Affinage

NLRP4

NACHT, LRR and PYD domains-containing protein 4 · UniProt Q96MN2

Round 2 corrected
Length
994 aa
Mass
113.4 kDa
Annotated
2026-04-29
56 papers in source corpus 15 papers cited in narrative 15 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NLRP4 is a cytoplasmic NLR family member that functions predominantly as a negative regulator of innate immune signaling and autophagy. It suppresses type I interferon production by scaffolding a signalosome in which DYRK2-mediated phosphorylation of TBK1 at Ser527 enables NLRP4 to recruit the E3 ligase DTX4 for K48-linked ubiquitination and proteasomal degradation of TBK1 at Lys670, a process gated by USP38-dependent removal of competing K33-linked ubiquitin chains (PMID:22388039, PMID:26407194, PMID:27692986). NLRP4 also inhibits NF-κB signaling through direct association with IKKα and suppression of IKK kinase activity, and negatively regulates the cGAS–STING–IRF3/7 axis (PMID:12093792, PMID:34927309). In parallel, NLRP4 restrains autophagy by binding Beclin 1 via its PYD and associating with the class C VPS complex, yet upon bacterial infection it is recruited to pathogen-containing vacuoles where it engages ARHGDIA to redirect Rho GTPase–actin dynamics for xenophagy (PMID:21209283, PMID:29099277).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2002 Medium

    Initial characterization established that NLRP4 suppresses NF-κB signaling by directly binding IKKα and inhibiting IKK kinase activity, positioning it as a negative regulator of innate inflammatory signaling rather than a canonical inflammasome activator.

    Evidence Co-immunoprecipitation, NF-κB reporter assays, EMSA, and in vitro kinase assays in HEK293 cells

    PMID:12093792

    Open questions at the time
    • Single-lab study without independent replication
    • Mechanism by which NLRP4 inhibits IKK kinase activity not defined
    • Endogenous expression context not examined
  2. 2002 Medium

    A parallel study reported that NLRP4 co-expression with ASC synergistically activated NF-κB and caspase-1-dependent IL-1β processing, suggesting inflammasome-like function; this was later contradicted by structural and biochemical evidence showing NLRP4 PYD does not interact with ASC.

    Evidence Co-expression in HEK cells, NF-κB reporter and caspase-1 activity assays

    PMID:12019269

    Open questions at the time
    • ASC interaction was subsequently refuted by crystal structure and three orthogonal binding assays (PMID:22928810)
    • Overexpression artifacts not excluded
  3. 2011 High

    NLRP4 was shown to be a negative regulator of autophagy, binding Beclin 1 through its PYD with the highest affinity among NLRs tested and associating with the class C VPS complex to restrain autophagosome/endosome maturation, establishing a non-inflammasome function for the protein.

    Evidence Co-immunoprecipitation, siRNA knockdown, confocal microscopy, and bacterial infection assays with Group A Streptococcus

    PMID:21209283

    Open questions at the time
    • Structural basis of Beclin 1–PYD interaction not resolved
    • Whether NLRP4 dissociation from Beclin 1 during infection is actively regulated remains unknown
  4. 2012 High

    The central mechanism of NLRP4-mediated type I IFN suppression was elucidated: NLRP4 recruits the E3 ligase DTX4 to TBK1, promoting site-specific K48-linked ubiquitination at Lys670 and proteasomal degradation, establishing a direct biochemical pathway for IFN attenuation.

    Evidence Co-immunoprecipitation, siRNA knockdown, K48-linkage-specific ubiquitination assays, TBK1 degradation immunoblots, dsRNA/dsDNA stimulation

    PMID:22388039

    Open questions at the time
    • How NLRP4 is activated or derepressed to engage TBK1 was not defined
    • Physiological triggers for NLRP4–DTX4 complex assembly unclear
  5. 2012 High

    Crystal structure of NLRP4 PYD at 2.3 Å resolved its six-helix death-domain fold with a uniquely elongated α3 helix, and definitively demonstrated that it does not interact with ASC, clarifying why NLRP4 does not form a canonical inflammasome.

    Evidence X-ray crystallography, co-immunoprecipitation, yeast two-hybrid, NMR chemical shift perturbation

    PMID:22928810

    Open questions at the time
    • No full-length NLRP4 structure available
    • Binding partners that do engage the PYD (beyond Beclin 1) not structurally mapped
  6. 2015 High

    DYRK2 was identified as the kinase that phosphorylates TBK1 at Ser527, establishing this modification as a prerequisite for NLRP4 and DTX4 recruitment, thereby defining the upstream gating event for the NLRP4-dependent TBK1 degradation pathway.

    Evidence In vitro kinase assays, Ser527 mutagenesis, co-immunoprecipitation, ubiquitination assays, interferon reporter assays

    PMID:26407194

    Open questions at the time
    • Whether DYRK2 phosphorylation is the sole gating event or acts cooperatively with additional signals is unknown
  7. 2016 High

    USP38 was placed within the NLRP4 signalosome as a deubiquitinase that edits K33-linked ubiquitin chains from TBK1 Lys670 to permit subsequent K48-linked ubiquitination by DTX4/TRIP, establishing a sequential ubiquitin-editing mechanism for TBK1 turnover.

    Evidence USP38 CRISPR knockout, K33- and K48-linkage-specific ubiquitination assays, in vitro deubiquitination, in vivo viral infection models

    PMID:27692986

    Open questions at the time
    • How the switch from K33 to K48 ubiquitin chains is temporally coordinated is not fully resolved
    • Whether additional DUBs participate in NLRP4 signalosome ubiquitin editing is unknown
  8. 2017 High

    NLRP4 was found to bind ARHGDIA at pathogen-containing vacuoles, directing Rho GTPase activation and actin dynamics for xenophagy; ARHGDIA Tyr156 phosphorylation gates this interaction, linking NLRP4 to cytoskeletal control during antibacterial autophagy.

    Evidence Co-immunoprecipitation, immunofluorescence, siRNA knockdown, ARHGDIA Y156 mutagenesis, GAS infection assays, autophagic flux assays

    PMID:29099277

    Open questions at the time
    • Kinase responsible for ARHGDIA Tyr156 phosphorylation not identified
    • Whether NLRP4-ARHGDIA interaction operates beyond GAS infection is untested
  9. 2022 Medium

    NLRP4 was demonstrated to suppress the cGAS–STING–IRF3/IRF7 axis, broadening its role as a negative regulator of cytosolic nucleic acid sensing beyond TBK1 degradation alone.

    Evidence NLRP4 siRNA knockdown, IFN-α/β ELISA, IRF3/IRF7 reporter assays, Lewis lung cancer tumor models, flow cytometry for CD8+ T cells

    PMID:34927309

    Open questions at the time
    • Direct biochemical interaction with cGAS or STING components not shown
    • Whether suppression occurs through TBK1 degradation or an independent mechanism is unresolved
  10. 2025 Medium

    A new axis was reported in which NLRP4 suppresses PP2A phosphatase activity to activate PI3K/Akt–NF-κB signaling, driving chemokine reprogramming that shapes the tumor immune microenvironment, revealing context-dependent pro-tumorigenic functions.

    Evidence NLRP4 stable overexpression, co-immunoprecipitation, proteomics, bulk RNA-seq, PP2A inhibitor rescue, subcutaneous tumor models

    PMID:40087771

    Open questions at the time
    • Mechanism by which NLRP4 inhibits PP2A catalytic activity is undefined
    • Apparent contradiction with canonical NF-κB-suppressive role not reconciled
    • Single-study claim requiring independent replication

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include how NLRP4 is itself activated or regulated at the protein level, the full-length structure and oligomeric state, the mechanism linking NLRP4 to mitochondrial ROS and DNA repair, and reconciliation of its context-dependent pro- versus anti-inflammatory roles.
  • No full-length structure or cryo-EM model
  • Ligand or danger signal that activates NLRP4 is unknown
  • NLRP4 post-translational regulation poorly characterized
  • Context-dependent switching between NF-κB suppression and PP2A-mediated NF-κB activation unexplained

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0060090 molecular adaptor activity 3
Localization
GO:0005829 cytosol 3 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-168256 Immune System 5 R-HSA-162582 Signal Transduction 3 R-HSA-9612973 Autophagy 3 R-HSA-392499 Metabolism of proteins 2
Partners
ARHGDIABECN1DTX4DYRK2IKBKASGT1TBK1USP38
Complex memberships
NLRP4-Beclin1-class C VPS complexNLRP4-DTX4-TBK1 signalosome

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 NLRP4 (then called PAN2/PAAD-NACHT-containing protein 2) suppresses NF-κB activation induced by TNF-α and IL-1β signaling, acting downstream of TRAF2, TRAF6, RIP, IRAK2, and NIK as well as IKKα and IKKβ. Co-immunoprecipitation demonstrated direct association of NLRP4 with IKKα, and in vitro kinase assays showed NLRP4 inhibits IKKα/β activity. Co-immunoprecipitation, NF-κB reporter assays, EMSA, in vitro kinase assays, overexpression in HEK293 cells The Journal of biological chemistry Medium 12093792
2002 NLRP4 (as PYPAF7) recruits to distinct cytoplasmic loci upon co-expression with ASC and synergistically activates NF-κB and caspase-1-dependent IL-1β processing. Pro-caspase-1 was identified as a binding partner of ASC in this pathway. Co-expression and co-localization in HEK cells, NF-κB reporter assays, caspase-1 activity assays, mammalian two-hybrid screen The Journal of biological chemistry Medium 12019269
2004 The NACHT domain of NLRP4 (as PAN2) participates in heterotypic NACHT-domain interactions, co-immunoprecipitating with NACHT domains from CLAN, Nod1, Nod2, cryopyrin, NAC, and NAIP when co-expressed in HEK-293T cells, suggesting NLRP4 can form protein-interaction networks with other NLR family members. Co-immunoprecipitation in HEK-293T cells, NF-κB reporter assays The Biochemical journal Low 15107016
2007 NLRP4, as a member of the NLR family, interacts with SGT1 and HSP90. Knockdown of SGT1 or chemical inhibition of HSP90 abrogated NLR-dependent inflammasome activity, placing SGT1 and HSP90 as conserved regulators of NLR function including NLRP4-containing complexes. siRNA knockdown, chemical inhibition (geldanamycin), co-immunoprecipitation, inflammasome activity assays Nature immunology Medium 17435760
2011 NLRP4 negatively regulates autophagy by binding Beclin1 through its PYD (NACHT domain region), with NLRP4 showing the strongest affinity among tested NLRs to the Beclin1 evolutionarily conserved domain. Upon Group A Streptococcus infection, NLRP4 is recruited to sub-plasma membrane phagosomes and transiently dissociates from Beclin1 to permit autophagic responses. NLRP4 also physically associates with the class C vacuolar protein-sorting (VPS) complex to negatively regulate autophagosome and endosome maturation. Co-immunoprecipitation, siRNA knockdown, immunofluorescence/confocal microscopy, bacterial infection assays, autophagic flux measurements Journal of immunology High 21209283
2012 NLRP4 negatively regulates type I interferon signaling by recruiting the E3 ubiquitin ligase DTX4 to TBK1, promoting K48-linked polyubiquitination of TBK1 at Lys670 and its proteasomal degradation. Knockdown of either NLRP4 or DTX4 abolished K48-linked ubiquitination and degradation of TBK1, and enhanced TBK1 phosphorylation and IRF3 activation. Co-immunoprecipitation, siRNA knockdown, ubiquitination assays (K48-specific), immunoblot for TBK1 degradation and phospho-IRF3, dsRNA/dsDNA stimulation assays Nature immunology High 22388039
2012 The crystal structure of the NLRP4 pyrin domain (PYD) was solved at 2.3 Å resolution, revealing a death domain superfamily fold with six α-helices. The NLRP4 PYD has unique structural features: an unusually long helix α3 and a distinct α2-α3 connecting loop compared to other PYDs. Despite a highly charged surface, NLRP4 PYD does not interact with the adaptor protein ASC, as demonstrated by co-immunoprecipitation, yeast two-hybrid, and NMR chemical shift perturbation analysis. X-ray crystallography (2.3 Å), co-immunoprecipitation, yeast two-hybrid, NMR chemical shift perturbation Biochemistry High 22928810
2014 Molecular dynamics simulations comparing NLRP4 PYD (as a representative native pyrin domain fold) with NLRP14 PYD revealed that intrinsic flexibility of NLRP pyrin domains is a key factor in their conformational dynamics, fold stability, and dimerization propensity. A charge relay system within NLRPs critically influences their conformational ensemble in solution. Molecular dynamics simulations, comparative structural analysis Protein science Low 25403012
2015 DYRK2 phosphorylates TBK1 at Ser527, and this phosphorylation is essential for the subsequent recruitment of NLRP4 and the E3 ubiquitin ligase DTX4 to TBK1, priming TBK1 for K48-linked ubiquitination and proteasomal degradation. This establishes DYRK2-mediated phosphorylation as an upstream event that gates NLRP4-DTX4-dependent TBK1 degradation. In vitro kinase assays, co-immunoprecipitation, ubiquitination assays, site-directed mutagenesis (Ser527), siRNA knockdown, interferon reporter assays PLoS pathogens High 26407194
2016 USP38 acts within the NLRP4 signalosome to negatively regulate type I IFN signaling. USP38 specifically cleaves K33-linked polyubiquitin chains from TBK1 at Lys670, removing them to allow subsequent K48-linked ubiquitination at the same site by DTX4 and TRIP (which are recruited via NLRP4). Knockout of USP38 increases K33-linked ubiquitination but abrogates K48-linked ubiquitination and TBK1 degradation. Co-immunoprecipitation, USP38 knockout (CRISPR), ubiquitination assays (K33- and K48-linkage specific), in vitro deubiquitination assays, interferon reporter assays, in vivo viral infection models Molecular cell High 27692986
2017 NLRP4 is recruited to Group A Streptococcus (GAS)-containing compartments and binds ARHGDIA (Rho GDP dissociation inhibitor α) to regulate Rho GTPase signaling, facilitating actin-mediated xenophagy. ARHGDIA Tyr156 phosphorylation acts as a regulatory gate for this interaction and for Rho-mediated autophagosome formation. Rho GTPases recruited via this NLRP4-ARHGDIA axis promote ATG9A recruitment to phagophores for autophagosome elongation. Co-immunoprecipitation, immunofluorescence microscopy, siRNA knockdown, bacterial infection assays (GAS), phosphorylation site mutagenesis (ARHGDIA Tyr156), autophagic flux assays Autophagy High 29099277
2017 NLRP4 negatively regulates both the TBK1/IRF3 and IKK/NF-κB signaling pathways in cardiac cells under fructose-induced injury. Overexpression of NLRP4 reduced pro-inflammatory cytokine release and TBK1 phosphorylation, while NLRP4 knockdown enhanced IKK/NF-κB activation, confirming NLRP4's role as a negative regulator of these inflammatory kinase cascades in cardiomyocytes. NLRP4 overexpression and siRNA knockdown, RT-qPCR, Western blotting for phospho-TBK1, phospho-IRF3, IKK activity, cytokine measurements, in vivo fructose-feeding mouse model Biomedicine & pharmacotherapy Medium 28486191
2022 NLRP4 knockdown in lung cancer cells enhanced type I IFN (IFN-α/β) production through the cGAS-STING-IRF3/IRF7 axis, placing NLRP4 as a negative regulator of cGAS-STING pathway signaling upstream of IRF3/IRF7 activation. NLRP4 siRNA knockdown, IFN-α/β ELISA, IRF3/IRF7 reporter assays, in vivo tumor models (Lewis lung cancer), flow cytometry for tumor-infiltrating CD8+ T cells Cancer science Medium 34927309
2024 NLRP4 upregulation promotes olaparib resistance in pancreatic cancer by enhancing DNA repair capacity and inducing mitochondrial ROS production that drives autophagy. Co-IP mass spectrometry identified NLRP4 as involved in the DNA damage response and autophagy pathways. NLRP4-generated mitochondrial ROS promote autophagy without directly affecting DNA damage, and inhibition of mitochondrial ROS (MitoQ) or autophagy (chloroquine) sensitizes cells to olaparib. Co-IP mass spectrometry, RNA sequencing, NLRP4 overexpression/knockdown, mitochondrial ROS measurement, DNA damage assays, olaparib resistance assays in vitro and in vivo Cell death & disease Medium 39187531
2025 NLRP4 overexpression suppresses PP2A (protein phosphatase 2A) activity and thereby activates the PI3K/Akt-NF-κB signaling axis in lung cancer, leading to chemokine reprogramming (CCL5 and CXCL2) that recruits TIGIT+TNFα+ NK cells and iNOS+ M1 macrophages. Co-IP and Western blot experiments validated NLRP4 interaction with components of this pathway. NLRP4 stable overexpression, co-immunoprecipitation, Western blotting, bulk RNA sequencing, proteomics, mass spectrometry, flow cytometry, multiplex immunofluorescence, subcutaneous tumor models in C57BL/6J mice Biomarker research Medium 40087771

Source papers

Stage 0 corpus · 56 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2003 NALPs: a novel protein family involved in inflammation. Nature reviews. Molecular cell biology 554 12563287
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2007 A crucial function of SGT1 and HSP90 in inflammasome activity links mammalian and plant innate immune responses. Nature immunology 356 17435760
2002 PYPAF7, a novel PYRIN-containing Apaf1-like protein that regulates activation of NF-kappa B and caspase-1-dependent cytokine processing. The Journal of biological chemistry 314 12019269
2012 NLRP4 negatively regulates type I interferon signaling by targeting the kinase TBK1 for degradation via the ubiquitin ligase DTX4. Nature immunology 247 22388039
2002 Functional screening of five PYPAF family members identifies PYPAF5 as a novel regulator of NF-kappaB and caspase-1. FEBS letters 245 12387869
2013 RNA decay machines: deadenylation by the Ccr4-not and Pan2-Pan3 complexes. Biochimica et biophysica acta 193 23337855
2003 Identification of Ser-386 of interferon regulatory factor 3 as critical target for inducible phosphorylation that determines activation. The Journal of biological chemistry 184 14703513
1996 The yeast Pan2 protein is required for poly(A)-binding protein-stimulated poly(A)-nuclease activity. The Journal of biological chemistry 153 8550599
2011 NLRP4 negatively regulates autophagic processes through an association with beclin1. Journal of immunology (Baltimore, Md. : 1950) 149 21209283
2004 Heterotypic interactions among NACHT domains: implications for regulation of innate immune responses. The Biochemical journal 129 15107016
2013 Proteomic analysis of podocyte exosome-enriched fraction from normal human urine. Journal of proteomics 126 23376485
2007 SGT1 is essential for Nod1 activation. Proceedings of the National Academy of Sciences of the United States of America 121 17420470
2016 USP38 Inhibits Type I Interferon Signaling by Editing TBK1 Ubiquitination through NLRP4 Signalosome. Molecular cell 119 27692986
2002 A novel PAAD-containing protein that modulates NF-kappa B induction by cytokines tumor necrosis factor-alpha and interleukin-1beta. The Journal of biological chemistry 86 12093792
2013 Structure of the PAN3 pseudokinase reveals the basis for interactions with the PAN2 deadenylase and the GW182 proteins. Molecular cell 83 23932717
2019 Molecular Basis for poly(A) RNP Architecture and Recognition by the Pan2-Pan3 Deadenylase. Cell 79 31104843
2012 Identification of PAN2 by quantitative proteomics as a leucine-rich repeat-receptor-like kinase acting upstream of PAN1 to polarize cell division in maize. The Plant cell 75 23175742
2008 Genetic variants in apoptosis and immunoregulation-related genes are associated with risk of chronic lymphocytic leukemia. Cancer research 64 19074885
2010 The genetics of NOD-like receptors in Crohn's disease. Tissue antigens 61 20403135
2015 DYRK2 Negatively Regulates Type I Interferon Induction by Promoting TBK1 Degradation via Ser527 Phosphorylation. PLoS pathogens 57 26407194
2014 Structural basis for Pan3 binding to Pan2 and its function in mRNA recruitment and deadenylation. The EMBO journal 55 24872509
2013 The P-body component USP52/PAN2 is a novel regulator of HIF1A mRNA stability. The Biochemical journal 50 23398456
2019 The intrinsic structure of poly(A) RNA determines the specificity of Pan2 and Caf1 deadenylases. Nature structural & molecular biology 49 31110294
2014 mRNA deadenylation by Pan2-Pan3. Biochemical Society transactions 48 24450649
2014 The structure of the Pan2-Pan3 core complex reveals cross-talk between deadenylase and pseudokinase. Nature structural & molecular biology 46 24880344
2012 The Caenorhabditis elegans GW182 protein AIN-1 interacts with PAB-1 and subunits of the PAN2-PAN3 and CCR4-NOT deadenylase complexes. Nucleic acids research 44 22402495
2012 Structural and functional analysis of the NLRP4 pyrin domain. Biochemistry 42 22928810
2002 Human pancreas protein 2 (PAN2) has a retinal reductase activity and is ubiquitously expressed in human tissues. FEBS letters 35 12435598
2002 Posttranscriptional regulation of the RAD5 DNA repair gene by the Dun1 kinase and the Pan2-Pan3 poly(A)-nuclease complex contributes to survival of replication blocks. The Journal of biological chemistry 33 11953437
2014 The CLRX.1/NOD24 (NLRP2P) pseudogene codes a functional negative regulator of NF-κB, pyrin-only protein 4. Genes and immunity 28 24871464
2014 Divergent roles for maize PAN1 and PAN2 receptor-like proteins in cytokinesis and cell morphogenesis. Plant physiology 26 24578508
2014 Intrinsic flexibility of NLRP pyrin domains is a key factor in their conformational dynamics, fold stability, and dimerization. Protein science : a publication of the Protein Society 21 25403012
2017 The intracellular microbial sensor NLRP4 directs Rho-actin signaling to facilitate Group A Streptococcus-containing autophagosome-like vacuole formation. Autophagy 20 29099277
2017 NLRP4 is an essential negative regulator of fructose-induced cardiac injury in vitro and in vivo. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 17 28486191
2023 Stomatal closure in maize is mediated by subsidiary cells and the PAN2 receptor. The New phytologist 15 37936339
2022 NLRP4 negatively regulates type I interferon response and influences the outcome in anti-programmed cell death protein (PD)-1/PD-ligand 1 therapy. Cancer science 14 34927309
2024 NLRP4 renders pancreatic cancer resistant to olaparib through promotion of the DNA damage response and ROS-induced autophagy. Cell death & disease 13 39187531
2018 Association of Genetic Variants of NLRP4 with Exacerbation of Asthma: The Effect of Smoking. DNA and cell biology 13 30526007
2021 Somatic Mutation of NLRP Genes in Gastric and Colonic Cancers. Pathology oncology research : POR 9 34257569
2022 Biallelic PAN2 variants in individuals with a syndromic neurodevelopmental disorder and multiple congenital anomalies. European journal of human genetics : EJHG 8 35304602
2002 Isolation and expression analysis of the human RNH2 gene encoding ribonuclease inhibitor 2. Journal of assisted reproduction and genetics 6 12182447
2022 The hyper-expression of NLRP4 characterizes the occurrence of macrophage activation syndrome assessing STING pathway in adult-onset Still's disease. Clinical and experimental immunology 4 35467709
2025 Human protein interaction networks of ancestral and variant SARS-CoV-2 in organ-specific cells and bodily fluids. Nature communications 2 40593736
2021 Pan2-Pan3 complex, together with Ccr4-Not complex, has a role in the cell growth on non-fermentable carbon sources. Biochemical and biophysical research communications 2 34280615
2025 NLRP4 unlocks an NK/macrophages-centered ecosystem to suppress non-small cell lung cancer. Biomarker research 1 40087771
2019 Author Correction: The intrinsic structure of poly(A) RNA determines the specificity of Pan2 and Caf1 deadenylases. Nature structural & molecular biology 1 31420603
2026 Pan2-Pan3 Complex-Mediated Deadenylation Enforces mRNA Quality Control for Infection of the Rice Blast Fungus. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41556236
2026 PAN2 maintains mRNA poly(A) tail homeostasis and regulates translation during spermiogenesis in mice. Nature communications 0 41714623
2025 Novel Missense Variant in the PAN2 Gene Associated With Congenital Anomalies and Neurodevelopmental Delay: Expanding the Phenotypic and Mutational Spectrum of PAN2-Related Disorders. Birth defects research 0 40491293
2025 Mechanisms governing poly(A)-tail-length specificity of the human PAN2-PAN3 deadenylase complex. Cell reports 0 41275497
2024 NLRP4 drives olaparib resistance in pancreatic cancer. Autophagy reports 0 40395525