopy of vRO distribution, viral titer assays, innate immune activation assays, ATL2 tethering vs. fusion mutant rescue experiments, synthetic peptide inhibition bioRxivpreprint Medium 41394679

Source papers

Stage 0 corpus · 90 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
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2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2021 Multilevel proteomics reveals host perturbations by SARS-CoV-2 and SARS-CoV. Nature 532 33845483
1994 Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides. Gene 492 8125298
2009 A class of dynamin-like GTPases involved in the generation of the tubular ER network. Cell 459 19665976
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2010 Systematic analysis of human protein complexes identifies chromosome segregation proteins. Science (New York, N.Y.) 421 20360068
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
1985 TCGF (IL 2)-receptor inducing factor(s). I. Regulation of IL 2 receptor on a natural killer-like cell line (YT cells). Journal of immunology (Baltimore, Md. : 1950) 397 2578514
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
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2019 ATL3 Is a Tubular ER-Phagy Receptor for GABARAP-Mediated Selective Autophagy. Current biology : CB 248 30773365
2016 An organelle-specific protein landscape identifies novel diseases and molecular mechanisms. Nature communications 211 27173435
1986 Cloning of cDNA for human T-cell replacing factor (interleukin-5) and comparison with the murine homologue. Nucleic acids research 202 3024129
2004 Comprehensive proteomic analysis of interphase and mitotic 14-3-3-binding proteins. The Journal of biological chemistry 185 15161933
2008 Atlastin GTPases are required for Golgi apparatus and ER morphogenesis. Human molecular genetics 170 18270207
2016 Cooperation of the ER-shaping proteins atlastin, lunapark, and reticulons to generate a tubular membrane network. eLife 150 27619977
2022 Calcium transients on the ER surface trigger liquid-liquid phase separation of FIP200 to specify autophagosome initiation sites. Cell 137 36198318
2019 Mapping the proximity interaction network of the Rho-family GTPases reveals signalling pathways and regulatory mechanisms. Nature cell biology 137 31871319
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2020 Systematic mapping of genetic interactions for de novo fatty acid synthesis identifies C12orf49 as a regulator of lipid metabolism. Nature metabolism 92 32694731
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1988 IL-2 receptor(p55)/Tac-inducing factor. Purification and characterization of adult T cell leukemia-derived factor. Journal of immunology (Baltimore, Md. : 1950) 88 2895791
2021 SARS-CoV-2-host proteome interactions for antiviral drug discovery. Molecular systems biology 86 34709727
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2017 A Single Adaptable Cochaperone-Scaffold Complex Delivers Nascent Iron-Sulfur Clusters to Mammalian Respiratory Chain Complexes I-III. Cell metabolism 78 28380382
1999 A novel ADP-ribosylation like factor (ARL-6), interacts with the protein-conducting channel SEC61beta subunit. FEBS letters 69 10508919
2020 Proteome-wide identification of HSP70/HSC70 chaperone clients in human cells. PLoS biology 65 32687490
1999 Gene expression in proliferating human erythroid cells. Genomics 65 10409428
2022 MYC multimers shield stalled replication forks from RNA polymerase. Nature 63 36424410
2006 Chemical interference of pathogen-associated molecular pattern-triggered immune responses in Arabidopsis reveals a potential role for fatty-acid synthase type II complex-derived lipid signals. The Journal of biological chemistry 62 17166839
2015 Temporal proteomics of NGF-TrkA signaling identifies an inhibitory role for the E3 ligase Cbl-b in neuroblastoma cell differentiation. Science signaling 61 25921289
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2013 Protrudin binds atlastins and endoplasmic reticulum-shaping proteins and regulates network formation. Proceedings of the National Academy of Sciences of the United States of America 56 23969831
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2011 Differentiation of mesenchymal stem cells derived from pancreatic islets and bone marrow into islet-like cell phenotype. PloS one 48 22194812
2022 NUDT21 limits CD19 levels through alternative mRNA polyadenylation in B cell acute lymphoblastic leukemia. Nature immunology 46 36138187
2021 Alzheimer's disease-causing presenilin-1 mutations have deleterious effects on mitochondrial function. Theranostics 46 34522215
1992 Lymphocyte transformation and thiol compounds; the role of ADF/thioredoxin as an endogenous reducing agent. Molecular immunology 43 1542302
2016 Mammalian knock out cells reveal prominent roles for atlastin GTPases in ER network morphology. Experimental cell research 41 27669642
2018 Circular RNA hsa_circ_0000993 inhibits metastasis of gastric cancer cells. Epigenomics 40 30215537
2009 Direct association of thioredoxin-1 (TRX) with macrophage migration inhibitory factor (MIF): regulatory role of TRX on MIF internalization and signaling. Antioxidants & redox signaling 34 19601712
2013 Characterizing the normal proteome of human ciliary body. Clinical proteomics 33 23914977
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1997 Role of intracellular redox status in apoptosis induction of human T-cell leukemia virus type I-infected lymphocytes by 13-cis-retinoic acid. Cancer research 27 9354458
2017 Drosophila Atlastin in motor neurons is required for locomotion and presynaptic function. Journal of cell science 25 28860117
2001 A mechanism of apoptosis induced by all-trans retinoic acid on adult T-cell leukemia cells: a possible involvement of the Tax/NF-kappaB signaling pathway. Leukemia research 25 11248329
1986 Systemic lupus erythematosus sera antilymphocyte reactivity: detection of antibodies to Tac-antigen positive T cell lines. Clinical and experimental immunology 25 3006953
2018 The Cuticle Mutant eca2 Modifies Plant Defense Responses to Biotrophic and Necrotrophic Pathogens and Herbivory Insects. Molecular plant-microbe interactions : MPMI 24 29130376
1990 Stepwise formation of the high-affinity complex of the interleukin 2 receptor. International immunology 21 2090200
1991 Isolation and characterization of a neu protein-specific activating factor from human ATL-2 cell conditioned medium. Biochemical and biophysical research communications 19 1681805
2006 Genetic interactions of a putative Arabidopsis thaliana ubiquitin-ligase with components of the Saccharomyces cerevisiae ubiquitination machinery. Current genetics 18 16897085
1997 Inhibition of proliferation and CD25 down-regulation by retinoic acid in human adult T cell leukemia cells. Leukemia 18 9067580
1992 Adult T-cell leukaemia-derived factor/thioredoxin expression on the HTLV-I transformed T-cell lines: heterogeneous expression in ALT-2 cells. Immunology 17 1398748
2021 Ryanodine receptor-mediated Ca2+ release and atlastin-2 GTPase activity contribute to IP3-induced dendritic Ca2+ signals in primary hippocampal neurons. Cell calcium 16 33812310
2013 Interleukin-2 inhibits HIV-1 replication in some human T cell lymphotrophic virus-1-infected cell lines via the induction and incorporation of APOBEC3G into the virion. The Journal of biological chemistry 12 23640893
2019 Defects of the endoplasmic reticulum and changes to lipid droplet size in mammary epithelial cells due to miR-30b-5p overexpression are correlated to a reduction in Atlastin 2 expression. Biochemical and biophysical research communications 11 30879769
2021 Epidermal Growth Factor Receptor Mutation Mechanisms in Nonsmall Cell Lung Cancer by Transcriptome Sequencing. Cancer biotherapy & radiopharmaceuticals 9 34009009
2021 Nodal modulator (NOMO) is required to sustain endoplasmic reticulum morphology. The Journal of biological chemistry 9 34224731
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2022 The endogenous HBZ interactome in ATL leukemic cells reveals an unprecedented complexity of host interacting partners involved in RNA splicing. Frontiers in immunology 8 35979358
2019 TMCC3 localizes at the three-way junctions for the proper tubular network of the endoplasmic reticulum. The Biochemical journal 8 31696206
2023 Construction and preclinical evaluation of a zirconium-89 labelled monoclonal antibody targeting PD-L2 in lung cancer. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 7 37852097
2024 The Auto-Regulation of ATL2 E3 Ubiquitin Ligase Plays an Important Role in the Immune Response against Alternaria brassicicola in Arabidopsis thaliana. International journal of molecular sciences 6 38397062
2022 StATL2-like could affect growth and cold tolerance of plant by interacting with StCBFs. Plant cell reports 6 35732839
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