Affinage

PLAA

Phospholipase A-2-activating protein · UniProt Q9Y263

Length
795 aa
Mass
87.2 kDa
Annotated
2026-06-10
32 papers in source corpus 16 papers cited in narrative 16 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

PLAA (yeast Doa1/Ufd3, C. elegans UFD-3) is a multi-domain ubiquitin adaptor that links ubiquitinated cargo to the p97/Cdc48 AAA-ATPase to direct protein fate across endolysosomal sorting, organelle-associated degradation, and DNA-damage responses (PMID:27044889, PMID:16705165). Its C-terminal PUL domain forms a six-helix Armadillo-repeat fold whose positively charged inner ridge engages the acidic C-terminus of p97/Cdc48, while the adjacent PFU domain provides a ubiquitin- and Hse1-binding surface (PMID:19887378, PMID:21063153). Through the PFU–Hse1/SH3 interaction PLAA couples ubiquitinated membrane cargo to the ESCRT machinery for MVB sorting (PMID:18508771, PMID:24607902), and as an adaptor within the Cdc48-Ufd1-Npl4 complex it recruits ubiquitinated outer-membrane substrates for mitochondria-associated degradation and forms a SUMO-specific complex with Cdc48 and the Wss1 metalloprotease that clears sumoylated targets after genotoxic stress (PMID:27044889, PMID:26349035). In human cells PLAA, together with p97, UBXD1, and the deubiquitylase YOD1, strips K48-linked ubiquitin conjugates from damaged lysosomes to promote selective autophagy (PMID:27753622). Biallelic and de novo PUL-domain mutations that weaken the PLAA–p97 interaction cause infantile-lethal epileptic encephalopathy, with mutant neurons accumulating K63-polyubiquitylated and synaptic membrane proteins and failing in synaptic vesicle recycling and neurotransmission (PMID:28413018, PMID:38650658). Independent of its ubiquitin-degradation role, PLAA's intrinsic disordered region directly binds the decapping regulator DCAP-1 to recruit it to cytoplasmic P-bodies (PMID:40560612). A separate body of work assigns PLAA a signaling function as an activator of phospholipase A2 downstream of the Pdia3 membrane receptor, driving arachidonic acid release, prostaglandin production, and PKC/CaMKII activation in chondrocytes (PMID:15368540, PMID:25158196).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2006 High

    Established that yeast Doa1/PLAA does more than maintain free ubiquitin pools, channeling ubiquitin into specific damage-induced modifications and acting as a dedicated factor for H2B monoubiquitination.

    Evidence Genetic epistasis with DNA-damage ubiquitination machinery plus Western blots for PCNA-Ub and H2B-Ub and ubiquitin-overexpression rescue in yeast

    PMID:16705165

    Open questions at the time
    • Did not define the direct physical mechanism by which Doa1 promotes H2B ubiquitination
    • No structural basis for substrate selection
  2. 2008 High

    Identified the PFU domain as the module coupling Doa1 to ESCRT-mediated endosomal sorting, separating this function from ubiquitin homeostasis.

    Evidence Direct PFU–Hse1/SH3 binding assay, structure-guided mutagenesis, GFP-Cps1 MVB sorting readout and genetic epistasis in yeast

    PMID:18508771

    Open questions at the time
    • Atomic detail of the PFU–SH3 interface not resolved
    • Human ortholog interaction not tested here
  3. 2009 High

    Resolved how the PUL domain recognizes p97/Cdc48, providing the structural basis for PLAA as a p97 cofactor and showing this interaction supports only a subset of PLAA functions.

    Evidence Crystal structure of the PUL domain–p97 C-terminal peptide complex with structure-guided mutagenesis and complementation in doa1Δ yeast

    PMID:19887378

    Open questions at the time
    • Which downstream processes require the p97 interaction versus not was only partially mapped
    • Role of p97 Tyr805 phosphorylation in regulation not functionally demonstrated
  4. 2010 Medium

    Provided a combined PFU-PUL structural view and proposed competition between Doa1 and Ufd2 for Cdc48 as a determinant of ubiquitinated-protein fate.

    Evidence 1.9 Å crystal structure of the yeast Doa1 PFU-PUL domain pair with structural comparison to Ufd2

    PMID:21063153

    Open questions at the time
    • Competition model not validated functionally
    • Single lab structural study with limited in vivo follow-up
  5. 2014 Medium

    Defined the solution architecture and critical residues of the Doa1/PFU:Hse1/SH3 complex, distinguishing the SH3-binding surface from the ubiquitin-binding surface.

    Evidence SAXS plus molecular docking and mutagenesis of the yeast Doa1–Hse1 interface

    PMID:24607902

    Open questions at the time
    • Low-resolution envelope rather than atomic structure
    • Not extended to human PLAA
  6. 2015 High

    Revealed an adaptor role for Doa1 in a Cdc48-Wss1 SUMO-targeted protease complex acting on sumoylated substrates during DNA damage.

    Evidence Co-IP of the Wss1/Cdc48/Doa1 complex, in vitro SUMO ligase assay, genetic analysis and fluorescence localization in yeast

    PMID:26349035

    Open questions at the time
    • Whether the human PLAA participates in an analogous SUMO-clearance complex unknown
    • Substrate range of the complex not defined
  7. 2016 High

    Showed Doa1/PLAA functions as a substrate-recruiting adaptor for Cdc48-Ufd1-Npl4 in mitochondria-associated degradation under oxidative stress.

    Evidence Genetic screen, reciprocal Co-IP with Cdc48-Ufd1-Npl4, ubiquitinated substrate binding assay and stress phenotyping in yeast

    PMID:27044889

    Open questions at the time
    • Conservation of MAD role in mammalian PLAA not established
    • Identity of physiological mitochondrial substrates limited
  8. 2016 High

    Placed human PLAA in the p97-UBXD1-PLAA-YOD1 (ELDR) machinery that removes K48-linked ubiquitin from damaged lysosomes to drive selective autophagy.

    Evidence Reciprocal Co-IP, lysosomal damage (LLOMe) assays, immunofluorescence localization, and disease-mutant MEF/patient tissue analysis in mammalian cells

    PMID:27753622

    Open questions at the time
    • How the complex selects the damaged-lysosome subpopulation not defined
    • Order of cofactor recruitment incompletely mapped
  9. 2017 High

    Connected PLAA loss-of-function to human disease, defining its essential role in K63-ubiquitin-mediated endolysosomal trafficking for synaptic vesicle recycling.

    Evidence Biallelic human mutations, mouse Plaa mutant model, K63-ubiquitin immunofluorescence, synaptic vesicle recycling assays and electrophysiology

    PMID:28413018

    Open questions at the time
    • Direct substrates accumulating at synapses not enumerated
    • Link between K63 accumulation and vesicle defect mechanistically incomplete
  10. 2022 Medium

    Implicated PLAA in cancer by showing it destabilizes METTL3 via ubiquitin-mediated degradation, modulating m6A-dependent TRPC3 mRNA stability and Ca2+ signaling.

    Evidence PLAA overexpression/knockdown in ovarian cancer lines, ubiquitin-degradation assay, MeRIP profiling, channel activity measurement and xenograft model

    PMID:35869392

    Open questions at the time
    • Whether PLAA acts directly or via an associated E3 on METTL3 unclear
    • Single lab; mechanism of METTL3 selection undefined
  11. 2024 Medium

    Provided patient-derived evidence that de novo PUL-domain missense variants weaken the PLAA–p97 interaction and perturb vesicle recycling, extending the genotype-phenotype link.

    Evidence Exome/genome sequencing with in vitro PLAA–p97 binding assays of patient variants and computational structural modeling

    PMID:38650658

    Open questions at the time
    • Functional consequences shown in vitro only
    • Limited cellular follow-up
  12. 2025 Medium

    Uncovered a degradation-independent PLAA function, with its intrinsic disordered region recruiting the decapping regulator DCAP-1 to P-bodies.

    Evidence C. elegans genetics, neuronal interactome proteomics, in vitro UFD-3–DCAP-1 binding, P-body imaging and IDR deletion analysis

    PMID:40560612

    Open questions at the time
    • Mammalian PLAA P-body role not tested
    • Functional output of P-body regulation on mRNA fate undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How PLAA's distinct activities — p97-coupled ubiquitin clearance, ESCRT-mediated sorting, P-body assembly, and Pdia3-dependent PLA2/lipid signaling — are integrated or partitioned within a single protein in mammalian cells remains unresolved.
  • No unified model reconciling the ubiquitin-adaptor and PLA2-activating functions
  • Tissue- and cargo-specific selection mechanisms unknown
  • Direct mammalian substrate repertoire largely uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0140096 catalytic activity, acting on a protein 3
Localization
GO:0005764 lysosome 1 GO:0005768 endosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-392499 Metabolism of proteins 2 R-HSA-5653656 Vesicle-mediated transport 2 R-HSA-9612973 Autophagy 1
Partners
DCAP-1HGSMETTL3PDIA3UBXD1VCPWSS1YOD1
Complex memberships
Cdc48-Ufd1-Npl4 complexWss1/Cdc48/Doa1 SUMO complexp97-UBXD1-PLAA-YOD1 (ELDR) complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 The C-terminal PUL domain of PLAA (human ortholog of yeast Doa1/Ufd3) forms a 6-mer Armadillo-containing domain whose positively charged inner ridge binds the C-terminus of p97/Cdc48; Tyr805 of p97 is buried in this ridge and implicated in phosphorylation-dependent regulation. Point mutants disrupting this interaction display only partial loss-of-function phenotypes, indicating the p97-PLAA interaction is required for a subset of PLAA-dependent processes. Crystal structure of PUL domain–p97 C-terminal peptide complex; structure-guided mutagenesis of yeast Doa1; functional complementation assays in doa1Δ cells The Journal of biological chemistry High 19887378
2010 Crystal structure of the PFU-PUL domain pair of yeast Doa1 at 1.9 Å reveals that the PUL domain adopts an Armadillo-like repeat fold with a positively charged concave surface that binds the negatively charged C-terminus of Cdc48; the PFU domain conserved surface is implicated in binding ubiquitin and Hse1. Structural comparison with Ufd2 suggests Doa1 and Ufd2 compete for Cdc48 binding to dictate fate of ubiquitinated proteins. X-ray crystallography at 1.9 Å resolution; structural comparison The Kobe journal of medical sciences Medium 21063153
2008 The PFU domain of yeast Doa1 binds directly to the SH3 domain of Hse1 (component of the ESCRT machinery), mediating Doa1's role in endosomal sorting. Loss of Doa1 causes missorting of MVB cargo GFP-Cps1 and reduces flux of ubiquitinated membrane proteins through the MVB pathway. This function is genetically separable from Doa1's role in maintaining ubiquitin levels. Direct binding assay (Hse1-SH3 pulldown of Doa1-PFU); site-directed mutations blocking PFU–SH3 interaction; GFP-Cps1 sorting assay; synthetic growth defect in doa1Δ vps27Δ double mutant; ubiquitin overexpression epistasis The Journal of biological chemistry High 18508771
2014 Solution structure of the Doa1/PFU:Hse1/SH3 complex determined by SAXS combined with molecular docking; Asn-438 of Doa1/PFU and Trp-254 of Hse1/SH3 are critical residues for the interaction (hydrogen bonding), whereas Phe-434, implicated in ubiquitin binding, is not required for this interaction. Small-angle X-ray scattering (SAXS); molecular docking; mutagenesis; biochemical binding assays Biochemical and biophysical research communications Medium 24607902
2016 Upon lysosomal damage, p97 translocates to lysosomes and cooperates with cofactors UBXD1, PLAA, and the deubiquitylase YOD1 (termed ELDR components) to selectively remove K48-linked ubiquitin conjugates from a subpopulation of damaged lysosomes and promote autophagosome formation. This complex acts downstream of K63-linked ubiquitination and p62 recruitment. Co-immunoprecipitation of p97 with PLAA, UBXD1, YOD1; lysosomal damage assay (LLOMe); immunofluorescence localization; analysis of p97 disease-mutant MEFs and patient tissue; tau fibril endocytosis model The EMBO journal High 27753622
2016 Yeast Doa1 (PLAA ortholog) forms a functional complex with Cdc48-Ufd1-Npl4 to mediate mitochondria-associated degradation (MAD) of ubiquitinated outer-membrane proteins. Doa1 directly interacts with ubiquitinated substrates and facilitates their recruitment to the Cdc48 complex. Loss of DOA1 causes accumulation and mislocalization of substrates on mitochondria, and is critical for cell survival under mitochondrial oxidative stress. Genetic screen for MAD regulators; Co-immunoprecipitation of Doa1 with Cdc48-Ufd1-Npl4; ubiquitinated substrate binding assay; doa1Δ phenotypic analysis under oxidative and ER stress The Journal of cell biology High 27044889
2015 Yeast Doa1 forms a SUMO-specific ternary complex with Cdc48 and Wss1 metalloprotease. Upon DNA damage, this Wss1/Cdc48/Doa1 complex is recruited to sumoylated targets and the Wss1 protease catalyzes SUMO chain extension (SUMO ligase activity) and subsequent self-cleavage and proteolysis. Doa1 acts as the adaptor in this complex. Upon genotoxic stress, Wss1 (and by extension the complex) is vacuolar. Co-immunoprecipitation (Wss1/Cdc48/Doa1 complex); in vitro SUMO ligase assay; genetic analysis (smt3-331, Camptothecin, UV); localization by fluorescence microscopy eLife High 26349035
2006 Yeast Doa1 channels ubiquitin from the proteasomal degradation pathway into pathways mediating DNA damage-induced ubiquitination of PCNA (monoubiquitination) and histone H2B monoubiquitination. In doa1Δ cells, damage-induced PCNA ubiquitination is absent; H2B ubiquitination is reduced basally and absent after DNA damage. The PCNA defect is rescued by ubiquitin overexpression but H2B monoubiquitination is not, indicating an additional specific role for Doa1 in H2B ubiquitination beyond simply supplying ubiquitin. Genetic interactions (doa1Δ with rad6, rad18, rad5, ubc13, mms2, bre1, lge1, cdc73, ubp8, ubp10, htb2); Western blot for PCNA-Ub and H2B-Ub; ubiquitin overexpression rescue experiments Molecular and cellular biology High 16705165
2017 Hypomorphic mutations in PLAA in humans and mice cause infantile-lethal neurodysfunction with seizures. PLAA functions as a ubiquitin adaptor protein for endolysosomal degradation; Plaa mutant neurons accumulate K63-polyubiquitylated proteins and synaptic membrane proteins, disrupting synaptic vesicle recycling and neurotransmission. Human genetics (biallelic PLAA mutations); mouse Plaa mutant model; immunofluorescence for K63-ubiquitylated proteins; synaptic vesicle recycling assays; electrophysiology of neurotransmission American journal of human genetics High 28413018
2024 De novo missense variants affecting conserved residues within the PUL domain of PLAA reduce PLAA–p97/VCP interaction, as shown by in vitro studies, and are associated with perturbed vesicle recycling. Computational modeling showed abnormal chain arrangements at the C-terminal PUL domain. Exome/genome sequencing; in vitro PLAA–p97 interaction assay with patient variants; computational structural modeling Frontiers in molecular neuroscience Medium 38650658
2005 PLAA (phospholipase A2-activating protein) is required for 1α,25(OH)2D3-dependent PKCα activation in rat growth plate chondrocytes. PLAA peptide increases arachidonic acid release and PLA2-specific activity in plasma membranes and matrix vesicles; its effect on PKC is blocked by PLA2 inhibitors (quinacrine, AACOCF3) and cyclooxygenase inhibitor indomethacin, indicating PLAA activates PLA2 leading to prostaglandin production acting via EP1 receptor. PLAA peptide also activates PLC-β1 and PLC-β3 via lysophospholipid. PLAA peptide treatment of primary chondrocytes; arachidonic acid release assay; PLA2 activity assay; PKC isoform activity measurement; pharmacological inhibitor studies; PLC isoform assays Journal of cellular physiology Medium 15368540
2014 PLAA and its membrane receptor partner Pdia3 are required for rapid 1α,25(OH)2D3-mediated activation of CaMKII in growth zone chondrocytes. Caveolae disruption abolishes CaMKII activation by 1α,25(OH)2D3 or PLAA peptide. Immunoprecipitation shows increased CaM binding to PLAA in response to 1α,25(OH)2D3, suggesting CaM links PLAA to CaMKII. Antibody blocking of PLAA and Pdia3; PLAA peptide treatment; caveolae disruption; CaMKII activity assay; co-immunoprecipitation of PLAA with calmodulin Connective tissue research Medium 25158196
2008 PLAA overexpression in HeLa cells increases PGE2, IL-6, activated cytosolic PLA2, COX-2, and NF-κB in response to TNF-α. PLAA promotes annexin A4 downregulation (annexin A4 acts as a PLA2 inhibitor) and clusterin downregulation, thereby amplifying PLA2-dependent inflammation. The plaa promoter contains a stimulatory Sp1-binding element in exon 1 that maintains basal expression and an inhibitory element. plaa(high)/plaa(low) HeLa Tet-off cell system; ELISA for PGE2, IL-6; Western blot for COX-2, NF-κB; microarray followed by functional assays; luciferase reporter assay; Sp1 decoy oligonucleotides and competitive binding assays Cellular signalling Medium 18291623
2009 PLAA overexpression enhances cisplatin-induced apoptosis in HeLa cells through: (1) accumulation of arachidonic acid causing mitochondrial cytochrome c leakage (blocked by siRNA-PLAA, rescued by exogenous arachidonic acid); (2) downregulation of cytoprotective clusterin; (3) upregulation of pro-apoptotic IL-32; (4) activation of JNK/c-Jun and FasL. PLAA induction by cisplatin also activates PLA2. plaa(high)/plaa(low) HeLa Tet-off cell system; siRNA-PLAA knockdown; caspase 3/8/9 activity assay; cytochrome c release assay; arachidonic acid rescue; proteomics for phospho-JNK/c-Jun and FasL Cellular signalling Medium 19258036
2022 PLAA inhibits the stability of METTL3 protein via ubiquitin-mediated degradation, reducing METTL3 expression, which in turn decreases TRPC3 mRNA stability (via m6A modification). Loss of PLAA leads to elevated METTL3, increased TRPC3, and enhanced intracellular Ca2+ signaling promoting ovarian cancer cell migration and invasion. PLAA overexpression/knockdown in ovarian cancer cell lines; ubiquitin-mediated METTL3 degradation assay; m6A-seq/MeRIP for TRPC3 mRNA; TRPC3 Ca2+ channel activity measurement; orthotopic xenograft mouse model Oncogene Medium 35869392
2025 The C. elegans PLAA ortholog UFD-3 directly interacts with the mRNA decapping complex regulatory subunit DCAP-1, and UFD-3's intrinsic disordered region (IDR) is required for recruitment of DCAP-1 to P-bodies. Loss of the IDR does not affect UFD-3's role in sorting ubiquitinated proteins through the MVB pathway, demonstrating that PLAA/UFD-3 regulates P-bodies through a pathway distinct from ubiquitin-dependent protein degradation. C. elegans genetics; unbiased proteomics (neuronal interactome); in vitro biochemical interaction assay (UFD-3–DCAP-1 direct binding); fluorescence imaging of P-bodies in C. elegans; IDR deletion mutant analysis Proceedings of the National Academy of Sciences of the United States of America Medium 40560612

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 VCP/p97 cooperates with YOD1, UBXD1 and PLAA to drive clearance of ruptured lysosomes by autophagy. The EMBO journal 289 27753622
2007 Weissellicin 110, a newly discovered bacteriocin from Weissella cibaria 110, isolated from plaa-som, a fermented fish product from Thailand. Applied and environmental microbiology 78 17293526
2016 Doa1 targets ubiquitinated substrates for mitochondria-associated degradation. The Journal of cell biology 77 27044889
2007 Expression of the mucus adhesion genes Mub and MapA, adhesion-like factor EF-Tu and bacteriocin gene plaA of Lactobacillus plantarum 423, monitored with real-time PCR. International journal of food microbiology 71 17399831
2015 Wss1 metalloprotease partners with Cdc48/Doa1 in processing genotoxic SUMO conjugates. eLife 66 26349035
2002 Fermentation and microflora of plaa-som, a thai fermented fish product prepared with different salt concentrations. International journal of food microbiology 47 11883675
2008 DOA1/UFD3 plays a role in sorting ubiquitinated membrane proteins into multivesicular bodies. The Journal of biological chemistry 40 18508771
2017 PLAA Mutations Cause a Lethal Infantile Epileptic Encephalopathy by Disrupting Ubiquitin-Mediated Endolysosomal Degradation of Synaptic Proteins. American journal of human genetics 37 28413018
2009 Structure and function of the PLAA/Ufd3-p97/Cdc48 complex. The Journal of biological chemistry 34 19887378
2022 PLAA suppresses ovarian cancer metastasis via METTL3-mediated m6A modification of TRPC3 mRNA. Oncogene 33 35869392
2006 Role of Doa1 in the Saccharomyces cerevisiae DNA damage response. Molecular and cellular biology 33 16705165
2005 Phospholipase A2 activating protein (PLAA) is required for 1alpha,25(OH)2D3 signaling in growth plate chondrocytes. Journal of cellular physiology 29 15368540
2010 Identification of lactic acid bacteria associated with the production of plaa-som, a traditional fermented fish product of Thailand. International journal of food microbiology 26 20167386
2009 Phospholipase A2-activating protein (PLAA) enhances cisplatin-induced apoptosis in HeLa cells. Cellular signalling 25 19258036
1999 HLA DOA1 and DOB1 loci in Honduran women with cervical dysplasia and invasive cervical carcinoma and their relationship to human papillomavirus infection. Human biology 25 10380373
2008 Alteration in the activation state of new inflammation-associated targets by phospholipase A2-activating protein (PLAA). Cellular signalling 19 18291623
1994 Expression of the Prevotella loescheii adhesin gene (plaA) is mediated by a programmed frameshifting hop. Journal of bacteriology 15 8144461
2007 Multiple functions of DOA1 in Candida albicans. Microbiology (Reading, England) 13 17379712
1999 The translational hop junction and the 5' transcriptional start site for the Prevotella loescheii adhesin encoded by plaA. Current microbiology 13 9841777
2014 Rapid 1α,25(OH)₂D ₃ membrane-mediated activation of Ca²⁺/calmodulin-dependent protein kinase II in growth plate chondrocytes requires Pdia3, PLAA and caveolae. Connective tissue research 11 25158196
2017 Disulfide loop cleavage of Legionella pneumophila PlaA boosts lysophospholipase A activity. Scientific reports 10 29176577
2005 Identification and molecular cloning of a gene encoding Phospholipase A2 (plaA) from Aspergillus nidulans. Biochimica et biophysica acta 10 16051517
2022 Distribution of Kazachstania Yeast in Thai Traditional Fermented Fish (Plaa-Som) in Northeastern Thailand. Journal of fungi (Basel, Switzerland) 9 36294595
2023 Degradation of α-Subunits, Doa1 and Doa4, are Critical for Growth, Development, Programmed Cell Death Events, Stress Responses, and Pathogenicity in the Watermelon Fusarium Wilt Fungus Fusarium oxysporum f. sp. niveum. Journal of agricultural and food chemistry 7 37486296
2010 Crystal structure of a PFU-PUL domain pair of Saccharomyces cerevisiae Doa1/Ufd3. The Kobe journal of medical sciences 6 21063153
2016 Doa1 is a MAD adaptor for Cdc48. The Journal of cell biology 5 27044894
2023 Structure-function relationships underpin disulfide loop cleavage-dependent activation of Legionella pneumophila lysophospholipase A PlaA. Molecular microbiology 4 38130174
2011 Identification and molecular cloning Moplaa gene, a homologue of Homo sapiens PLAA, in Magnaporthe oryzae. Microbiological research 4 21482087
2024 Allelic heterogeneity and abnormal vesicle recycling in PLAA-related neurodevelopmental disorders. Frontiers in molecular neuroscience 2 38650658
2014 Molecular determinants of the interaction between Doa1 and Hse1 involved in endosomal sorting. Biochemical and biophysical research communications 2 24607902
2025 PLAA/UFD-3 regulates P-bodies through its intrinsic disordered domain. Proceedings of the National Academy of Sciences of the United States of America 1 40560612
2020 The phospholipase A effector PlaA from Legionella pneumophila: expression, purification and crystallization. Acta crystallographica. Section F, Structural biology communications 1 32133999

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