Affinage

ATL2

Atlastin-2 · UniProt Q8NHH9

Length
583 aa
Mass
66.2 kDa
Annotated
2026-06-09
55 papers in source corpus 14 papers cited in narrative 14 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATL2 (atlastin-2) is a membrane-bound dynamin-like GTPase of the endoplasmic reticulum that drives homotypic fusion of ER tubules to build and maintain the three-way junctions of the polygonal ER network (PMID:18270207, PMID:30773365). Its function is redundant with the paralogs ATL1 and ATL3 and is conserved across distant orthologs, since re-expression of any single atlastin or the yeast and plant orthologs Sey1p and RHD3 rescues the loss of three-way junctions caused by combined atlastin knockout (PMID:27669642). This GTPase-dependent fusion activity is required broadly for ER-templated cellular processes: it shapes the dendritic ER that organizes RyR2 and IP3R1 channel distribution and supports normal IP3-evoked Ca2+ signaling (PMID:33812310), sustains lipid (phosphatidylcholine and cholesterol) synthesis and intracellular membrane homeostasis [PMID:bio_10.1101_2025.04.12.648519], and licenses the assembly of FIP200 autophagosome initiation sites on the ER surface (PMID:36198318). ATL2 activity at three-way junctions is regulated by Lunapark, which ubiquitinates ATL2 at lysines 56, 57, 282, and 302; a ubiquitination-site mutant fails to restore three-way junctions, establishing Lunapark-dependent ubiquitination as a positive determinant of ATL2 network-shaping activity (PMID:35894092), while TMCC3 binds atlastins and acts as a further positive modulator at junctions (PMID:31696206). ATL2 additionally mediates ER-mitochondria contact formation downstream of mutant presenilin-1 (PMID:34522215) and is co-opted by viruses: it maintains the reticular ER integrity needed for SV40 membrane penetration (PMID:37578227), and its membrane-tethering activity, separable from fusion, organizes the spatial distribution of flavivirus replication organelles (PMID:41394679). In vivo, ATL2 loss is embryonic lethal with disrupted cerebellar development through disorganized Bergmann glia [PMID:bio_10.1101_2025.04.12.648519].

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2008 Medium

    Established that ATL2 is an ER-localized GTPase whose activity is needed to build the reticular ER network, answering whether atlastins shape ER tubules in non-neuronal cells.

    Evidence siRNA knockdown and GTPase-deficient dominant-negative overexpression in HeLa cells with ER/Golgi morphology imaging

    PMID:18270207

    Open questions at the time
    • Did not directly demonstrate membrane fusion in vitro
    • Mechanism of three-way junction formation not resolved at molecular level
  2. 2016 High

    Resolved whether ATL2 acts redundantly with other atlastins by showing that any single atlastin or a distant ortholog restores ER network formation after triple knockout.

    Evidence CRISPR/Cas9 triple atlastin knockout in NIH-3T3 cells with paralog and ortholog rescue and morphology/differentiation assays

    PMID:27669642

    Open questions at the time
    • Redundancy obscures ATL2-specific contributions
    • Link between BMP signaling/ER stress and atlastin loss not mechanistically dissected
  3. 2019 Medium

    Distinguished ATL2's fusion-driven ER-shaping role from ATL3's ER-phagy receptor function, clarifying functional division of labor among paralogs.

    Evidence siRNA depletion and morphological comparison of ATL2 vs ATL3 in a focused mechanistic study

    PMID:30773365

    Open questions at the time
    • Did not test whether ATL2 has any independent non-fusion role
  4. 2019 Medium

    Identified TMCC3 as a direct atlastin-binding modulator at three-way junctions, addressing how atlastin activity is positively regulated in the network.

    Evidence Co-IP/binding assays, TMCC3 knockdown, and ATL2 overexpression rescue with ER morphology imaging

    PMID:31696206

    Open questions at the time
    • Molecular mechanism by which TMCC3 stimulates atlastin not defined
    • Direct binding to ATL2 specifically vs other atlastins not isolated
  5. 2021 Medium

    Connected ATL2 GTPase activity to dendritic Ca2+ signaling by showing it organizes ER Ca2+ channel distribution in neurons.

    Evidence GTPase-deficient ATL2 mutant expression in hippocampal neurons with live Ca2+ imaging and channel localization

    PMID:33812310

    Open questions at the time
    • Whether RyR2/IP3R aggregation is a direct or downstream consequence of ER disruption unresolved
    • No direct ATL2-channel interaction shown
  6. 2021 Medium

    Implicated ATL2 in ER-mitochondria contact formation downstream of an Alzheimer's-linked presenilin-1 mutation.

    Evidence Hippocampal expression profiling, ATL2 siRNA knockdown, and MAM contact quantification

    PMID:34522215

    Open questions at the time
    • Direct molecular role of ATL2 at MAMs not defined
    • Whether effect requires GTPase/fusion activity untested
  7. 2021 Medium

    Placed ATL2 in the autophagosome initiation pathway by showing it is required for FIP200 complex assembly on the ER.

    Evidence siRNA depletion, super-resolution imaging of FIP200 puncta, and VAPA/B epistasis

    PMID:36198318

    Open questions at the time
    • ATL2-specific contribution separate from ATL3 not isolated
    • Mechanistic link from ER Ca2+ transients to FIP200 recruitment incomplete
  8. 2021 Low

    Positioned ATL2 within the broader ER-shaping protein network alongside Climp63 in epistasis analysis of NOMO1.

    Evidence Genetic epistasis analysis with siRNA depletion and electron microscopy

    PMID:34224731

    Open questions at the time
    • ATL2 used as reference rather than directly manipulated
    • No direct functional interaction with NOMO1 established
  9. 2022 High

    Defined a regulatory mechanism for ATL2 by identifying Lunapark-mediated ubiquitination at specific lysines as required for three-way junction formation.

    Evidence Co-IP, ubiquitination assays, K-to-R site mutagenesis, and rescue of three-way junctions

    PMID:35894092

    Open questions at the time
    • How ubiquitination biochemically alters ATL2 GTPase/fusion activity unknown
    • Turnover vs activity-modulation role of the modification unresolved
  10. 2023 Medium

    Showed ATL2 supports viral membrane penetration indirectly by maintaining global ER reticular integrity rather than relocalizing to penetration foci.

    Evidence siRNA knockdown, confocal microscopy, and SV40 infectivity assays with ATL3 comparison

    PMID:37578227

    Open questions at the time
    • No direct ATL2 interaction with the penetration complex shown
    • Whether GTPase activity is required not tested
  11. 2024 Medium

    Demonstrated, via the Drosophila ortholog, that atlastin in muscle is required for autophagy and protein quality control, and that neuronal activity modulates this requirement.

    Evidence Drosophila atl null mutant, tissue-specific rescue, TrpA1 neuronal activation, and polyubiquitin aggregate quantification

    PMID:38166124

    Open questions at the time
    • Ortholog study may not map directly to mammalian ATL2
    • Molecular basis of activity-dependent proteostatic stress unknown
  12. 2025 Medium

    Separated ATL2's membrane-tethering activity from its fusion activity, showing tethering alone is sufficient to organize flavivirus replication organelles.

    Evidence ATL2 knockout with tethering-competent/fusion-defective mutant rescue, EM, and viral replication assays (preprint)

    PMID:41394679

    Open questions at the time
    • Preprint not yet peer-reviewed
    • How tethering spatially organizes vROs mechanistically unclear
  13. 2025 Medium

    Established the in vivo requirement for ATL2 in development and lipid homeostasis, showing knockout is embryonic lethal with cerebellar defects and reduced lipid synthesis.

    Evidence ATL2 knockout mice, cerebellar histology, glia positioning analysis, and lipidomics (preprint)

    PMID:bio_10.1101_2025.04.12.648519

    Open questions at the time
    • Preprint not yet peer-reviewed
    • Causal chain from ER fusion to lipid synthesis decline not mechanistically resolved
    • Cell-autonomous vs non-autonomous basis of cerebellar phenotype unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ATL2's distinct activities — tethering versus fusion — are differentially deployed across its many roles (Ca2+ signaling, autophagy initiation, MAMs, lipid synthesis, viral organelle organization) and how ubiquitination integrates these remain unresolved.
  • No structural model linking GTPase cycle to tethering vs fusion outcomes
  • Mechanistic coupling between ER shaping and downstream lipid/Ca2+/autophagy functions undefined
  • No reported human Mendelian disease link in this corpus

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 4 GO:0140657 ATP-dependent activity 1
Localization
GO:0005783 endoplasmic reticulum 4
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-1430728 Metabolism 1 R-HSA-9612973 Autophagy 1
Partners

Evidence

Reading pass · 14 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 ATL2 (atlastin-2) is a large, membrane-bound GTPase localized to the endoplasmic reticulum (ER) in non-neuronal tissues. Knockdown of ATL2 in HeLa cells by siRNA disrupts Golgi morphology, and expression of dominant-negative (GTPase-deficient) atlastin proteins causes prominent inhibition of ER reticularization, specifically blocking formation of three-way junctions in the ER tubular network. siRNA knockdown in HeLa cells, dominant-negative overexpression, fluorescence microscopy of ER and Golgi morphology Human molecular genetics Medium 18270207
2016 Triple CRISPR/Cas9 knockout of all three atlastins (Atl1/2/3) in NIH-3T3 cells causes marked disruption of ER morphology with prominent impairment of three-way ER tubule junction formation. This phenotype is rescued by re-expression of any single human atlastin (ATL1, ATL2, or ATL3), or distant orthologs from yeast (Sey1p) or Arabidopsis (RHD3), establishing ATL2 as functionally redundant with paralogs in ER network formation. Atlastins are also required for proper adipocyte-like differentiation of NIH-3T3 cells, and their loss alters BMP signaling and increases ER stress sensitivity. CRISPR/Cas9 triple knockout, rescue expression assays, fluorescence microscopy of ER morphology, differentiation assays Experimental cell research High 27669642
2019 ATL2 predominantly affects ER morphology by promoting ER tubule fusion (consistent with its GTPase activity), whereas ATL3 has a distinct role as an ER-phagy receptor. ATL2 depletion causes detectable alterations in ER morphology, distinguishing it functionally from ATL3 depletion which barely alters ER morphology. siRNA depletion, fluorescence microscopy of ER morphology, functional comparison with ATL3 Current biology : CB Medium 30773365
2021 ATL2 GTPase activity is required for normal IP3-induced dendritic Ca2+ signaling in hippocampal neurons. GTPase-deficient ATL2 mutants cause ER morphological alterations, delay the onset and increase the rising time of IP3-evoked Ca2+ signals, and cause RyR2 and IP3R1 channel aggregation and RyR2 redistribution in dendrites. Expression of GTPase-deficient ATL2 mutants in primary hippocampal neurons, live Ca2+ imaging, fluorescence microscopy of ER morphology and Ca2+ channel distribution Cell calcium Medium 33812310
2022 Lunapark (Lnp) ubiquitinates ATL2 at lysines 56, 57, 282, and 302. Lnp localization to ER three-way junctions is required for ATL2 ubiquitination. Expression of an ATL2 ubiquitination-site mutant (K→R substitutions) fails to rescue the decrease in three-way junctions caused by ATL2 knockdown, indicating that Lnp-mediated ubiquitination of ATL2 is required for proper tubular ER network formation. Co-IP, ubiquitination assays, site-directed mutagenesis, siRNA knockdown, rescue expression, fluorescence microscopy of ER three-way junctions Journal of biochemistry High 35894092
2019 TMCC3 physically binds to atlastins (including ATL2) through its C-terminal transmembrane domains and localizes to ER three-way junctions. TMCC3 knockdown decreases three-way junctions and expands ER sheets; this phenotype is partially rescued by ATL2 overexpression, placing TMCC3 as a positive modulator of atlastin activity at three-way junctions. Co-IP/binding assays, siRNA knockdown, ATL2 overexpression rescue, fluorescence microscopy of ER morphology The Biochemical journal Medium 31696206
2021 ATL2 expression is upregulated by the Alzheimer's disease-linked PS1 M146V mutation and contributes to elevated ER-mitochondria contacts (MAMs). Downregulation of ATL2 after PS1 mutant induction rescued the abnormally elevated ER-mitochondria interactions back to normal levels, identifying ATL2 as a mediator of ER-mitochondria contact sites downstream of mutant presenilin-1. Comparative hippocampal gene expression profiling, ATL2 siRNA knockdown, ER-mitochondria contact site quantification, Western blotting Theranostics Medium 34522215
2021 ATL2 and ATL3 are required for the association of multiple FIP200 autophagosome initiation complexes on the ER surface. Depletion of ATL2/3 impairs the assembly of FIP200 puncta into autophagosome formation sites, placing ATL2 in the pathway linking ER Ca2+ transients to autophagosome initiation. siRNA depletion, multi-modal SIM analysis, live imaging of FIP200 puncta, epistasis with VAPA/B Cell Medium 36198318
2023 ATL2 supports the reticular ER morphology required for the integrity of the ATL3-dependent membrane penetration complex during SV40 (polyomavirus) infection. Unlike ATL3, ATL2 does not reorganize to ER-foci (membrane penetration sites); instead it maintains the overall ER tubular network that is critical for the ATL3-containing complex. ATL2 knockdown impairs SV40 infection. siRNA knockdown, confocal microscopy, viral infectivity assays, mechanistic comparison with ATL3 Journal of virology Medium 37578227
2025 ATL2 depletion reduces the spatial distribution of flavivirus (DENV, ZIKV) viral replication organelles (vROs) within infected cells, decreases virus production, and induces innate immune responses. A tethering-competent but fusion-defective ATL2 mutant is sufficient to rescue DENV and ZIKV replication in ATL2-knockout cells, demonstrating that ATL2's membrane-tethering activity (not its fusion activity) is required for vRO organization. ATL2 knockout, ATL2 tethering/fusion mutant rescue, confocal and electron microscopy, viral replication assays, innate immune response measurement bioRxivpreprint Medium 41394679
2025 ATL2 knockout mice are embryonic lethal with compromised cerebellar development. ATL2 is highly expressed in neuroglia and its loss disorganizes Bergmann glia positioning, interfering with granule cell migration. ATL2-null cells show reduced intracellular membrane area associated with decreased phosphatidylcholine and cholesterol synthesis, indicating ATL2's GTPase-mediated ER fusion activity is required for sustained lipid synthesis and membrane homeostasis. ATL2 knockout mice, cerebellar histology, glia positioning analysis, lipidomics, membrane area quantification bioRxivpreprint Medium bio_10.1101_2025.04.12.648519
2021 A genetic epistasis analysis placing ATL2 within the network of ER-shaping proteins: NOMO1 depletion causes ER morphology collapse, and this was analyzed in the context of known ER-shaping proteins including Atlastin2 and Climp63, establishing ATL2 as part of the functional network maintaining ER structural integrity. Genetic epistasis analysis, siRNA depletion, electron microscopy of ER morphology The Journal of biological chemistry Low 34224731
2019 miR-30b-5p overexpression in mouse mammary epithelial cells causes downregulation of ATL2 expression, leading to fragmented ER tubular network and increased lipid droplet size, suggesting ATL2 plays a role in lipid droplet formation and ER morphology maintenance in mammary epithelial cells. Transgenic mouse model with miR-30b-5p overexpression, electron microscopy of ER, lipid droplet quantification, miRNA target validation Biochemical and biophysical research communications Low 30879769
2024 In Drosophila, loss of the atlastin ortholog (atl) from muscle causes autophagy defects and accumulation of polyubiquitin protein aggregates. Increased neuronal excitability enhances this proteomic stress specifically when atl is absent from muscle (not neuron), demonstrating that atlastin in muscle is required for autophagy and protein quality control, and that neuronal activity modulates this requirement. Drosophila atl2 null mutant, TrpA1 neuronal activation, polyubiquitin aggregate quantification, tissue-specific rescue experiments PloS one Medium 38166124

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
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
1990 Adult T-cell leukemia-derived factor/thioredoxin, produced by both human T-lymphotropic virus type I- and Epstein-Barr virus-transformed lymphocytes, acts as an autocrine growth factor and synergizes with interleukin 1 and interleukin 2. Proceedings of the National Academy of Sciences of the United States of America 264 2172979
2019 ATL3 Is a Tubular ER-Phagy Receptor for GABARAP-Mediated Selective Autophagy. Current biology : CB 251 30773365
1986 Cloning of cDNA for human T-cell replacing factor (interleukin-5) and comparison with the murine homologue. Nucleic acids research 202 3024129
2008 Atlastin GTPases are required for Golgi apparatus and ER morphogenesis. Human molecular genetics 170 18270207
2022 Calcium transients on the ER surface trigger liquid-liquid phase separation of FIP200 to specify autophagosome initiation sites. Cell 144 36198318
1985 Low frequency of somatic mutation in beta-chain variable region genes of human T-cell receptors. Proceedings of the National Academy of Sciences of the United States of America 128 3865189
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
1991 Characterization of a neu/c-erbB-2 protein-specific activating factor. Proceedings of the National Academy of Sciences of the United States of America 81 1717981
2000 Binding of stromal derived factor-1alpha (SDF-1alpha) to CXCR4 chemokine receptor in normal human megakaryoblasts but not in platelets induces phosphorylation of mitogen-activated protein kinase p42/44 (MAPK), ELK-1 transcription factor and serine/threonine kinase AKT. European journal of haematology 61 10997882
2021 SalvGlandDx - a comprehensive salivary gland neoplasm specific next generation sequencing panel to facilitate diagnosis and identify therapeutic targets. Neoplasia (New York, N.Y.) 58 33878706
1994 Impaired growth in Rabson-Mendenhall syndrome: lack of effect of growth hormone and insulin-like growth factor-I. The Journal of clinical endocrinology and metabolism 53 8077364
2021 Alzheimer's disease-causing presenilin-1 mutations have deleterious effects on mitochondrial function. Theranostics 48 34522215
2011 Differentiation of mesenchymal stem cells derived from pancreatic islets and bone marrow into islet-like cell phenotype. PloS one 48 22194812
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 42 27669642
2018 Circular RNA hsa_circ_0000993 inhibits metastasis of gastric cancer cells. Epigenomics 40 30215537
2013 Characterizing the normal proteome of human ciliary body. Clinical proteomics 34 23914977
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
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
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 Nodal modulator (NOMO) is required to sustain endoplasmic reticulum morphology. The Journal of biological chemistry 10 34224731
2021 Epidermal Growth Factor Receptor Mutation Mechanisms in Nonsmall Cell Lung Cancer by Transcriptome Sequencing. Cancer biotherapy & radiopharmaceuticals 9 34009009
1998 Thiol compounds rescue growth inhibition by retinoic acid on HTLV-I (+) T lymphocytes; possible mechanism of retinoic-acid-induced growth inhibition of adult T-cell leukemia cells. Hematopathology and molecular hematology 9 9608357
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
2022 StATL2-like could affect growth and cold tolerance of plant by interacting with StCBFs. Plant cell reports 6 35732839
2022 Construction and Preclinical Evaluation of a 124/125I-Labeled Specific Antibody Targeting PD-L2 in Lung Cancer. Molecular pharmaceutics 6 36579764
2020 Activation of Early Defense Signals in Seedlings of Nicotiana benthamiana Treated with Chitin Nanoparticles. Plants (Basel, Switzerland) 6 32397652
2022 Lunapark ubiquitinates atlastin-2 for the tubular network formation of the endoplasmic reticulum. Journal of biochemistry 5 35894092
2022 MiR-30e-5p deficiency exerts an inhibitory effect on inflammation in rheumatoid arthritis via regulating Atl2 expression. Archives of rheumatology 5 37235116
2001 New T-lymphocytic cell lines for studying cell infectability by human immunodeficiency virus. European journal of haematology 4 11737246
2023 The atlastin ER morphogenic proteins promote formation of a membrane penetration site during non-enveloped virus entry. Journal of virology 3 37578227
1991 Hepatocyte growth inhibitory factor derived from HTLV-I(+) T cell lines: effect on the epidermal growth factor-dependent proliferation of rat hepatocytes. Clinical immunology and immunopathology 3 1900462
2025 Pseudomonas syringae lytic transglycosylase HrpH interacts with host ubiquitin ligase ATL2 to modulate plant immunity. Cell reports 2 39752255
2024 Motor neuron activity enhances the proteomic stress caused by autophagy defects in the target muscle. PloS one 2 38166124
2023 Transcriptome analysis during ToLCBaV disease development in contrasting tomato genotypes. 3 Biotech 2 37304404
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
2025 Primary Sweat Gland Adenocarcinoma of the Skin With ATL2::PRKD3 Fusion: A Potential Cutaneous Analog of Cribriform Adenocarcinoma of the Salivary Glands? Genes, chromosomes & cancer 1 41225782
2025 Homotypic endoplasmic reticulum membrane tethering is critical for flavivirus replication. bioRxiv : the preprint server for biology 1 41394679
2005 Human leukocyte antigen-class II-negative long-term cultured human T-cell leukemia virus type-I-infected T-cell lines with progressed cytological properties significantly induce superantigen-dependent normal T-cell proliferation. Pathology international 1 15871724
1994 Possible involvement of protein kinase C activation in down-regulation of CD3 antigen on adult T cell leukaemia cells. British journal of haematology 1 8199035
2026 In silico prediction of faba bean necrotic yellows virus proteins and their interactions with host protein SnRK1 through expression analysis. International journal of biological macromolecules 0 41520974
2025 Connecting tubules: mechanisms of endoplasmic reticulum membrane fusion. Biochemical Society transactions 0 40587263

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