Affinage · Plasmodium

Showing PF3D7_1019900 — ATG8 is a alias.

ATG8

PF3D7_1019900 · autophagy-related protein 8

Annotated
2026-09-08
34 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ATG8 (PF3D7_1019900) is a ubiquitin-like protein of Plasmodium falciparum that, in contrast to its yeast and mammalian counterparts, functions predominantly in apicoplast biology rather than canonical autophagy during blood-stage development (PMID:22900071, PMID:29295911). In intraerythrocytic parasites it exists almost exclusively as a membrane-associated, phosphatidylethanolamine-conjugated (lipidated) form and localizes to the apicoplast, a four-membrane plastid, with no accumulation of classical autophagosome-like structures (PMID:22900071, PMID:25426852). Membrane association and apicoplast targeting depend on its C-terminal glycine and its LIR docking site (LDS), whereas the N-terminal helix and the apicomplexan-specific loop are dispensable for apicoplast-specific function (PMID:24025672, PMID:36625582). Conditional depletion is lethal to blood-stage parasites and is fully rescued by isopentenyl pyrophosphate; ATG8-depleted parasites lose the apicoplast without defects in protein import or membrane expansion, establishing that its sole essential blood-stage role is in apicoplast inheritance—fission and segregation to daughter parasites (PMID:29295911). Lipidation is executed by an ATG8 conjugation system in which the E1-like enzyme Atg7 (P. berghei) loads ATG8 onto the E2-like Atg3, engaged through an Atg8-family-interacting (AIM) motif whose PfATG8–PfAtg3 co-crystal structure was solved to 2.2 Å (PMID:22982544, PMID:39714137); membrane deconjugation is performed principally by the cysteine protease Atg4, with OTU providing partial but irreversible compensation (P. berghei) (PMID:37910326). Upstream, PfATG18 acting through its PI3P interaction controls ATG8 membrane association and apicoplast inheritance (PMID:29089429). In liver-stage parasites, ATG8 additionally participates in microneme clearance via autophagosome-like structures and apicoplast biogenesis, and dysregulation of ATG8 levels impairs merozoite maturation and infectivity (PMID:27353755, PMID:39714137). The PfATG8–PfAtg3 interface and the apicomplexan-specific loop have been exploited as antimalarial targets (PMID:24786226, PMID:26748931).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2012 High

    Established that ATG8 in P. falciparum is a lipidated, membrane-associated protein directed to the apicoplast rather than to classical autophagosomes, redefining its expected function away from canonical autophagy.

    Evidence Fluorescence and immuno-EM localization plus membrane lipidation assay in intraerythrocytic parasites

    PMID:22900071

    Open questions at the time
    • Did not define which enzymes catalyze lipidation
    • Did not establish the essential function of the apicoplast localization
  2. 2012 High

    Resolved the structural basis of how ATG8 is engaged by the conjugation machinery, identifying an AIM in Atg3 and a unique apicomplexan loop as the binding interface.

    Evidence 2.2 Å co-crystal structure of PfATG8 with an Atg3 peptide, in vitro binding, and small-molecule inhibition

    PMID:22982544

    Open questions at the time
    • Whether the apicomplexan loop is required in vivo was not tested
    • Structure did not address lipidation on membranes
  3. 2013 High

    Defined the C-terminal glycine as the determinant of ATG8 membrane and apicoplast association, and documented starvation-responsive autophagosome-like structures, framing dual apicoplast and autophagy-associated roles.

    Evidence C-terminal glycine mutagenesis, colocalization with RAB7, acidification assays, and immuno-EM in P. falciparum

    PMID:24025672 PMID:24275162

    Open questions at the time
    • Whether starvation-induced vesicle behavior reflects an essential function was not resolved
    • Proteomic ribophagy/nucleophagy associations were not functionally confirmed
  4. 2013 High

    Showed that the parasite ATG8 system is functionally divergent from other orthologs and restricted to apicoplast biology in liver stages, not autophagic cell death.

    Evidence Transgenic expression across the P. falciparum lifecycle, EM in P. berghei liver stages, yeast complementation, and mammalian autophagy assays

    PMID:23388496 PMID:24342964

    Open questions at the time
    • Mechanism of the novel interaction with membranes not defined
    • Did not distinguish apicoplast biogenesis from inheritance
  5. 2014 Medium

    Confirmed ATG8 as a constitutively membrane-integral protein distinct from the cytosol/membrane equilibrium of other orthologs and largely insensitive to autophagy inhibitors.

    Evidence Subcellular fractionation, western blot, IFA, and pharmacological/doxycycline perturbation in P. falciparum

    PMID:25426852

    Open questions at the time
    • Partial apicoplast colocalization left additional membrane pools unexplained
    • Did not test essentiality directly
  6. 2014 Medium

    Validated the ATG8–Atg3 interaction and ATG8 lipidation as druggable antimalarial nodes acting in both blood and liver stages.

    Evidence SPR-based inhibitor screening, lipidation assay, and blood/liver-stage growth inhibition (Malaria Box)

    PMID:24786226

    Open questions at the time
    • Cellular target engagement not directly proven
    • Selectivity over host homologs not fully established
  7. 2016 High

    Demonstrated that ATG8 levels must be tightly balanced: overexpression drives aberrant microneme clearance and apicoplast collapse, blocking liver-stage maturation and infectivity.

    Evidence ATG8 gain-of-function transgenic P. berghei with organelle-marker imaging and mouse infectivity assays

    PMID:27353755

    Open questions at the time
    • Whether microneme clearance is a physiological ATG8 function or an overexpression artifact
    • Molecular link between ATG8 dosage and apicoplast collapse unresolved
  8. 2016 Medium

    Confirmed the apicomplexan A-loop as an exploitable, host-divergent target by structure-guided inhibitors that block ATG8–Atg3 binding and shift ATG8 lipidation.

    Evidence Virtual screening against the PfATG8 A-loop, lipidation-state assay, and blood/liver-stage growth inhibition

    PMID:26748931

    Open questions at the time
    • In vivo efficacy not established
    • Later work questioned the A-loop's functional requirement in vivo
  9. 2017 Medium

    Placed PfATG18 upstream of ATG8, showing that PI3P-dependent ATG18 controls ATG8 membrane/apicoplast localization and apicoplast inheritance.

    Evidence Conditional knockdown of PfATG18, ATG8 localization readout, and PI3P interaction assay

    PMID:29089429

    Open questions at the time
    • Direct biochemical interaction between ATG18 and ATG8 not shown
    • ATG8 localization is an indirect downstream readout
  10. 2017 Medium

    Identified OTU as an ATG8 deconjugating (delipidating) protease linked to apicoplast development, extending the enzymatic control of ATG8 turnover.

    Evidence Degradation-tag knockdown of PfOTU, apicoplast marker IFA, deconjugation assay, and IPP rescue

    PMID:28423214

    Open questions at the time
    • Relationship between OTU and Atg4 not resolved here
    • Deconjugation role inferred rather than shown to be primary
  11. 2018 High

    Established the single essential blood-stage function of ATG8 as apicoplast inheritance (fission/segregation), decoupled from autophagy, protein import, and membrane expansion.

    Evidence Conditional depletion with IPP rescue, apicoplast FISH, import, membrane expansion, and inheritance assays in P. falciparum

    PMID:29295911

    Open questions at the time
    • Molecular mechanism by which ATG8 drives fission/segregation unknown
    • Interactors executing segregation not identified
  12. 2023 High

    Defined the enzymatic logic of ATG8 deconjugation, showing Atg4 as the primary delipidase required for liver-stage differentiation and OTU as an irreversible, non-recycling backup.

    Evidence Individual and attempted double KO of Atg4 and Otu in P. berghei, ATG8 deconjugation assays, western blot, and sporozoite infection

    PMID:37910326

    Open questions at the time
    • Timing/spatial regulation of deconjugation during replication unclear
    • Whether irreversible OTU cleavage serves a distinct signaling role unknown
  13. 2023 High

    Mapped the structural determinants of ATG8's apicoplast function, showing the LDS is required and the N-terminal helix and apicomplexan loop are dispensable in vivo, overturning the earlier in vitro emphasis on the loop.

    Evidence Functional complementation with ATG8 domain mutants, apicoplast localization, and lipidation assays in P. falciparum and T. gondii

    PMID:36625582

    Open questions at the time
    • Identity of LDS-binding effectors mediating apicoplast function not defined
    • Reconciliation with A-loop inhibitor strategy not fully resolved
  14. 2024 High

    Placed the E1-like Atg7 at the apex of ATG8 lipidation, showing it is required for ATG8 membrane conjugation and for downstream microneme exocytosis, organelle biogenesis, and merozoite formation.

    Evidence Conditional knockdown of Atg7 in P. berghei with lipidation western blots, ATG8/organelle IFA, and blood/liver-stage growth assays

    PMID:39714137

    Open questions at the time
    • Whether Atg7 has ATG8-independent activities not resolved
    • Coupling between lipidation and specific effector recruitment unmapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular mechanism by which lipidated, LDS-competent ATG8 drives apicoplast fission and segregation—and the effectors it recruits at the apicoplast membrane—remains unresolved.
  • No ATG8 effector proteins executing apicoplast fission identified
  • Mechanistic link between LDS engagement and organelle division unknown
  • Species-divergent liver-stage microneme role not mechanistically integrated with the blood-stage inheritance role

Mechanism profile

Synthesis pass · controlled-vocabulary classification
Partners
ATG3 (E2-LIKE; AIM/A-LOOP INTERACTION, CO-CRYSTAL STRUCTURE) [#2, #14]ATG4 (PRIMARY DECONJUGATING CYSTEINE PROTEASE; P. BERGHEI) [#13]ATG7 (E1-LIKE ACTIVATING ENZYME; P. BERGHEI) [#15]GRASP (COLOCALIZES WITH ATG8-POSITIVE AUTOPHAGOSOMES; P. BERGHEI) [#18]OTU (BACKUP DECONJUGATING PROTEASE, IRREVERSIBLE CLEAVAGE) [#10, #13]PFATG18 (PI3P-DEPENDENT, UPSTREAM REGULATOR OF ATG8 MEMBRANE ASSOCIATION) [#9]PFATG5 (PARTIAL COLOCALIZATION) [#16]PFRAB7 (COLOCALIZATION ON MATURING VESICLES) [#0]
Complex memberships
ATG8 conjugation system (ATG8–Atg7–Atg3)

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 P. falciparum ATG8 (PfATG8) requires its C-terminal glycine for association with autophagosome membranes and for localization to the apicoplast membrane and apicoplast-targeted vesicles; mutation of this glycine abolishes both localizations. Amino acid starvation provoked increased colocalization of PfATG8-labeled vesicles with PfRAB7, and acidification of co-labeled structures consistent with RAB7-mediated autophagosome maturation. Immuno-electron microscopy detected PfATG8 on double-membrane-bound vesicles and near/within the food vacuole, consistent with autophagosome fusion with the endosomal system. C-terminal glycine mutagenesis, immunofluorescence colocalization with PfRAB7, acidification assay, immuno-electron microscopy Autophagy High 24025672
2012 P. falciparum ATG8 (PfAtg8) is expressed during intra-erythrocytic development and associates with membranes as a lipid-conjugated form. Fluorescence microscopy and immunoelectron microscopy demonstrate that PfAtg8 localizes to the apicoplast (a four-membrane-bound non-photosynthetic plastid). Autophagosome-like structures are not observed in the erythrocytic stages, suggesting the Atg8 conjugation system is used for the apicoplast rather than classical autophagy. Fluorescence microscopy, immunoelectron microscopy, membrane association/lipidation assay PloS one High 22900071
2012 The co-crystal structure of P. falciparum ATG8 (PfAtg8) with an Atg3 peptide (residues 103–110) was solved to 2.2 Å resolution, identifying an Atg8 family interacting motif (AIM) in PfAtg3 that binds PfAtg8. In vitro interaction studies confirmed the binding. A unique apicomplexan loop in PfAtg8 (absent from human Atg8 homologs) was found to be important for Atg3 binding. The full-length PfAtg8–PfAtg3 protein-protein interaction was inhibited at low micromolar concentrations by 1,2,3-trihydroxybenzene. X-ray crystallography (2.2 Å co-crystal structure), in vitro binding assay, small-molecule inhibition Journal of structural biology High 22982544
2013 PfATG8 localizes to the apicoplast and cytosolic vesicles throughout asexual and sexual erythrocytic stages. In apicoplast-minus parasites, immunofluorescence of PfATG8 is consistent with a role in apicoplast biogenesis. Treatment with the autophagy inhibitors bafilomycin A1 and chloroquine caused dramatic morphological changes to the apicoplast and parasite death. Deep proteomic analysis of PfATG8-associated components suggested possible involvement in ribophagy and piecemeal microautophagy of the nucleus. Immunofluorescence assay (IFA), pharmacological inhibition (bafilomycin A1, chloroquine), mass spectrometry-based proteomics of ATG8-associated proteins Autophagy Medium 24275162
2013 In P. berghei liver-stage parasites, PbAtg8 localizes to the apicoplast. Relocalization of PbAtg8 to autophagosome-like vesicles was not observed in dying parasites, indicating that PbAtg8 function during liver stage is restricted to apicoplast biology rather than classical autophagic cell death. Immunofluorescence/live imaging of PbAtg8 in liver-stage parasites, examination of dying parasites Autophagy Medium 23388496
2013 The ATG8-conjugation system (PfATG8, PfATG3, PfATG7) is active across the P. falciparum lifecycle. In P. berghei liver stages, PbATG8 associates with the limiting membranes of the apicoplast, and this association increases as the apicoplast expands during hepatocyte replication. P. berghei ATG8 cannot functionally complement an atg8Δ yeast mutant, and does not localize to autophagosomes in starved mammalian cells, indicating a novel mechanism of interaction compared to other orthologs. Transgenic mCherry-PfATG8 expression across lifecycle stages, EM and colocalization studies in P. berghei, yeast complementation assay, mammalian cell autophagy assay Autophagy High 24342964
2014 In P. falciparum, PfAtg8 is found exclusively in the pellet (membrane) fraction as an integral membrane protein throughout asexual and sexual stages, in contrast to yeast/mammalian Atg8 which distributes between cytosolic and membrane fractions. Starvation decreased PfAtg8 levels ~3-fold. ATG8-associated puncta and expression were not altered by E64, pepstatin, 3-methyladenine, or chloroquine. PfAtg8 showed partial colocalization with the apicoplast; doxycycline-induced apicoplast disruption did not affect ATG8 localization. Subcellular fractionation, western blotting, immunofluorescence, pharmacological inhibitor treatment, doxycycline-mediated apicoplast disruption PloS one Medium 25426852
2014 Inhibitors of the PfAtg8–PfAtg3 protein-protein interaction were identified from the Malaria Medicine Venture Malaria Box using surface plasmon resonance. These inhibitors prevent PfAtg8 lipidation with phosphatidylethanolamine and inhibit P. falciparum growth in blood and liver stages. Surface plasmon resonance-based inhibitor screening, PfAtg8 lipidation assay, P. falciparum growth inhibition assay (blood stage and liver stage) Journal of medicinal chemistry Medium 24786226
2016 In P. berghei liver forms, overexpression of ATG8 impairs development into late liver stages and produces small merosomes with immature merozoites unable to establish blood infection. Micronemes were found to colocalize with PbATG8-containing structures before expulsion. PbATG8 overexpression caused delayed clearance of micronemes via ATG8-containing autophagosomes and abnormally fast apicoplast proliferation followed by apicoplast collapse. PbATG8 was not incorporated into the progeny of mutant parasites. ATG8 overexpression (gain-of-function transgenic line), immunostaining (ACP for apicoplast, microneme markers), colocalization analysis, mouse infectivity assay mBio High 27353755
2017 P. falciparum ATG18 (PfATG18) regulates membrane association and apicoplast localization of ATG8. Conditional knockdown of PfATG18 results in loss of the apicoplast, and its interaction with phosphatidylinositol 3-phosphate (PI3P) is critical for apicoplast inheritance and for proper ATG8 apicoplast localization. Conditional knockdown of PfATG18, immunofluorescence of ATG8 localization, PI3P interaction assay mBio Medium 29089429
2017 P. falciparum OTU-like cysteine protease (PfOTU) provides evidence of a biological function in membrane deconjugation (delipidation) of ATG8, which may be linked to apicoplast protein import. Knockdown of PfOTU resulted in abnormal apicoplast development. Degradation-tag-mediated knockdown of PfOTU, immunofluorescence of apicoplast markers, isoprenoid (IPP) rescue experiment Cellular microbiology Medium 28423214
2018 Conditional depletion of P. falciparum ATG8 (PfATG8) is lethal to blood-stage parasites, and this growth inhibition is fully rescued by isopentenyl pyrophosphate (IPP), which rescues apicoplast metabolic defects. IPP-rescued, ATG8-depleted parasites lose their apicoplast. Loss of ATG8 does not affect apicoplast protein import or membrane expansion but prevents apicoplast inheritance by daughter parasites, establishing that PfATG8's essential function is specifically in apicoplast fission/segregation during replication, not in autophagy. Conditional expression regulation, IPP rescue assay, fluorescence in situ hybridization (FISH) for apicoplast genome, apicoplast protein import assay, membrane expansion assay, apicoplast inheritance assay mBio High 29295911
2016 Virtual library screening targeting the unique apicomplexan A-loop of PfAtg8, which mediates PfAtg3 binding and is absent from human Atg8 homologs, identified small molecules that inhibit the PfAtg8–PfAtg3 interaction, shift the lipidation state of PfAtg8, and inhibit P. falciparum growth in blood and liver stages. Virtual screening targeting PfAtg8 A-loop, PfAtg8 lipidation state assay, P. falciparum blood- and liver-stage growth inhibition assay ChemMedChem Medium 26748931
2023 In P. berghei, Atg4 is the primary deconjugating (delipidating) enzyme for ATG8; Atg4 KO sporozoites showed elevated ATG8 levels and impaired ATG8 deconjugation. Atg4 KO sporozoites invade hepatocytes and develop into early liver stages normally but fail to complete nuclear and organelle differentiation, unable to mature into hepatic merozoites. OTU (Otu) can partially compensate for deconjugation but cleaves at the N-terminal side of glycine, thereby irreversibly inactivating ATG8 rather than recycling it. Simultaneous deletion of both Atg4 and Otu was lethal, confirming their combined essentiality for ATG8 deconjugation. Gene disruption (individual KO of Atg4 and Otu; simultaneous double-KO refractory), in vitro and in vivo ATG8 deconjugation assay, western blot for ATG8 levels, mouse sporozoite infection assay Cellular and molecular life sciences : CMLS High 37910326
2023 Functional complementation experiments in P. falciparum showed that the LC3-interacting region (LIR) docking site (LDS) of PfATG8 is required for apicoplast localization and function, likely via ATG8 lipidation. The N-terminal helix of PfATG8 is dispensable for apicoplast-specific function. The unique apicomplexan-specific loop, previously implicated in membrane conjugation machinery interaction in vitro, is not required for membrane conjugation or apicoplast-specific effector function in P. falciparum or Toxoplasma gondii. Functional complementation with ATG8 domain mutants, apicoplast localization assay, lipidation assay mBio High 36625582
2024 In P. berghei, Atg7 (E1-like enzyme) is essential for ATG8 lipidation onto membranes. Depletion of Atg7 abolishes ATG8 membrane localization and lipidation, impairs microneme exocytosis, and blocks organelle biogenesis and merozoite formation during liver-stage development. Atg7 is also required for blood-stage parasite development. Conditional knockdown of Atg7 (degradation-tag system), western blot for ATG8 lipidation, immunofluorescence for ATG8 membrane localization and organelle markers, microneme exocytosis assay, blood and liver stage growth assay mBio High 39714137
2018 PfAtg8 is expressed in intraerythrocytic stages and basal autophagy is constitutively active, mediating intraerythrocytic development and RBC re-invasion. PfAtg8 shows punctate localization throughout the parasite and responds to both autophagy inducers and inhibitors. PfAtg8 partially colocalizes with PfAtg5, which itself is present on double-membrane-bound vesicles and partially colocalizes with ER, mitochondria, and apicoplast. Immunofluorescence, western blot for autophagy protein expression, autophagy induction/inhibition assays, colocalization analysis Cell death discovery Low 30302277
2013 Distribution of PfATG8 immunofluorescence signal differs between chloroquine-sensitive and chloroquine-resistant trophozoite-stage P. falciparum parasites at LD50 (cytocidal) but not IC50 (cytostatic) concentrations, suggesting an autophagy-like process is altered in chloroquine-resistant parasites. Indirect immunofluorescence of PfATG8 in synchronized CQS vs CQR trophozoites, quantitative trait loci analysis PloS one Low 24278114
2034 In P. berghei liver stage, GRASP associates with PbATG8-containing autophagosomes that contain micronemes; however, GRASP-KO parasites can still expel micronemes, indicating GRASP is not strictly required for ATG8-autophagosome-mediated microneme clearance. GRASP gene knockout, colocalization of GRASP with PbATG8-positive autophagosomes, microneme expulsion assay in KO parasites Molecular microbiology Low 40143578

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Plasmodium falciparum ATG8 implicated in both autophagy and apicoplast formation. Autophagy 79 24025672
2012 Autophagy-related Atg8 localizes to the apicoplast of the human malaria parasite Plasmodium falciparum. PloS one 69 22900071
2013 The multifunctional autophagy pathway in the human malaria parasite, Plasmodium falciparum. Autophagy 66 24275162
2018 ATG8 Is Essential Specifically for an Autophagy-Independent Function in Apicoplast Biogenesis in Blood-Stage Malaria Parasites. mBio 61 29295911
2013 Features of autophagic cell death in Plasmodium liver-stage parasites. Autophagy 56 23388496
2017 Autophagy-Related Protein ATG18 Regulates Apicoplast Biogenesis in Apicomplexan Parasites. mBio 45 29089429
2012 Structural characterization and inhibition of the Plasmodium Atg8-Atg3 interaction. Journal of structural biology 45 22982544
2014 Characterization of the autophagy marker protein Atg8 reveals atypical features of autophagy in Plasmodium falciparum. PloS one 42 25426852
2014 Identification of an Atg8-Atg3 protein-protein interaction inhibitor from the medicines for Malaria Venture Malaria Box active in blood and liver stage Plasmodium falciparum parasites. Journal of medicinal chemistry 40 24786226
2013 Characterization of the ATG8-conjugation system in 2 Plasmodium species with special focus on the liver stage: possible linkage between the apicoplastic and autophagic systems? Autophagy 36 24342964
2016 Overexpression of Plasmodium berghei ATG8 by Liver Forms Leads to Cumulative Defects in Organelle Dynamics and to Generation of Noninfectious Merozoites. mBio 33 27353755
2013 A process similar to autophagy is associated with cytocidal chloroquine resistance in Plasmodium falciparum. PloS one 33 24278114
2013 Autophagy in Plasmodium, a multifunctional pathway? Computational and structural biotechnology journal 33 24688742
2013 Plasmodium falciparum erythrocytic stage parasites require the putative autophagy protein PfAtg7 for normal growth. PloS one 26 23825614
2018 Basal and starvation-induced autophagy mediates parasite survival during intraerythrocytic stages of Plasmodium falciparum. Cell death discovery 25 30302277
2017 Plasmodium falciparum OTU-like cysteine protease (PfOTU) is essential for apicoplast homeostasis and associates with noncanonical role of Atg8. Cellular microbiology 19 28423214
2016 Virtual Screening and Experimental Validation Identify Novel Inhibitors of the Plasmodium falciparum Atg8-Atg3 Protein-Protein Interaction. ChemMedChem 18 26748931
2018 Characterization of Plasmodium Atg3-Atg8 Interaction Inhibitors Identifies Novel Alternative Mechanisms of Action in Toxoplasma gondii. Antimicrobial agents and chemotherapy 14 29158278
2023 Regulation of Atg8 membrane deconjugation by cysteine proteases in the malaria parasite Plasmodium berghei. Cellular and molecular life sciences : CMLS 12 37910326
2018 Structure-based drug design, synthesis and biological assays of P. falciparum Atg3-Atg8 protein-protein interaction inhibitors. Journal of computer-aided molecular design 11 29383466
2024 Autophagy protein Atg7 is essential for maintaining malaria parasite cellular homeostasis and organelle biogenesis. mBio 10 39714137
2024 LC3B labeling of the parasitophorous vacuole membrane of Plasmodium berghei liver stage parasites depends on the V-ATPase and ATG16L1. Molecular microbiology 7 38574236
2024 Plasmodium berghei liver stage parasites exploit host GABARAP proteins for TFEB activation. Communications biology 7 39572689
2023 Structure-Function Relationship for a Divergent Atg8 Protein Required for a Nonautophagic Function in Apicomplexan Parasites. mBio 7 36625582
2021 Plasmodium UIS3 avoids host cell-autonomous exclusion that requires GABARAPs but not LC3 and autophagy. Parasitology international 6 33771680
2021 Chemoprophylaxis vaccination with a Plasmodium liver stage autophagy mutant affords enhanced and long-lasting protection. NPJ vaccines 6 34376691
2019 Structural Analysis of PfSec62-Autophagy Interacting Motifs (AIM) and PfAtg8 Interactions for Its Implications in RecovER-phagy in Plasmodium falciparum. Frontiers in bioengineering and biotechnology 5 31608276
2025 Metamorphosis and development of malaria parasites in the liver are regulated by unconventional autophagy. Autophagy reports 2 40395990
2024 Drug-induced ER stress leads to induction of programmed cell death pathways of the malaria parasite. Parasitology research 1 38976068
2023 Biological functions and structural biology of Plasmodium falciparum autophagy-related proteins: The under-explored options for novel antimalarial drug design. Chemical biology & drug design 1 36869438
2026 Hepatocyte Autophagy in Malaria: Current Concepts, Emerging Mechanisms, and Future Therapeutic Directions. Pathogens (Basel, Switzerland) 0 41599054
2026 Divergent Autophagy Pathways in Plasmodium: Mechanisms, Functions, and Therapeutic Potential. Molecular microbiology 0 42473197
2025 The Plasmodium GRASP Homolog Modulates Liver Stage Development, Subsequent Blood Infection and Virulence in Mice. Molecular microbiology 0 40143578
2022 The ART of Resistance. Autophagy reports 0 40396048