Affinage

ATG9A

Autophagy-related protein 9A · UniProt Q7Z3C6

Length
839 aa
Mass
94.4 kDa
Annotated
2026-06-09
100 papers in source corpus 53 papers cited in narrative 53 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATG9A is the sole multispanning transmembrane core autophagy protein, functioning as a lipid scramblase whose homotrimeric, domain-swapped architecture creates a solvated central pore connected to branched lateral cavities that flip phospholipids between membrane leaflets; pore mutations cripple scrambling and yield markedly smaller autophagosomes, establishing that scramblase activity drives phagophore membrane expansion (PMID:33106659, PMID:32610138). ATG9A directly couples to the rod-shaped lipid transfer protein ATG2A in a 3:1 (ATG9A trimer: ATG2A) assembly, aligning the ATG9A lateral pore with the ATG2A lipid-transfer cavity so that lipids extracted from donor membranes are received and redistributed across the growing bilayer (PMID:36347259, PMID:39174844). ATG9A integrates into autophagy initiation through a C-terminal HORMA dimer-interacting region that engages the ATG13-ATG101 dimer by β-sheet complementation, a contact required for PINK1/Parkin-NDP52 mitophagy (PMID:36791199), and ATG9A vesicles serve as mobile delivery platforms that bring PI4KIIIβ and PI4P production to nascent autophagosomes (PMID:30917996). The protein operates within an elaborate trafficking itinerary: it is exported from the TGN as a specific AP-4 cargo and propelled to the cell periphery via RUSC2-kinesin-1 (PMID:29180427, PMID:30262884, PMID:34432492), cycles through recycling endosomes via AP-2 sorting motifs, SNX4-BAR complexes, and retromer (PMID:27587839, PMID:32513819, PMID:33468622), and its trafficking is further tuned by palmitoylation, ubiquitination, and partner GTPases (PMID:40394978, PMID:35196483). Beyond autophagosome biogenesis, ATG9A acts as a hub for membrane repair and homeostasis, organizing IQGAP1-ESCRT-III (CHMP2A) complexes to protect the plasma membrane and to close autophagosomes (PMID:34257406, PMID:39745851), repairing damaged lysosomes by delivering PI4K2A (PMID:40460835), negatively regulating STING-TBK1 innate immune assembly (PMID:19926846), targeting the TNFR1 cytotoxic complex IIa for lysosomal degradation as a cell-death checkpoint (PMID:36520901), and mobilizing lipids from lipid droplets to mitochondria (PMID:34799570). ATG9A additionally has autophagy-independent roles in directed cell migration through β1-integrin delivery (PMID:35180289), Golgi integrity via MARCH9-mediated K63-ubiquitination and GRASP55 (PMID:35977480), and unconventional secretion of galectins (PMID:40335523). Disruption of AP-4-dependent ATG9A trafficking underlies neuronal pathology, including impaired axonal autophagosome generation and accumulation of mutant huntingtin aggregates (PMID:29698489, PMID:31142229).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2009 High

    Established the first non-autophagosome-biogenesis function of ATG9A by showing it restrains innate immune signaling, distinguishing this role from canonical autophagy.

    Evidence Atg9a vs Atg7 knockout macrophages with STING-TBK1 assembly and IFN readouts

    PMID:19926846

    Open questions at the time
    • Molecular basis of how ATG9A physically limits STING-TBK1 assembly not defined
    • Whether scramblase activity is required for this immune role untested
  2. 2016 Medium

    Mapped the trafficking determinants of ATG9A, answering how the protein navigates biosynthetic and recycling compartments to reach autophagy sites.

    Evidence Mutagenesis of AP-2, V515-C519, and L340-L354 motifs with localization and autophagy-flux readouts; TRAPPC8 and SMPD1 perturbations

    PMID:27070082 PMID:27316455 PMID:27587839 PMID:27663665

    Open questions at the time
    • How individual sorting steps are coordinated kinetically unresolved
    • Structural basis of self-interaction during biosynthetic transit unknown
  3. 2017 High

    Identified the AP-4 export pathway that delivers ATG9A from the TGN to the periphery, explaining the cellular logic of an 'ATG9A reservoir' for autophagosome biogenesis.

    Evidence AP-4 knockout cells, patient fibroblasts, organellar proteomics, and RUSC2 knockdown with ATG9A localization and LC3B lipidation

    PMID:29180427 PMID:30262884

    Open questions at the time
    • Signal recognized by AP-4 on ATG9A not structurally defined at this stage
    • Functional consequence of vesicle clustering near autophagosomes not mechanistically dissected
  4. 2020 High

    Resolved the central question of ATG9A's molecular activity, showing it is a lipid scramblase whose trimeric pore architecture is essential for autophagosome membrane expansion.

    Evidence Cryo-EM structures (2.9 Å), in vitro scrambling assays, MD simulations, and pore mutagenesis with autophagosome-size readout

    PMID:32610138 PMID:33106659

    Open questions at the time
    • Lipid-headgroup selectivity of scrambling not fully defined
    • In vivo regulation of pore opening unknown
  5. 2020 Medium

    Connected ATG9A to a network of cargo adaptors, motors, and GTPases, defining how its peripheral distribution and autophagosome delivery are spatially controlled.

    Evidence FHF complex AP-MS, OPTN co-IP/phase-separation, Rab1B and SNX4 perturbations with ATG9A localization and mitophagy/autophagy readouts

    PMID:28522593 PMID:32073997 PMID:32513819 PMID:32556086

    Open questions at the time
    • Hierarchy and hand-off among the multiple motors/adaptors not established
    • Direct vs indirect nature of several interactions unconfirmed
  6. 2021 High

    Revealed ATG9A as a membrane-protection and lipid-mobilization hub beyond autophagy, organizing ESCRT machinery at the plasma membrane and transferring fatty acids from lipid droplets to mitochondria.

    Evidence ATG9A knockout cells with PM permeabilization assays, IQGAP1-ESCRT interaction studies, and lipid-droplet/FA-transfer/respiration assays in cells and C. elegans

    PMID:34257406 PMID:34799570

    Open questions at the time
    • Whether scramblase activity underlies PM protection and lipid transfer untested
    • Direct ATG9A-ESCRT contacts vs IQGAP1-bridged contacts not separated
  7. 2022 High

    Demonstrated post-translational control of ATG9A activity and a checkpoint function in cell death, broadening its regulatory and pathological significance.

    Evidence TRAF6/A20 ubiquitination assays with VPS34 readout; MARCH9 K63-ubiquitination with GRASP55/Golgi readout; ATG9A knockout mice with TNFR1 complex IIa lysosomal targeting and lethality/skin-disease models

    PMID:35196483 PMID:35977480 PMID:36520901

    Open questions at the time
    • Integration of competing ubiquitination signals on ATG9A unresolved
    • Mechanism of LC3-independent lysosomal targeting of complex IIa not structurally defined
  8. 2024 High

    Determined the structural basis of ATG9A-ATG2A coupling, answering how scrambled lipids are sourced and channeled into the growing phagophore.

    Evidence Cryo-EM of ATG2A-WIPI4-ATG9A (3:1 trimer:ATG2A), cryo-ET of vesicle tethering, and MD simulations of lipid extraction

    PMID:36347259 PMID:39174844

    Open questions at the time
    • Rate and directionality of lipid flux through the coupled channel not measured in cells
    • Regulation of complex assembly/disassembly during phagophore growth unknown
  9. 2025 High

    Positioned ATG9A as a central hub spanning all stages of autophagosome membrane biogenesis and extended its vesicle-delivery role to lysosome repair and unconventional secretion.

    Evidence Co-IP and SolVit closure assays for ATG9A-IQGAP1-CHMP2A; ATG9A KO with lysosome-repair and galectin-secretion assays and SNARE complex mapping

    PMID:39745851 PMID:40335523 PMID:40460835

    Open questions at the time
    • How a single protein partitions between distinct vesicle pools and functions is unresolved
    • Whether scramblase activity is required for closure, repair, and secretion not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How ATG9A's single biochemical activity (lipid scrambling) mechanistically underlies its many context-specific roles—autophagosome closure, membrane repair, immune regulation, secretion, and migration—remains unresolved.
  • No unifying model linking scramblase activity to non-autophagic functions
  • Regulation of vesicle-pool identity and functional specialization unknown
  • Structural state of ATG9A in repair/secretion complexes uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008289 lipid binding 4 GO:0005215 transporter activity 3 GO:0060090 molecular adaptor activity 3 GO:0140096 catalytic activity, acting on a protein 3
Localization
GO:0005794 Golgi apparatus 5 GO:0031410 cytoplasmic vesicle 5 GO:0005768 endosome 4 GO:0005783 endoplasmic reticulum 4 GO:0005886 plasma membrane 3 GO:0005764 lysosome 2
Pathway
R-HSA-5653656 Vesicle-mediated transport 6 R-HSA-9612973 Autophagy 5 R-HSA-168256 Immune System 3 R-HSA-1430728 Metabolism 2 R-HSA-5357801 Programmed Cell Death 2
Partners
ATG101ATG13ATG2ACHMP2AIQGAP1OPTNPI4KBTRAF6
Complex memberships
ATG9A-ATG13-ATG101 (ULK1 complex via HDIR)ATG9A-ATG2A-WIPI4 lipid transfer complexATG9A-IQGAP1-CHMP2A (ESCRT-III) closure complex

Evidence

Reading pass · 53 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2020 ATG9A is a lipid scramblase that equilibrates phospholipids across membrane bilayers in vitro. Cryo-EM structures reveal a homotrimeric architecture with a solvated central pore connected laterally to the cytosol through cavities within each protomer. Molecular dynamics simulations suggest the central pore opens laterally to accommodate lipid headgroups, enabling lipid flipping. Mutations in the pore reduce scrambling activity and yield markedly smaller autophagosomes, establishing that lipid scrambling by ATG9A is essential for autophagosome membrane expansion. Cryo-EM structure determination, in vitro lipid scrambling assay, molecular dynamics simulation, mutagenesis with functional readout (autophagosome size) Nature structural & molecular biology High 33106659
2020 Cryo-EM structure of human ATG9A at 2.9-Å resolution reveals a homotrimeric domain-swapped architecture, multiple membrane spans, and a network of branched cavities consistent with a membrane transporter function. Mutational analyses support a role for the cavities in ATG9A function. Structure-guided molecular simulations predict ATG9A causes membrane bending, explaining its localization to small vesicles and highly curved autophagosome edges. Cryo-EM structure determination (2.9 Å), mutagenesis, molecular dynamics simulation Cell reports High 32610138
2022 ATG9A and ATG2A form a heteromeric complex essential for autophagosome formation. Using peptide arrays, crosslinking, hydrogen-deuterium exchange mass spectrometry, and cryo-EM, several interfaces mediating ATG9A–ATG2A interaction were identified. The model proposes direct lipid transfer from ATG2A into the lipid-binding perpendicular branch of ATG9A. Mutational analyses of these interfaces combined with functional autophagy assays confirmed their importance. Peptide arrays, crosslinking MS, HDX-MS, cryo-EM, mutagenesis + functional autophagy assays Molecular cell High 36347259
2024 Cryo-EM structures of human ATG2A–WIPI4 (3.2 Å) and ATG2A–WIPI4–ATG9A (7 Å) complexes reveal a 3:1 stoichiometry of ATG9A trimer to ATG2A, with the ATG9A lateral pore directly aligned with the ATG2A lipid transfer cavity. The ATG9A trimer contacts both the N-terminal and C-terminal tip of rod-shaped ATG2A. Cryo-electron tomography showed ATG2A tethers lipid vesicles at different orientations, and MD simulations propose a mechanism for lipid extraction from donor membranes. Cryo-EM structure determination, cryo-electron tomography, molecular dynamics simulation Nature structural & molecular biology High 39174844
2023 X-ray crystallographic structure (2.4 Å) of the ATG9A C-terminal tail bound to the ATG13–ATG101 HORMA dimer reveals a 'HORMA dimer-interacting region' (HDIR) in the extreme C-terminus of ATG9A. The HDIR binds the HORMA domain of ATG101 by β-sheet complementation, occupying a deep cleft at the ATG13–ATG101 interface. Disruption of this complex in cells impairs PINK1/Parkin-dependent mitophagy mediated by cargo receptor NDP52. X-ray crystallography (2.4 Å), cell-based mitophagy assays with structure-guided mutants Science advances High 36791199
2009 ATG9A co-localizes with STING and LC3 after dsDNA stimulation. Loss of Atg9a (but not Atg7) greatly enhances STING–TBK1 assembly induced by dsDNA, leading to aberrant innate immune activation. Thus ATG9A negatively regulates STING–TBK1 complex formation and innate immune signaling downstream of dsDNA sensing. Atg9a knockout mouse macrophages, co-localization (immunofluorescence), genetic epistasis (Atg9a KO vs Atg7 KO), measurement of STING–TBK1 assembly and IFN production Proceedings of the National Academy of Sciences of the United States of America High 19926846
2017 AP-4 promotes signal-mediated export of ATG9A from the trans-Golgi network (TGN) to the peripheral cytoplasm. AP-4 deficiency causes retention of ATG9A at the TGN, impairs LC3B lipidation, and blocks maturation of preautophagosomal structures. ATG9A is identified as a specific AP-4 cargo. AP-4 KO cells, immunofluorescence localization of ATG9A, LC3B lipidation assay, preautophagosomal structure analysis Proceedings of the National Academy of Sciences of the United States of America High 29180427
2018 AP-4 deficiency causes missorting of ATG9A in multiple cell types including patient-derived cells. RUSC2 facilitates transport of AP-4-derived ATG9A-positive vesicles from the TGN to the cell periphery. These vesicles cluster near autophagosomes, suggesting they constitute the 'ATG9A reservoir' required for autophagosome biogenesis. Dysregulation of autophagy accompanies ATG9A missorting. Dynamic Organellar Maps proteomics, AP-4 KO cells and patient-derived fibroblasts, immunofluorescence, RUSC2 knockdown experiments Nature communications High 30262884
2019 ATG9A vesicles are enriched in BAR-domain proteins (Arfaptins) and phosphoinositide-metabolizing enzymes. Arfaptin2 regulates starvation-dependent distribution of ATG9A vesicles. ATG9A vesicles deliver PI4-kinase PI4KIIIβ to the autophagosome initiation site. PI4KIIIβ interacts with both ATG9A and ATG13 to control PI4P production at the initiation membrane and the autophagic response. Quantitative proteomics of immunoisolated ATG9A vesicles, Co-IP (ATG9A–PI4KIIIβ–ATG13), siRNA knockdown, PI4P production assay The Journal of cell biology High 30917996
2020 The autophagy adaptor OPTN forms a complex with ATG9A vesicles. Disruption of OPTN–ATG9A interactions prevents mitophagy. OPTN–ATG9A interaction is required for de novo synthesis of autophagosomal membranes near ubiquitinated mitochondria, defining an OPTN–ATG9A axis for mitophagy initiation. Phase-separated fluorescent foci assay, Co-IP, mitophagy induction with mitochondria-targeted ubiquitin chains, disruption of OPTN–ATG9A interaction with functional readout The Journal of cell biology High 32556086
2021 ATG9A depletion increases lipid droplet size and/or number and blocks fatty acid transfer from lipid droplets to mitochondria, impairing mitochondrial respiration. ATG9A localizes to vesicular-tubular clusters (VTCs) tightly associated with an ER subdomain enriched in TMEM41B and in proximity to phagophores, lipid droplets, and mitochondria, establishing a non-autophagic role for ATG9A in lipid mobilization. ATG9A KO in human cell lines and C. elegans, lipid droplet imaging, fatty acid transfer assay (fluorescent lipid tracking), mitochondrial respiration assay, immunofluorescence localization Nature communications High 34799570
2021 ATG9A organizes, together with IQGAP1, components of the ESCRT system at the plasma membrane (PM). ATG9A and ESCRTs cooperate to protect the PM from damage by a broad spectrum of agents including gasdermin, MLKL, and coronavirus ORF3a. ATG9A KO sensitizes the PM to permeabilization. ATG9A KO cells, ESCRT co-localization/interaction studies, PM permeabilization assays with multiple agents, IQGAP1 interaction experiments Nature cell biology High 34257406
2025 ATG9A facilitates autophagosome closure by partnering with IQGAP1 and the key ESCRT-III component CHMP2A. This function is distinct from its roles in phagophore initiation and expansion, making ATG9A a central hub governing all major stages of autophagosome membrane biogenesis. Co-IP (ATG9A–IQGAP1–CHMP2A), KO cells with autophagosome closure assay (SolVit), high-content microscopy The Journal of cell biology High 39745851
2022 TRAF6 E3 ubiquitin ligase mediates K48/K63-linked non-proteolytic ubiquitination of ATG9A in response to ROS. A20 deubiquitinase reverses this modification. Ubiquitinated ATG9A shows enhanced association with Beclin 1 and promotes assembly of the VPS34–UVRAG complex, stimulating autophagy. ATG9A ubiquitination mutants impair VPS34 activation and autophagy under oxidative stress. Ubiquitination assays (K48/K63-specific), Co-IP (ATG9A–Beclin 1–VPS34–UVRAG), TRAF6 KO/overexpression, A20 deubiquitinase assay, VPS34 activity assay Cell reports High 35196483
2022 ATG9A and FIP200 promote degradation of cytotoxic TNFR1 complex IIa through an LC3-independent lysosomal targeting pathway, constituting a cell-death checkpoint that prevents TNF-induced apoptosis. This mechanism counteracts TNFR1-mediated embryonic lethality and inflammatory skin disease in mouse models. ATG9A KO mice, co-immunoprecipitation, lysosomal targeting assay, cell death assays, mouse embryonic lethality model, inflammatory skin disease model Science High 36520901
2016 ATG9A contains AP-2-binding sorting motifs in its N-terminal cytosolic stretch. Mutations in these motifs prevent autophagy and cause abnormal accumulation of ATG9A at recycling endosomes. Knockdown of TRAPPC8 (a TRAPPIII subunit) similarly causes ATG9A accumulation in recycling endosomes and autophagy defects, demonstrating that ATG9A trafficking through recycling endosomes is essential for autophagosome formation. Mutagenesis of AP-2 binding motifs, immunofluorescence localization, siRNA knockdown of TRAPPC8, autophagy flux assay Journal of cell science High 27587839
2018 SNX18 regulates ATG9A trafficking from recycling endosomes by recruiting Dynamin-2. ATG9A is recruited to SNX18-induced tubules from recycling endosomes and accumulates in juxtanuclear recycling endosomes in cells lacking SNX18. SNX18–Dynamin-2 binding is required for ATG9A trafficking and for formation of ATG16L1- and WIPI2-positive autophagosome precursor membranes. SNX18 KO/knockdown, immunofluorescence, SNX18–Dynamin-2 interaction assay, autophagosome precursor membrane quantification EMBO reports Medium 29437695
2021 ATG9A interacts with ATG13 and ATG101 (ULK1 complex members) independently of ULK1. Deletion of ATG13 or ATG101 causes aberrant ATG9A accumulation at stalled p62/SQSTM1–ubiquitin clusters. This ULK1-independent ATG13 complex regulates ATG9A distribution. BioID quantitative proteomics, KO/reconstitution, split-mVenus interaction assay, immunofluorescence EMBO reports Medium 34369648
2020 The FTS-Hook-FHIP (FHF) complex interacts with AP-4 through direct binding of the AP-4 μ4 subunit to coiled-coil domains in Hook1 and Hook2. Knockdown of FHF subunits disperses AP-4 and ATG9A from the perinuclear region, consistent with FHF coupling AP-4/ATG9A vesicles to the microtubule retrograde motor dynein-dynactin. Affinity purification–mass spectrometry, Co-IP (μ4–Hook1/Hook2), siRNA knockdown with ATG9A/AP-4 localization readout Molecular biology of the cell Medium 32073997
2021 RUSC2 couples ATG9A-containing AP-4 vesicles to the plus-end-directed microtubule motor kinesin-1 via an interaction between a disordered region of RUSC2 and kinesin-1 light chain, driving peripheral distribution of ATG9A vesicles. WDR47 counteracts this interaction as a negative regulator. Co-IP (RUSC2–kinesin-1 light chain), ATG9A localization assays in KO/knockdown cells, WDR47 overexpression experiments Molecular biology of the cell Medium 34432492
2017 Small GTPase Rab1B associates with ATG9A vesicles. Knockdown of Rab1B suppresses autophagy and causes ATG9A accumulation in intermediate membrane structures at autophagosome formation sites, placing Rab1B upstream of proper ATG9A-dependent autophagosome development. Immunoisolation of ATG9A vesicles with proteomic analysis, Rab1B siRNA knockdown, immunofluorescence of ATG9A localization FASEB journal Medium 28522593
2018 In AP-4 ε KO mice, ATG9A is more concentrated in the TGN and depleted from peripheral cytoplasm in neurons. This mislocalization is associated with increased accumulation of mutant huntingtin aggregates in axons, linking AP-4-dependent ATG9A trafficking to autophagic clearance of protein aggregates in neurons. AP-4 ε KO mouse model, immunohistochemistry, patient fibroblast analysis, mutant HTT aggregate assay PLoS genetics Medium 29698489
2019 In AP-4 KO neurons, ATG9A is retained in the TGN, depleting axonal ATG9A and causing defective axonal autophagosome generation, aberrant expansions of the distal axon, and impaired axonal extension. AP-4 epsilon subunit KO mouse model, immunofluorescence of ATG9A/autophagosomes, axonal morphology analysis Autophagy Medium 31142229
2022 Upon heat stress, the E3 ubiquitin ligase MARCH9 ubiquitinates ATG9A via K63-linked conjugation. Non-degradable ubiquitinated ATG9A disperses from the Golgi and inhibits GRASP55 oligomerization, causing Golgi fragmentation. ATG9A KO or MARCH9 KO prevents Golgi fragmentation under heat and other Golgi stresses, revealing a non-autophagic role for ATG9A in Golgi dynamics. MARCH9 overexpression/KO, ubiquitination assays, ATG9A KO, GRASP55 oligomerization assay, Golgi morphology quantification Cell reports Medium 35977480
2021 ATG9A acetylation within the ER lumen (regulated by AT-1/SLC33A1) controls reticulophagy induction. Despite luminal acetylation, ATG9A engages reticulophagy receptors FAM134B and SEC62 on the cytosolic side of the ER. Interactome analysis identified CALR and HSPB1 as ATG9A partners that regulate reticulophagy induction as a function of ATG9A acetylation state. Two mouse models of AT-1 dysregulation (overexpression and haploinsufficiency), ATG9A interactome analysis, reticulophagy assays iScience Medium 33870132
2021 BECN2 recruits inflammasome sensors (NLRP3, AIM2, NLRP1, NLRC4) onto ATG9A+ vesicles forming a BECN2–ATG9A–sensor complex upon ULK1 activation, directing sensor degradation through a ULK1- and ATG9A-dependent but BECN1–WIPI2–ATG16L1–LC3-independent non-canonical autophagic pathway. SNARE proteins SEC22A, STX5, and STX6 mediate this pathway. BECN2 KO mice, Co-IP (BECN2–ATG9A–sensors), siRNA knockdown, inflammasome activity assays, SNARE interaction experiments Autophagy Medium 34152938
2022 ATG9A plays a critical role in chemotactic migration of human cell lines including glioma cells. ATG9A-positive vesicles are targeted to the migration front of polarized cells, where their exocytosis correlates with protrusive activity. ATG9A is critical for efficient delivery of β1 integrin to the leading edge and normal adhesion dynamics. ATG9A siRNA depletion, TIRF live-cell microscopy of ATG9A-pHluorin construct, β1 integrin trafficking assay, lamellipodium formation quantification The Journal of cell biology Medium 35180289
2018 VAMP7 localizes to ATG9A-resident vesicles at recycling endosomes. Hrb recruits VAMP7 and ATG9A from the plasma membrane to recycling endosomes. VAMP7 forms a SNARE complex with Syntaxin16 and SNAP-47, which mediates fusion of ATG9A-resident vesicles during autophagosome formation in pancreatic β-cells. VAMP7-deficient β-cells, Co-IP (VAMP7–Hrb–Syntaxin16–SNAP-47), immunofluorescence, siRNA knockdown of SNARE components, autophagy assay Endocrinology Medium 30215699
2018 Atg9a conditional KO in mouse brain causes progressive axonal degeneration with aberrant membrane structures and accumulation of SQSTM1/p62 and NBR1 at early postnatal stages. ATG9A is also required for neurite outgrowth independently of ATG7 and ATG16L1, demonstrating an autophagy-independent function of ATG9A in neurite extension. Brain-specific conditional Atg9a KO mice, electron microscopy, immunohistochemistry, Western blot, primary neuronal culture neurite outgrowth assay in multiple KO backgrounds, DTI-MRI Autophagy Medium 28513333
2016 Excess sphingomyelin (due to SMPD1 deficiency) causes ATG9A to concentrate in transferrin receptor-positive juxtanuclear recycling endosomes instead of its normal trafficking itinerary, impairing autophagosome maturation and closure. Ectopic ATG9A expression reverts this autophagy defect, and exogenous C12-sphingomyelin induces similar juxtanuclear ATG9A accumulation in healthy cells. Niemann-Pick patient fibroblasts, SMPD1 siRNA knockdown, ATG9A localization (immunofluorescence), ectopic ATG9A rescue, ceramide/sphingomyelin treatment, smpd1-KO mouse tissue Autophagy Medium 27070082
2016 A conserved glycine residue (G516) in the C-terminal V515-C519 motif of human ATG9A is required for its transport from the ER to the Golgi apparatus. Mutation of this motif severely impairs ER-to-Golgi transport. ATG9A self-interacts, and this self-interaction promotes its trafficking through the Golgi, but the molecular mechanism of self-interaction differs from yeast. Sequential mutagenesis of V515-C519 motif, immunofluorescence localization, co-immunoprecipitation for self-interaction Biochemical and biophysical research communications Medium 27663665
2016 Deletion of amino acids L340–L354 causes ER retention of ATG9A. Mutation of the L711YM713 sequence in the C-terminal region impairs ATG9A transport through the Golgi. Some newly synthesized ATG9A can bypass the Golgi to reach the plasma membrane. ATG9A oligomerization helps its sorting through biosynthetic compartments. Sequential deletions and point mutations, immunofluorescence localization in HeLa cells, co-transfection rescue experiments Biochimica et biophysica acta Medium 27316455
2020 The SNX4–SNX7 heterodimer is an autophagy-specific SNX-BAR complex required for efficient ATG9A trafficking from the Golgi region to sites of autophagosome assembly. SNX4 disruption causes mis-trafficking/retention of ATG9A in the Golgi region and impairs LC3 lipidation and autophagosome assembly. siRNA and CRISPR-Cas9 KO of SNX4, immunofluorescence of ATG9A localization, LC3 lipidation assay, autophagosome assembly imaging Journal of cell science Medium 32513819
2021 SNX4 mediates recycling of ATG9A from endolysosomes to early endosomes, from where ATG9A is recycled to the TGN in a retromer-dependent (VPS35-dependent) manner. SNX4 depletion causes ATG9A accumulation on endolysosomes and inhibits starvation-induced autophagosome biogenesis and autophagic flux. siRNA depletion of SNX4/VPS35, immunofluorescence of ATG9A on endolysosomes/early endosomes, autophagy flux assay Journal of cell science Medium 33468622
2020 ATG9A localizes to neurons of the mouse CNS, particularly highly expressed in Purkinje cells where it is found in the ER, TGN, lysosomes/late endosomes, and axon terminals, as determined by immunohistochemistry with a specific antibody recognizing both non-glycosylated (~94 kDa) and glycosylated (~105 kDa) forms. Antibody production, immunohistochemistry, subcellular fractionation/immunoblotting The journal of histochemistry and cytochemistry Medium 20124090
2014 miR-34a directly binds the ATG9A 3'-UTR but not a mutated version, inhibiting ATG9A protein expression and autophagic activity in cardiomyocytes. ATG9A overexpression or Ang II treatment upregulates autophagic activity and cardiomyocyte hypertrophy; ATG9A knockdown reverses these effects, placing ATG9A downstream of miR-34a in the regulation of cardiac hypertrophy. 3'-UTR luciferase reporter assay, miR-34a overexpression/inhibition, ATG9A knockdown/overexpression, autophagy assays (LC3 II/I, p62, TEM, flow cytometry) PloS one Medium 24728149
2020 ATG9A interacts with F-actin and NMMHC IIA in response to oxygen-glucose deprivation/reoxygenation (OGD/R). NMMHC IIA-actin interaction contributes to ATG9A trafficking and autophagosome formation. Inhibition of NMMHC IIA (blebbistatin) or F-actin polymerization (cytochalasin D) suppresses ATG9A trafficking and autophagy induction. Co-IP (NMMHC IIA–ATG9A–F-actin), siRNA knockdown, blebbistatin/cytochalasin D treatment, ATG9A trafficking assay, mouse MCAO model Cell death & disease Medium 32513915
2025 ATG9A-containing vesicles deliver PI4K2A to damaged lysosomes, playing a critical role in lysosome repair. ARFIP2, a component of ATG9A vesicles, binds and sequesters PI4P on lysosomes, balancing OSBPL-dependent lipid transfer and promoting retrieval of ATG9A vesicles through AP-3 recruitment. ATG9A KO cells, live-cell imaging of ATG9A vesicle dynamics upon lysosomal damage, Co-IP (ATG9A–ARFIP2–PI4K2A), PI4P assays, intracellular bacterial damage models Developmental cell Medium 40460835
2025 ATG9A undergoes S-palmitoylation at Cys155 and Cys156 (2CS mutation abolishes this). S-palmitoylation coordinates ATG9A trafficking from the TGN to phagophores and is required for efficient autophagy initiation. Acyl-biotin exchange assay, 2-bromopalmitate inhibition, mutagenesis (2CS), ATG9A trafficking and autophagy initiation assays Autophagy Medium 40394978
2025 ATG9A vesicles function as carriers for galectin-9 unconventional secretion, independently of canonical autophagy, secretory autophagy, or LC3-dependent pathways. The N-terminus of ATG9A and both carbohydrate recognition domains of galectin-9 are critical for this process. TMED10 mediates incorporation of galectin-9 into ATG9A vesicles, which fuse with the plasma membrane via the STX13–SNAP23–VAMP3 SNARE complex. ATG9A also regulates secretion of galectin-4, galectin-8, and annexin A6 but not IL-1β, galectin-3, or FGF2. ATG9A KO cells, domain mapping (N-terminus mutants), Co-IP (ATG9A–TMED10–galectin-9), SNARE complex identification, galectin secretion assays Nature communications Medium 40335523
2024 SEC31a (outer coat protein of COPII vesicles) interacts with ATG9A of autophagosomal seed vesicles, mediating recruitment of COPII vesicles as a membrane source for autophagosome formation during osteogenic differentiation of mesenchymal stem cells. Co-IP (SEC31a–ATG9A), SEC31a siRNA in MSCs and in vivo, autophagosome number/size quantification, osteogenesis assay Advanced science Medium 39361436
2024 IRP2 (but not IRP1) is required for ATG9A endosomal trafficking. IRP2 ablation results in defective AMPK activation and impaired ATG9A endosomal trafficking, leading to decreased engulfment of NCOA4-ferritin complex by endosomes and dysregulated endosomal microferritinophagy. IRP2 KO cells, ATG9A localization assay, ferritinophagy assay (NCOA4-ferritin complex), AMPK activation assay The Journal of biological chemistry Medium 39276939
2024 RHOD (atypical Rho GTPase) interacts with ATG9A upon starvation and accompanies ATG9A trafficking from the Golgi toward phagophores. RHOD promotes Golgi fragmentation to facilitate ATG9A vesicle export from the TGN. WHAMM forms a complex with RHOD and participates in ATG9A trafficking in a RHOD-dependent manner. RHOD mutants lacking the exon II effector region (required for ATG9A binding) or the CAAX box fail to stimulate ATG9A trafficking. Co-IP (RHOD–ATG9A–WHAMM), BiFC interaction assay, PUP-IT proximity labeling, RHOD KO plus domain-disrupting mutants, ATG9A trafficking assay Autophagy Medium 40143438
2020 HIF-1 transcription factor binds the ATG9A promoter under hypoxia. Lentiviral knockdown of ATG9A in intestinal epithelial cells prevents epithelial barrier formation by >95% and causes significant mislocalization of tight junction proteins and defects in the actin cytoskeleton including mislocalization of vasodilator-stimulated phosphoprotein. ChIP-chip (HIF-1α antibody + promoter microarray), luciferase promoter assay, HIF-1 KO, lentiviral ATG9A KD, tight junction protein localization, actin cytoskeleton imaging Molecular biology of the cell Medium 32726170
2019 ATG9A promotes HIV-1 infectivity in an envelope glycoprotein-dependent manner. ATG9A KO reduces infectivity of WT HIV-1 by ~4–8-fold in HeLa and Jurkat T cells without affecting virus release. Pseudotyping with VSV-G rescues infectivity, and the Nef–ATG9A interaction is not required for this function. ATG9A KO (HeLa, Jurkat), virus release assay, infectivity assay, pseudotyping rescue, tandem affinity purification–MS (Nef interactome) Retrovirology Medium 31269971
2016 Atg9a deficiency prevents a form of necrosis observed at the bone surface during mouse embryonic development. This necrosis is unaffected by Atg5 KO, establishing Atg9a-dependent necrosis as distinct from canonical autophagy-dependent cell death and indicating an active role for Atg9a in developmental morphogenesis of the bone surface. Atg9a KO and Atg5 KO mouse embryos, vital staining with propidium iodide for plasma membrane disruption (in vivo), bone surface morphology analysis Nature communications Medium 27811852
2023 In synaptic terminals, ATG9A does not co-assemble into synaptophysin-positive synaptic vesicle condensates but localizes on a distinct class of vesicles that assembles with synapsin into a separate phase. ATG9A undergoes activity-dependent exo-endocytosis at synapses, demonstrating differential sorting of ATG9A vesicles relative to synaptic vesicles. Ectopic expression in fibroblasts, live-cell imaging of condensate formation, nerve terminal analysis, activity-dependent exo-endocytosis assay Nature communications Medium 36709207
2024 Tepsin directly binds LC3B (but not other mammalian ATG8 family members) via a LIR motif, with micromolar affinity at the established LC3B LIR docking site. Loss of tepsin dysregulates ATG9A export from the TGN and ATG9A distribution at the cell periphery. Reintroduction of tepsin with mutated LIR or missing N-terminus fails to fully rescue ATG9A trafficking defects. Biochemical binding assays with purified recombinant proteins, calorimetry, structural modeling, siRNA KD, ATG9A localization assay, mRFP-GFP-LC3B reporter Molecular biology of the cell Medium 38381558
2025 ATG9A virtually all resides within a subtype of intracellular nanovesicles (INVs), termed ATG9A-flavor INVs, which constitute ~20% of all INVs. Perturbing ATG9A-flavor INVs impairs the starvation-induced autophagy response. The INV proteome is enriched for transmembrane cargo molecules including integrins and transporters. In-cell vesicle capture assays, quantitative imaging analysis of ATG9A co-localization with INV markers, autophagy induction assay upon perturbation Journal of cell science Low 40067248
2023 HSF4 directly transcriptionally activates the ATG9a gene in the lens. ChIP assay and luciferase reporter assay confirm HSF4 binding to the ATG9a promoter. Loss of HSF4 reduces ATG9a expression, impairs autophagosome biogenesis, and causes defective organelle clearance in lens fibers. ChIP assay, luciferase reporter assay, HSF4 KO mouse (HSF4del42), immunofluorescence and immunoblotting of ATG9a and autophagy markers Investigative ophthalmology & visual science Low 37266953
2023 ATG9A supports Chlamydia trachomatis infection via autophagy-independent mechanisms mediated by its binding ability to clathrin adaptor proteins, as shown by rescue experiments with ATG9A mutants defective in clathrin adaptor binding. ATG9A-deficient HeLa cells, Chlamydia proliferation assay, rescue with ATG9A mutants defective in clathrin adaptor binding Microbiology spectrum Low 37707289
2025 ATG9A interacts with PLA2G6 (iPLA2β). ATG9A–PLA2G6 interaction accelerates phosphatidylcholine degradation, perturbing fatty acid metabolism and causing mitochondrial dysfunction. Liver-specific ATG9A overexpression enhances autophagic flux but impairs autophagosome degradation and disrupts hepatic lipid metabolism. Co-IP (ATG9A–PLA2G6), liver-specific ATG9A overexpression mouse model, phosphatidylcholine/fatty acid metabolic assays, mitochondrial function assay Autophagy Low 41358570
2024 ATG9A mRNA expression is regulated by m6A modification in arsenic-exposed microglia. FTO (m6A eraser) demethylates ATG9A mRNA, and its loss increases m6A modification and reduces ATG9A expression. ATG9A knockdown significantly attenuates ferritin degradation (ferritinophagy) in arsenic-treated microglial cells. m6A sequencing, FTO knockin/KO mouse models, ATG9A siRNA knockdown, ferritinophagy assay Journal of hazardous materials Low 40816185

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Atg9a controls dsDNA-driven dynamic translocation of STING and the innate immune response. Proceedings of the National Academy of Sciences of the United States of America 704 19926846
2020 Structure, lipid scrambling activity and role in autophagosome formation of ATG9A. Nature structural & molecular biology 253 33106659
2020 Critical role of mitochondrial ubiquitination and the OPTN-ATG9A axis in mitophagy. The Journal of cell biology 165 32556086
2019 ATG9A shapes the forming autophagosome through Arfaptin 2 and phosphatidylinositol 4-kinase IIIβ. The Journal of cell biology 160 30917996
2020 Structure of Human ATG9A, the Only Transmembrane Protein of the Core Autophagy Machinery. Cell reports 141 32610138
2017 AP-4 mediates export of ATG9A from the trans-Golgi network to promote autophagosome formation. Proceedings of the National Academy of Sciences of the United States of America 141 29180427
2016 Atg9A trafficking through the recycling endosomes is required for autophagosome formation. Journal of cell science 134 27587839
2018 AP-4 vesicles contribute to spatial control of autophagy via RUSC-dependent peripheral delivery of ATG9A. Nature communications 127 30262884
2022 ATG9A and ATG2A form a heteromeric complex essential for autophagosome formation. Molecular cell 117 36347259
2021 The autophagy protein ATG9A enables lipid mobilization from lipid droplets. Nature communications 107 34799570
2018 Altered distribution of ATG9A and accumulation of axonal aggregates in neurons from a mouse model of AP-4 deficiency syndrome. PLoS genetics 96 29698489
2018 Atg9a deficiency causes axon-specific lesions including neuronal circuit dysgenesis. Autophagy 89 28513333
2018 SNX18 regulates ATG9A trafficking from recycling endosomes by recruiting Dynamin-2. EMBO reports 80 29437695
2018 ATG7 and ATG9A loss-of-function variants trigger autophagy impairment and ovarian failure. Genetics in medicine : official journal of the American College of Medical Genetics 73 30224786
2021 ATG9A protects the plasma membrane from programmed and incidental permeabilization. Nature cell biology 72 34257406
2022 K48/K63-linked polyubiquitination of ATG9A by TRAF6 E3 ligase regulates oxidative stress-induced autophagy. Cell reports 71 35196483
2019 Axonal autophagosome maturation defect through failure of ATG9A sorting underpins pathology in AP-4 deficiency syndrome. Autophagy 69 31142229
2017 Activation of miR-34a impairs autophagic flux and promotes cochlear cell death via repressing ATG9A: implications for age-related hearing loss. Cell death & disease 66 28981097
2014 miR-34a modulates angiotensin II-induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity. PloS one 66 24728149
2019 The lncRNA NEAT1/miR-29b/Atg9a axis regulates IGFBPrP1-induced autophagy and activation of mouse hepatic stellate cells. Life sciences 60 31610195
2017 Small GTPase Rab1B is associated with ATG9A vesicles and regulates autophagosome formation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 56 28522593
2016 Excess sphingomyelin disturbs ATG9A trafficking and autophagosome closure. Autophagy 52 27070082
2023 Structural basis for ATG9A recruitment to the ULK1 complex in mitophagy initiation. Science advances 48 36791199
2021 BioID reveals an ATG9A interaction with ATG13-ATG101 in the degradation of p62/SQSTM1-ubiquitin clusters. EMBO reports 42 34369648
2023 Synaptic vesicle proteins and ATG9A self-organize in distinct vesicle phases within synapsin condensates. Nature communications 41 36709207
2010 Atg9A protein, an autophagy-related membrane protein, is localized in the neurons of mouse brains. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 40 20124090
2020 Two different axes CALCOCO2-RB1CC1 and OPTN-ATG9A initiate PRKN-mediated mitophagy. Autophagy 38 32892694
2020 A heterodimeric SNX4--SNX7 SNX-BAR autophagy complex coordinates ATG9A trafficking for efficient autophagosome assembly. Journal of cell science 37 32513819
2015 Role of the Atg9a gene in intrauterine growth and survival of fetal mice. Reproductive biology 37 26370455
2016 Aberrant methylation of ATG2B, ATG4D, ATG9A and ATG9B CpG island promoter is associated with decreased mRNA expression in sporadic breast carcinoma. Gene 36 27265029
2014 Age-enhanced endoplasmic reticulum stress contributes to increased Atg9A inhibition of STING-mediated IFN-β production during Streptococcus pneumoniae infection. Journal of immunology (Baltimore, Md. : 1950) 36 24670807
2022 ATG9A prevents TNF cytotoxicity by an unconventional lysosomal targeting pathway. Science (New York, N.Y.) 35 36520901
2021 The phosphatidylinositol 3-phosphate-binding protein SNX4 controls ATG9A recycling and autophagy. Journal of cell science 33 33468622
2020 HANR Enhances Autophagy-Associated Sorafenib Resistance Through miR-29b/ATG9A Axis in Hepatocellular Carcinoma. OncoTargets and therapy 30 32210579
2020 NMMHC IIA triggers neuronal autophagic cell death by promoting F-actin-dependent ATG9A trafficking in cerebral ischemia/reperfusion. Cell death & disease 30 32513915
2024 Structural basis for lipid transfer by the ATG2A-ATG9A complex. Nature structural & molecular biology 28 39174844
2018 VAMP7 Regulates Autophagosome Formation by Supporting Atg9a Functions in Pancreatic β-Cells From Male Mice. Endocrinology 28 30215699
2020 The FTS-Hook-FHIP (FHF) complex interacts with AP-4 to mediate perinuclear distribution of AP-4 and its cargo ATG9A. Molecular biology of the cell 27 32073997
2021 BECN2 (beclin 2) Negatively Regulates Inflammasome Sensors Through ATG9A-Dependent but ATG16L1- and LC3-Independent Non-Canonical Autophagy. Autophagy 26 34152938
2018 ATG9A Is Overexpressed in Triple Negative Breast Cancer and Its In Vitro Extinction Leads to the Inhibition of Pro-Cancer Phenotypes. Cells 26 30563263
2022 Nondegradable ubiquitinated ATG9A organizes Golgi integrity and dynamics upon stresses. Cell reports 25 35977480
2017 TMEM74 promotes tumor cell survival by inducing autophagy via interactions with ATG16L1 and ATG9A. Cell death & disease 25 29048433
2016 ATG9A loss confers resistance to trastuzumab via c-Cbl mediated Her2 degradation. Oncotarget 23 27050377
2024 NDRG1 overcomes resistance to immunotherapy of pancreatic ductal adenocarcinoma through inhibiting ATG9A-dependent degradation of MHC-1. Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy 22 38228036
2024 IL-4 activates ULK1/Atg9a/Rab9 in asthma, NLRP3 inflammasomes, and Golgi fragmentation by increasing autophagy flux and mitochondrial oxidative stress. Redox biology 22 38373380
2020 The HIF target ATG9A is essential for epithelial barrier function and tight junction biogenesis. Molecular biology of the cell 22 32726170
2016 Vital staining for cell death identifies Atg9a-dependent necrosis in developmental bone formation in mouse. Nature communications 22 27811852
2014 Lentivirus-mediated Bos taurus bta-miR-29b overexpression interferes with bovine viral diarrhoea virus replication and viral infection-related autophagy by directly targeting ATG14 and ATG9A in Madin-Darby bovine kidney cells. The Journal of general virology 22 25234643
2025 ATG9A and ARFIP2 cooperate to control PI4P levels for lysosomal repair. Developmental cell 21 40460835
2022 The core autophagy protein ATG9A controls dynamics of cell protrusions and directed migration. The Journal of cell biology 21 35180289
2024 Emerging roles of ATG9/ATG9A in autophagy: implications for cell and neurobiology. Autophagy 19 39099167
2025 ATG9A facilitates the closure of mammalian autophagosomes. The Journal of cell biology 18 39745851
2021 RUSC2 and WDR47 oppositely regulate kinesin-1-dependent distribution of ATG9A to the cell periphery. Molecular biology of the cell 18 34432492
2019 The autophagy protein ATG9A promotes HIV-1 infectivity. Retrovirology 17 31269971
2018 Deregulation of ATG9A by impaired AR signaling induces autophagy in prostate stromal fibroblasts and promotes BPH progression. Cell death & disease 17 29568063
2022 miR-34a/ATG9A/TFEB Signaling Modulates Autophagy in Cochlear Hair Cells and Correlates with Age-related Hearing Loss. Neuroscience 16 35367291
2021 ATG9A regulates proteostasis through reticulophagy receptors FAM134B and SEC62 and folding chaperones CALR and HSPB1. iScience 15 33870132
2021 High-throughput imaging of ATG9A distribution as a diagnostic functional assay for adaptor protein complex 4-associated hereditary spastic paraplegia. Brain communications 15 34729478
2018 MiR-29a inhibited intestinal epithelial cells autophagy partly by decreasing ATG9A in ulcerative colitis. Anti-cancer drugs 14 29916896
2023 circAP1M2 activates ATG9A-associated autophagy by inhibiting miR-1249-3p to promote cisplatin resistance in oral squamous cell carcinoma. Journal of cellular physiology 13 37661341
2022 Trehalose Protects Keratinocytes against Ultraviolet B Radiation by Activating Autophagy via Regulating TIMP3 and ATG9A. Oxidative medicine and cellular longevity 13 35450405
2023 Ap4b1-knockout mouse model of hereditary spastic paraplegia type 47 displays motor dysfunction, aberrant brain morphology and ATG9A mislocalization. Brain communications 12 36632189
2023 ATG9B is a tissue-specific homotrimeric lipid scramblase that can compensate for ATG9A. Autophagy 11 37938170
2023 ATG9A modulated by miR-195-5p can boost the malignant progression of cervical cancer cells. Epigenetics 10 37782756
2025 YBX1 promotes 5-Fluorouracil resistance in gastric cancer via m5C-dependent ATG9A mRNA stabilization through autophagy. Oncogene 9 40251390
2024 SEC31a-ATG9a Interaction Mediates the Recruitment of COPII Vesicles for Autophagosome Formation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 9 39361436
2023 S100a9 inhibits Atg9a transcription and participates in suppression of autophagy in cardiomyocytes induced by β1-adrenoceptor autoantibodies. Cellular & molecular biology letters 9 37723445
2022 Autophagy-associated immune dysregulation and hyperplasia in a patient with compound heterozygous mutations in ATG9A. Autophagy 9 35838483
2019 ATG9A supplies PtdIns4P to the autophagosome initiation site. Autophagy 9 31204568
2024 Iron regulatory protein two facilitates ferritinophagy and DNA damage/repair through guiding ATG9A trafficking. The Journal of biological chemistry 7 39276939
2022 A noncanonical autophagy function of ATG9A for Golgi integrity and dynamics. Autophagy 7 36198086
2022 Atg9A-mediated mitophagy is required for decidual differentiation of endometrial stromal cells. Reproductive biology 7 36343573
2020 The structure of human ATG9A and its interplay with the lipid bilayer. Autophagy 7 33016201
2025 Autophagy-independent role of ATG9A vesicles as carriers for galectin-9 secretion. Nature communications 6 40335523
2025 S-palmitoylation coordinates the trafficking of ATG9A to mediate autophagy initiation. Autophagy 6 40394978
2023 HSF4 Transcriptionally Activates Autophagy by Regulating ATG9a During Lens Terminal Differentiation. Investigative ophthalmology & visual science 6 37266953
2023 Tracking the transition from an ATG9A vesicle to an autophagosome. Autophagy 6 37405380
2024 miRNA family miR-29 inhibits PINK1-PRKN dependent mitophagy via ATG9A. bioRxiv : the preprint server for biology 5 38293184
2024 Tepsin binds LC3B to promote ATG9A trafficking and delivery. Molecular biology of the cell 5 38381558
2016 A conserved glycine residue in the C-terminal region of human ATG9A is required for its transport from the endoplasmic reticulum to the Golgi apparatus. Biochemical and biophysical research communications 5 27663665
2025 ATG2A-WDR45/WIPI4-ATG9A complex-mediated lipid transfer and equilibration during autophagosome formation. Autophagy 4 40116844
2024 HCMV miR-UL70-3p downregulates the rapamycin-induced autophagy by targeting the autophagy-related protein 9A (ATG9A). International reviews of immunology 4 38164951
2022 Chemotactic cell migration: the core autophagy protein ATG9A is at the leading edge. Autophagy 4 35468023
2016 Molecular determinants that mediate the sorting of human ATG9A from the endoplasmic reticulum. Biochimica et biophysica acta 4 27316455
2025 ATG9A vesicles are a subtype of intracellular nanovesicle. Journal of cell science 3 40067248
2025 Anoctamin-5 deficiency enhances ATG9A-dependent autophagy, inducing osteogenesis and gnathodiaphyseal dysplasia-like bone formation. JCI insight 3 40067389
2025 Progress on multifunctional transmembrane protein ATG9A. Cell communication and signaling : CCS 3 40598533
2025 ATG9A-mediated autophagy prevents inflammatory skin disease by limiting TNFR1-driven STING activation and ZBP1-dependent cell death. Immunity 3 41118755
2023 A novel role of ATG9A and RB1CC1/FIP200 in mediating cell-death checkpoints to repress TNF cytotoxicity. Autophagy 3 36892222
2023 ATG9A supports Chlamydia trachomatis infection via autophagy-independent mechanisms. Microbiology spectrum 3 37707289
2021 Downregulation of microRNA-96-5p protects TM3 cells against zearalenone toxicity via targeting ATG9A. Experimental and therapeutic medicine 3 34584554
2025 RHOD mediates ATG9A trafficking to promote autophagosome formation during autophagy in cancer. Autophagy 2 40143438
2025 ATG9A controls all stages of autophagosome biogenesis. Autophagy 2 40241347
2025 TERT/FOXO1 signaling promotes islet β-cell dysfunction in type 2 diabetes mellitus by regulating ATG9A-mediated autophagy. World journal of diabetes 2 40487620
2024 The differential expression patterns of Atg9a and Atg9b in cells of the reproductive organs. Clinical and experimental reproductive medicine 2 38757275
2024 Ubiquitin-mediated recruitment of the ATG9A-ATG2 lipid transfer complex drives clearance of phosphorylated p62 aggregates. Molecular biology of the cell 2 39718773
2023 Imaging ATG9A, a Multi-Spanning Membrane Protein. Journal of visualized experiments : JoVE 2 37395569
2023 Tepsin binds LC3B to promote ATG9A export and delivery at the cell periphery. bioRxiv : the preprint server for biology 2 37502979
2025 m6A modification of ATG9A regulates ferritinophagy in microglial activation induced by arsenic. Journal of hazardous materials 1 40816185
2025 ATG9A-PLA2G6 axis reprograms phospholipid metabolism to drive metabolic liver disease and hepatocellular carcinoma. Autophagy 1 41358570

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