Affinage

PSTPIP2

Proline-serine-threonine phosphatase-interacting protein 2 · UniProt Q9H939

Length
334 aa
Mass
38.9 kDa
Annotated
2026-06-10
25 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

PSTPIP2 (MAYP) is an F-BAR/PCH-domain adaptor expressed predominantly in myeloid cells that acts as a negative regulator of innate immune activation while also shaping actin-dependent cell motility (PMID:15788569, PMID:16397132, PMID:19608749). Through direct F-actin bundling it suppresses CSF-1-induced membrane ruffling and promotes filopodia formation and directional chemotaxis in macrophages (PMID:15788569). PSTPIP2 restrains signaling downstream of the CSF-1 receptor: its loss elevates CSF-1-stimulated ERK1/2 phosphorylation, proliferation, and cytokine output (MIP-1α, IL-6), and re-expression normalizes this hyperactivation (PMID:19608749, PMID:22923495). Mechanistically, PSTPIP2 recruits two classes of inhibitory enzymes — PEST-family tyrosine phosphatases through a W232-dependent interface and the inositol phosphatase SHIP1 plus Csk through C-terminal tyrosine residues — to dampen Src-family kinase activity (including LYN) and limit IL-1β processing, reactive oxygen species production, and CXCL2 secretion in neutrophils; the PEST-PTP interface is dominant for disease control while the SHIP1 interface contributes specifically to IL-1β restraint (PMID:24407241, PMID:26304991, PMID:36605205). Both its membrane-deforming F-BAR activity and tyrosine phosphorylation are required to suppress osteoclastogenesis (PMID:22923495). Loss-of-function or destabilizing missense mutations (L98P/cmo, I282N/Lupo) cause macrophage- and neutrophil-driven, inflammasome-independent autoinflammatory bone disease (chronic multifocal osteomyelitis) in mice, in which neutrophil serine proteases drive IL-1β processing (PMID:16122996, PMID:16397132, PMID:24395802). PSTPIP2 expression is epigenetically controlled — silenced by DNMT3a/3b-mediated promoter hypermethylation and activated by H3K27 acetylation — and its restoration suppresses STAT1/NF-κB-driven inflammation and tissue injury across liver and kidney models (PMID:29993036, PMID:33311489, PMID:35149186).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2005 High

    Established the biochemical activity of PSTPIP2 as a direct F-actin bundler and linked that activity to control of macrophage morphology and motility downstream of CSF-1R.

    Evidence In vitro bundling with purified protein plus bidirectional gain/loss-of-function in macrophages scoring ruffling, filopodia, and chemotaxis

    PMID:15788569

    Open questions at the time
    • Did not identify the upstream kinases or adaptors coupling CSF-1R to PSTPIP2
    • Did not connect actin function to inflammatory phenotypes
  2. 2005 Medium

    Identified PSTPIP2 as the genetic cause of murine chronic multifocal osteomyelitis, tying the gene to autoinflammatory bone disease.

    Evidence Positional cloning of the cmo locus and identification of the L98P missense mutation by Sanger sequencing

    PMID:16122996

    Open questions at the time
    • Did not establish how L98P alters protein function
    • Did not identify the responsible cell type
  3. 2006 High

    Showed the disease is macrophage-autonomous and that the Lupo (I282N) mutation acts by destabilizing the protein and abolishing inducible upregulation.

    Evidence Positional cloning, bone marrow transplantation, clodronate macrophage depletion, and Western blot for protein stability

    PMID:16397132

    Open questions at the time
    • Did not define the signaling pathway hyperactivated by PSTPIP2 loss
    • Did not resolve which downstream cytokines drive bone pathology
  4. 2009 High

    Defined PSTPIP2 as a negative regulator of CSF-1R signaling, with loss elevating ERK activation and cytokine output rescuable by re-expression.

    Evidence BMT, retroviral PSTPIP2 rescue in macrophages, ERK phosphorylation and cytokine ELISA

    PMID:19608749

    Open questions at the time
    • Did not map the molecular interface restraining CSF-1R signaling
    • Did not distinguish actin vs. enzyme-recruitment contributions
  5. 2012 High

    Separated PSTPIP2 functions into a tyrosine-phosphorylation/F-BAR module controlling osteoclast fusion and a PEST-phosphatase module controlling TRAP expression, and validated CSF-1R as a druggable driver.

    Evidence Domain mutagenesis in osteoclastogenesis assays plus PLX3397 treatment of cmo mice

    PMID:22923495

    Open questions at the time
    • Did not identify the kinase phosphorylating PSTPIP2
    • Did not enumerate the C-terminal binding partners beyond PEST-PTPs
  6. 2014 High

    Established that cmo bone pathology is driven by neutrophil-derived IL-1β through inflammasome-independent serine protease processing rather than NLRP3/caspase-1.

    Evidence Genetic epistasis with IL-1RI, IL-1α/β, NLRP3 and caspase-1 knockouts plus ex vivo neutrophil stimulation with protease inhibitors

    PMID:24395802

    Open questions at the time
    • Did not identify the specific serine protease
    • Did not link the PSTPIP2 molecular interfaces to neutrophil IL-1β control
  7. 2014 Medium

    Showed PSTPIP2 binds LYN and recruits PEST phosphatases via W232 to suppress CSK, modulating Src-family kinase activity in a hematopoietic differentiation context.

    Evidence Co-IP, LYN epistasis with dominant-negative/constitutively active constructs, and W232A mutagenesis in K562 and primary megakaryocytes

    PMID:24407241

    Open questions at the time
    • Single-lab Co-IP without structural validation of the LYN interaction
    • Relevance to bone disease not directly tested
  8. 2015 Medium

    Identified SHIP1 and Csk as additional inhibitory partners binding the C-terminal tyrosines, defining a PEST-phosphatase-independent route to suppress neutrophil IL-1β processing.

    Evidence Co-IP with domain mapping plus SHIP1 inhibitor treatment of stimulated neutrophils

    PMID:26304991

    Open questions at the time
    • Did not quantify relative in vivo contributions of SHIP1 vs. PEST-PTPs
    • No structural model of the tyrosine-dependent SHIP1 interface
  9. 2022 High

    Resolved the in vivo division of labor between the two interfaces, showing PEST-PTP binding is required to prevent disease and dominates ROS/CXCL2 control while both interfaces equally restrain IL-1β.

    Evidence Knock-in mice with point mutations disrupting PEST-PTP or SHIP1 binding sites, with disease scoring and IL-1β/ROS/CXCL2 assays

    PMID:36605205

    Open questions at the time
    • Did not address how F-BAR/actin activity integrates with enzyme recruitment in disease
    • Did not define the CXCL2 feedback loop molecularly
  10. 2022 Medium

    Extended PSTPIP2 function to synovial macrophage polarization and tissue-barrier formation under hormonal control.

    Evidence Pstpip2-Cre reporter mice, macrophage-specific Esr2 conditional knockout, and AAV-PSTPIP2 overexpression with polarization/dynamics imaging

    PMID:36324152

    Open questions at the time
    • Mechanistic link between ERβ and PSTPIP2 expression not defined
    • Single-lab study
  11. 2018 Medium

    Showed PSTPIP2 expression is epigenetically silenced by DNMT3a/3b promoter hypermethylation and that it directs macrophage M1/M2 polarization via STAT1/STAT6.

    Evidence RRBS methylation sequencing, ChIP for DNMT3a/3b, AAV9 overexpression, and bidirectional knockdown with STAT phosphorylation readouts

    PMID:29993036

    Open questions at the time
    • Direct PSTPIP2-STAT interaction not demonstrated
    • Causal relationship between methylation and disease severity untested
  12. 2022 Medium

    Confirmed DNMT3a as the principal writer silencing PSTPIP2 in liver injury and linked restored expression to suppressed STAT1/NF-κB inflammation.

    Evidence ChIP and methylation-specific PCR, DNMT3a knockdown, and AAV9-PSTPIP2 rescue in ethanol-fed mice

    PMID:35149186

    Open questions at the time
    • Mechanism of NF-κB suppression by PSTPIP2 not resolved
    • Single-lab study
  13. 2020 Medium

    Broadened PSTPIP2 regulation to H3K27-acetylation-driven activation and an anti-apoptotic role in renal tubular epithelium.

    Evidence AAV-PSTPIP2 overexpression, siRNA knockdown, ChIP for H3K27ac, and TSA HDAC inhibition with apoptosis readouts

    PMID:33311489

    Open questions at the time
    • Molecular link between PSTPIP2 and the apoptotic machinery not defined
    • Function outside myeloid cells mechanistically unclear
  14. 2024 Medium

    Placed PSTPIP2 upstream of an NF-κB/IL-19/IL-20Rβ axis controlling neutrophil NET formation in nephropathy.

    Evidence Kidney-specific Pstpip2 knock-in, Ly6G neutrophil depletion, PAD4 inhibition, and IL-19/IL-20Rβ signaling experiments

    PMID:38314821

    Open questions at the time
    • Direct PSTPIP2 control of NF-κB not biochemically demonstrated
    • Single-lab pathway reconstruction
  15. 2011 Medium

    Demonstrated that PSTPIP2 membrane-curvature activity is co-opted by HCV to build NS4B-induced membranous webs for viral replication.

    Evidence Lentiviral RNAi in replicon/infected cells, detergent-resistant membrane fractionation, and a curvature-defective mutant rescue

    PMID:22130530

    Open questions at the time
    • Did not connect membrane-deforming activity to its immune-regulatory roles
    • Host vs. viral determinants of recruitment unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How PSTPIP2's actin/membrane-deforming F-BAR activity is mechanistically integrated with its enzyme-recruitment scaffolding to produce its cell-type-specific anti-inflammatory outputs, and the structural basis of its partner interfaces, remain unresolved.
  • No structural model of PSTPIP2 bound to PEST-PTP, SHIP1, Csk, or LYN
  • Identity of the kinase(s) phosphorylating PSTPIP2 not established
  • Direct biochemical mechanism linking PSTPIP2 to STAT1/STAT3/NF-κB not demonstrated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 4 GO:0008092 cytoskeletal protein binding 1
Localization
GO:0005886 plasma membrane 2 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3
Partners
CSKLYNPTP-PESTSHIP1

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 PSTPIP2 directly bundles F-actin in vitro and colocalizes with cortical and filopodial F-actin in vivo in macrophages. Overexpression decreased CSF-1-induced membrane ruffling and increased filopodia formation and directional motility, while reduced PSTPIP2 expression produced the opposite phenotype, establishing PSTPIP2 as a negative regulator of membrane ruffling and positive regulator of filopodia and chemotaxis downstream of CSF-1R. In vitro F-actin bundling assay with purified MAYP/PSTPIP2, overexpression and RNAi knockdown in macrophages with quantification of membrane ruffling, filopodia, and chemotaxis, colocalization imaging Molecular biology of the cell High 15788569
2005 A missense mutation c.293T→C in pstpip2 (L98P) co-segregates with the cmo autoinflammatory phenotype in mice, and the cmo locus was refined to a 1.3 Mb region on chromosome 18 containing pstpip2, identifying this gene as the genetic cause of chronic multifocal osteomyelitis. Positional cloning via backcross breeding, Sanger sequencing of candidate genes in refined interval Bone Medium 16122996
2006 A second missense mutation (I282N, Lupo) in MAYP/PSTPIP2 causes macrophage-mediated autoinflammatory disease transferable by bone marrow transplantation and dependent on macrophages (suppressible by clodronate liposomes). The I282N mutation renders the protein unstable, reducing expression ~3-fold in macrophages; LPS-stimulated MAYP upregulation is abolished. MAYP is expressed in monocytes/macrophages and a Mac1+ granulocyte subfraction, and LPS increases its expression in macrophages. Positional cloning of Lupo mutation, bone marrow transplantation, clodronate liposome depletion, Western blot for protein stability, cytokine measurement in vitro Blood High 16397132
2009 PSTPIP2 deficiency (cmo, L98P) causes loss of detectable PSTPIP2 protein in macrophages, mast cells, and osteoclasts. cmo disease is lymphocyte-independent and cured by bone marrow transplantation. PSTPIP2-deficient macrophages show elevated MIP-1α and IL-6 production and increased CSF-1-stimulated ERK1/2 phosphorylation and proliferation; retroviral re-expression of wild-type PSTPIP2 normalizes cytokine production, establishing PSTPIP2 as a negative regulator of CSF-1R signaling in macrophages. Bone marrow transplantation, retroviral rescue of PSTPIP2 expression in macrophages, flow cytometry, Western blot, cytokine ELISA, ERK phosphorylation assays Blood High 19608749
2012 PSTPIP2 suppresses osteoclastogenesis via two separable functional domains: (1) tyrosine phosphorylation and a functional F-BAR domain are required for inhibiting both TRAP expression and osteoclast precursor fusion; (2) interaction with PEST-type phosphatases is required only for suppression of TRAP expression but not fusion. Elevated MIP-1α production in PSTPIP2-deficient macrophages is CSF-1R-dependent, and pharmacological CSF-1R/c-Kit inhibition (PLX3397) ameliorates disease in cmo mice. In vitro osteoclastogenesis assays with purified PSTPIP2-mutant precursors, domain mutagenesis (F-BAR, tyrosine, PEST-phosphatase binding), PLX3397 pharmacological treatment of cmo mice, serum MIP-1α measurement Blood High 22923495
2014 In cmo mice, IL-1β (but not IL-1α) plays a critical role in bone pathology via IL-1RI signaling. Disease is independent of the NLRP3 inflammasome and caspase-1. Neutrophils (not macrophages) from cmo mice secrete elevated IL-1β in response to ATP, silica, and Pseudomonas aeruginosa, and this response is sensitive to serine protease inhibitors, implicating neutrophil serine proteases in inflammasome-independent IL-1β processing. Genetic epistasis (IL-1RI-deficient cmo mice, IL-1α/β knockout cmo mice, NLRP3/caspase-1 knockout cmo mice), ex vivo neutrophil and macrophage stimulation assays, serine protease inhibitor treatment Proceedings of the National Academy of Sciences of the United States of America High 24395802
2014 PSTPIP2 interacts with LYN kinase and impairs megakaryocyte differentiation by recruiting PEST phosphatases to suppress CSK activity, leading to enhanced Src family kinase activation and reduced ERK phosphorylation. A W232A mutant of PSTPIP2 (defective in PEST phosphatase interaction) fails to inhibit differentiation and promotes megakaryocyte differentiation instead. PSTPIP2 is a GATA-1-repressed gene in megakaryocytes. Co-immunoprecipitation (PSTPIP2–LYN), ectopic expression and siRNA knockdown in K562 cells, dominant-negative and constitutively active LYN constructs for epistasis, W232A mutagenesis, flow cytometry for CD41 and ploidy, ERK phosphorylation assay, primary mouse bone marrow megakaryocyte assays Cell death & disease Medium 24407241
2015 PSTPIP2 binds both SHIP1 and Csk (inhibitory enzymes) in addition to previously known PEST phosphatases. SHIP1 binds to the C-terminal tyrosine residues of PSTPIP2 that are critical for its PEST-phosphatase-independent inhibitory function. In neutrophils, the SHIP1-binding C-terminal region of PSTPIP2 is required for suppression of IL-1β processing; pharmacological SHIP1 inhibition enhances IL-1β processing. Co-immunoprecipitation of PSTPIP2 with SHIP1 and Csk, domain mapping of SHIP1 binding site, SHIP1 inhibitor treatment of neutrophils, IL-1β processing assays with neutrophil stimulation (silica, Ab aggregates, LPS) Journal of immunology Medium 26304991
2011 PSTPIP2 localizes to detergent-resistant membranes (lipid rafts) containing the HCV RNA replication complex and is required for formation of NS4B-induced membranous webs. A membrane curvature-defective PSTPIP2 mutant fails to support HCV replication, demonstrating that the membrane-deforming activity of PSTPIP2 is essential for membranous web formation and HCV replication. lentiviral RNAi knockdown in HCV replicon and infected cells (HCV RNA/protein quantification), subcellular fractionation to detergent-resistant membranes, membranous web formation assay, curvature-defective PSTPIP2 mutant rescue experiment Journal of virology Medium 22130530
2018 PSTPIP2 promoter hypermethylation in hepatic macrophages (mediated by DNMT3a and DNMT3b) silences PSTPIP2 expression during liver fibrosis. PSTPIP2 overexpression suppresses M1 polarization by inhibiting STAT1 activity and promotes M2 polarization by enhancing STAT6 activity. Knockdown promotes M1 and suppresses M2 polarization in vitro. RRBS genome-wide methylation sequencing of isolated hepatic macrophages, ChIP assay for DNMT3a/3b binding to PSTPIP2 promoter, AAV9-PSTPIP2 overexpression in mice, STAT1/STAT6 phosphorylation Western blot, siRNA knockdown in RAW264.7 cells Oncogene Medium 29993036
2022 Disruption of the PEST-PTP binding site in PSTPIP2 causes symptomatic autoinflammatory disease, while disruption of the SHIP1 binding site does not. Both PEST-PTPs and SHIP1 contribute equally to control of IL-1β production in neutrophils, but PEST-PTPs have a dominant role in controlling reactive oxygen species production and CXCL2 chemokine secretion, the latter creating a positive feedback loop for neutrophil recruitment. Generation of knock-in mouse strains with point mutations disrupting PEST-PTP or SHIP1 binding sites, disease symptom scoring, IL-1β and ROS assays in neutrophils, CXCL2 measurement Frontiers in immunology High 36605205
2022 PSTPIP2 regulates synovial macrophage polarization and dynamics in an ERβ-dependent manner, forming an F4/80+PSTPIP2hi immunological barrier in the joint lining layer. This was established using Pstpip2CreR26-ZsGreen reporter mice and Esr2fl/fl/Adgre-Cre conditional knockout mice. Pstpip2CreR26-ZsGreen reporter mouse imaging, macrophage-specific Esr2 (ERβ) conditional knockout (Esr2fl/fl/Adgre-Cre), AAV-PSTPIP2 overexpression, macrophage polarization and dynamics assays Arthritis research & therapy Medium 36324152
2020 PSTPIP2 suppresses cisplatin-induced apoptosis in renal tubular epithelial cells. H3K27 acetylation at the PSTPIP2 promoter drives its expression, and HDAC inhibition (TSA) upregulates PSTPIP2; silencing PSTPIP2 abolishes this anti-apoptotic effect in vitro. AAV-PSTPIP2 overexpression in mice, epithelial cell-specific overexpression, siRNA knockdown in vitro, ChIP assay validating H3K27ac binding to PSTPIP2 promoter, TSA HDAC inhibitor treatment Cell death & disease Medium 33311489
2024 In aristolochic acid nephropathy, PSTPIP2 suppresses NET formation via the NF-κB/IL-19/IL-20Rβ pathway: damaged renal tubular epithelial cells release IL-19 via PSTPIP2-mediated NF-κB inhibition, and IL-19 signals through IL-20Rβ on neutrophils to induce NETs, which in turn promote RTEC apoptosis. Conditional Pstpip2 knock-in reduced neutrophil infiltration, IL-19, and NETs; Ly6G neutrophil depletion and PAD4 inhibition phenocopied PSTPIP2 protection. Conditional kidney-specific Pstpip2 knock-in mice, Ly6G-neutralizing antibody (neutrophil depletion), PAD4 inhibitor, in vitro IL-19/IL-20Rβ signaling experiments in damaged RTECs, NF-κB pathway analysis eLife Medium 38314821
2022 DNMT3a directly binds the Pstpip2 promoter (shown by ChIP assay) and is the principal epigenetic regulator of PSTPIP2 expression during alcohol-induced liver injury; DNMT3a silencing restores PSTPIP2 expression and reduces inflammation. PSTPIP2 overexpression regulates inflammatory responses through STAT1 and NF-κB signaling pathways in macrophages. ChIP assay for DNMT3a at Pstpip2 promoter, methylation-specific PCR, DNMT3a siRNA knockdown, AAV9-PSTPIP2 overexpression in EtOH-fed mice, STAT1/NF-κB Western blot Pharmacological research Medium 35149186
2024 PSTPIP2 protects hepatocytes from apoptosis via STAT3 signaling: PSTPIP2 overexpression reduced caspase-dependent apoptosis in EtOH-induced ALI mice and in a stable PSTPIP2-overexpressing AML-12 cell line, with STAT3 identified as a direct downstream signaling pathway regulated by PSTPIP2. AAV9-PSTPIP2 overexpression in EtOH-fed mice, lentivirus-stable PSTPIP2-overexpressing AML-12 cells, caspase activity assays, STAT3 phosphorylation Western blot Biochemical pharmacology Low 38824967

Source papers

Stage 0 corpus · 25 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 A missense mutation in pstpip2 is associated with the murine autoinflammatory disorder chronic multifocal osteomyelitis. Bone 159 16122996
2006 Mutation of mouse Mayp/Pstpip2 causes a macrophage autoinflammatory disease. Blood 120 16397132
2014 Inflammasome-independent IL-1β mediates autoinflammatory disease in Pstpip2-deficient mice. Proceedings of the National Academy of Sciences of the United States of America 97 24395802
2009 Genetic susceptibility factors in a cohort of 38 patients with SAPHO syndrome: a study of PSTPIP2, NOD2, and LPIN2 genes. The Journal of rheumatology 67 20032092
2005 The PCH family member MAYP/PSTPIP2 directly regulates F-actin bundling and enhances filopodia formation and motility in macrophages. Molecular biology of the cell 64 15788569
2012 PSTPIP2 deficiency in mice causes osteopenia and increased differentiation of multipotent myeloid precursors into osteoclasts. Blood 63 22923495
2009 Primed innate immunity leads to autoinflammatory disease in PSTPIP2-deficient cmo mice. Blood 63 19608749
2018 PSTPIP2 connects DNA methylation to macrophage polarization in CCL4-induced mouse model of hepatic fibrosis. Oncogene 62 29993036
2020 PSTPIP2 inhibits cisplatin-induced acute kidney injury by suppressing apoptosis of renal tubular epithelial cells. Cell death & disease 39 33311489
2015 PSTPIP2, a Protein Associated with Autoinflammatory Disease, Interacts with Inhibitory Enzymes SHIP1 and Csk. Journal of immunology (Baltimore, Md. : 1950) 29 26304991
2011 Proline-serine-threonine phosphatase-interacting protein 2 (PSTPIP2), a host membrane-deforming protein, is critical for membranous web formation in hepatitis C virus replication. Journal of virology 29 22130530
2015 Increased neutrophil infiltration, IL-1 production and a SAPHO syndrome-like phenotype in PSTPIP2-deficient mice. Rheumatology (Oxford, England) 25 25602062
2021 Role of the F-BAR Family Member PSTPIP2 in Autoinflammatory Diseases. Frontiers in immunology 20 34262554
2024 Histone deacetylase-mediated silencing of PSTPIP2 expression contributes to aristolochic acid nephropathy-induced PANoptosis. British journal of pharmacology 19 38073114
2018 PSTPIP2 Inhibits the Inflammatory Response and Proliferation of Fibroblast-Like Synoviocytes in vitro. Frontiers in pharmacology 18 30564127
2014 PSTPIP2 dysregulation contributes to aberrant terminal differentiation in GATA-1-deficient megakaryocytes by activating LYN. Cell death & disease 16 24407241
2022 DNMT3a-mediated methylation of PSTPIP2 enhances inflammation in alcohol-induced liver injury via regulating STAT1 and NF-κB pathway. Pharmacological research 14 35149186
2019 PSTPIP2 attenuates joint damage and suppresses inflammation in adjuvant-induced arthritis. European journal of pharmacology 14 31325437
2023 PSTPIP2 alleviates obesity associated adipose tissue inflammation and insulin resistance in diabetes mice through promoting M2 macrophage polarization via activation of PPARγ. Journal of diabetes and its complications 11 37150118
2024 PSTPIP2 ameliorates aristolochic acid nephropathy by suppressing interleukin-19-mediated neutrophil extracellular trap formation. eLife 10 38314821
2022 PSTPIP2 regulates synovial macrophages polarization and dynamics via ERβ in the joint microenvironment. Arthritis research & therapy 8 36324152
2022 Molecular interactions of adaptor protein PSTPIP2 control neutrophil-mediated responses leading to autoinflammation. Frontiers in immunology 8 36605205
2024 PSTPIP2 protects against alcoholic liver injury and invokes STAT3-mediated suppression of apoptosis. Biochemical pharmacology 3 38824967
2023 PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects. Allergologia et immunopathologia 3 37695226
2025 Disruption of Morrbid alleviates autoinflammatory osteomyelitis in Pstpip2-deficient mice. Disease models & mechanisms 1 40503910

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