Affinage

ARPC1B

Actin-related protein 2/3 complex subunit 1B · UniProt O15143

Length
372 aa
Mass
41.0 kDa
Annotated
2026-06-09
34 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARPC1B is a hematopoietically-enriched regulatory subunit of the Arp2/3 complex that mediates WASP-stimulated nucleation of branched actin networks, an activity that the ARPC1A isoform cannot compensate for despite its compensatory upregulation (PMID:28368018, PMID:34673575). Loss of ARPC1B abolishes Arp2/3 complex assembly and disables WASP-dependent actin branching, weakening the cortical F-actin cytoskeleton and crippling actin-driven processes across immune and platelet lineages: lamellipodia extension, immunological synapse assembly, polarized lytic granule secretion, neutrophil pseudopod-based and post-transmigration migration, B-cell receptor confinement, and proplatelet formation (PMID:28368018, PMID:30254128, PMID:31710310, PMID:34673575, PMID:34135903, PMID:38224139). In T cells, ARPC1B additionally supports retromer/WASH-dependent recycling of TCR, CD8, and GLUT1 to the plasma membrane, coupling its actin role to surface receptor homeostasis and signaling (PMID:31710310). Patient frameshift mutations cause an inborn error of immunity with microthrombocytopenia, defective T-cell and thrombocyte development, and increased radiosensitivity; causality is established by rescue with wild-type but not mutant ARPC1B in zebrafish and in patient-derived T cells (PMID:28368018, PMID:29127144, PMID:30254128, PMID:35967303). ARPC1B activity is tuned by Thr21 phosphorylation within its first WD repeat—by PAK1 to control cortical Arp2/3 localization and motility, and by Aurora A to govern centrosomal homeostasis and mitotic entry—and its abundance is stabilized against ubiquitin-mediated degradation by NAA30-dependent N-terminal acetylation (PMID:14749719, PMID:20603326, PMID:41615304). In non-hematopoietic cancer contexts, ARPC1B exerts non-canonical scaffolding roles, stabilizing partner proteins (IFI16/HuR, STAT1, IGF2BP3) against ubiquitination to sustain oncogenic signaling, immunosuppression, and glycolytic reprogramming (PMID:36380368, PMID:39841088, PMID:41803983).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2004 High

    Established that ARPC1B is a phosphoregulated subunit, showing PAK1 phosphorylates it on Thr21 to control its localization with Arp2/3 at cortical nucleation sites and cell motility.

    Evidence In vitro kinase assay, co-IP, T21A mutagenesis, and motility assays

    PMID:14749719

    Open questions at the time
    • Did not address tissue specificity of this regulation
    • Did not test whether T21 phosphorylation alters actin nucleation kinetics directly
  2. 2010 High

    Revealed a second kinase axis where ARPC1B is both an activator and Thr21 substrate of Aurora A, linking it to centrosomal homeostasis and mitotic entry beyond cortical actin.

    Evidence Immunofluorescence colocalization with gamma-tubulin, in vitro kinase assay, Aurora A activity assay, siRNA depletion, phosphomutant overexpression

    PMID:20603326

    Open questions at the time
    • Whether the centrosomal role depends on Arp2/3 complex assembly is unresolved
    • Relationship between the PAK1 and Aurora A Thr21 inputs not reconciled
  3. 2017 High

    Defined ARPC1B as a non-redundant, hematopoietically-restricted Arp2/3 subunit whose loss is causative for human disease, abolishing complex assembly and causing microthrombocytopenia and defective platelet/thrombocyte and T-cell development.

    Evidence Patient platelet proteomics, spreading assays, megakaryocyte KO cell lines, and zebrafish loss-of-function with human cDNA rescue versus mutant variant

    PMID:28368018 PMID:29127144

    Open questions at the time
    • Molecular basis for ARPC1A's inability to substitute not defined at this stage
    • Did not establish the biochemical defect in actin nucleation
  4. 2018 High

    Localized the T-cell defect to Arp2/3-dependent lamellipodia and immunological synapse assembly, with lentiviral gene correction confirming cell-intrinsic causality.

    Evidence Confocal imaging, proliferation and migration assays, lentiviral rescue in patient T cells across six unrelated patients

    PMID:30254128

    Open questions at the time
    • Did not address whether defects extend beyond actin to membrane trafficking
  5. 2019 High

    Uncovered a dual mechanism in CTLs whereby ARPC1B drives synapse actin and lytic granule secretion and also supports retromer/WASH-dependent surface recycling of TCR, CD8, and GLUT1.

    Evidence Patient CTL cytotoxicity, synapse imaging, surface receptor flow cytometry, and retromer/WASH functional assessment

    PMID:31710310

    Open questions at the time
    • Direct molecular link between ARPC1B and the WASH/retromer machinery not mapped
    • Whether surface depletion is a primary or secondary consequence unclear
  6. 2021 High

    Provided the biochemical basis for ARPC1B's non-redundancy by showing it specifically mediates WASP-stimulated branched actin nucleation, the loss of which weakens cortical actin and dysregulates BCR tonic signaling.

    Evidence WASP-stimulated actin nucleation assays, podosome/lamellipodia assays, BCR diffusion (FRAP/single-molecule), calcium imaging, and phospho-Akt in patient cells

    PMID:34673575

    Open questions at the time
    • Structural determinant of WASP-specific stimulation in ARPC1B vs ARPC1A not defined
  7. 2021 Medium

    Refined the neutrophil migration defect, showing ARPC1B/Arp2/3 branched actin is dispensable for transmigration efficiency but essential for subendothelial crawling and 3D matrix locomotion.

    Evidence Flow-based transmigration, subendothelial crawling, 3D collagen migration, and vessel-on-a-chip assays in patient neutrophils

    PMID:34135903

    Open questions at the time
    • No genetic rescue performed
    • Single lab; molecular distinction between migration modes not resolved
  8. 2024 Medium

    Used a genetic iPSC model to attribute the migration defect to a switch from pseudopod to filopodia and dissected cell-intrinsic neutrophil from extrinsic endothelial contributions.

    Evidence ARPC1B-KO iPSC-derived neutrophils, primary deficient endothelial cells, and blood vessel-on-a-chip live imaging

    PMID:38224139

    Open questions at the time
    • Single lab
    • Mechanism of the pseudopod-to-filopod switch not defined at molecular level
  9. 2022 Medium

    Extended ARPC1B function to genome maintenance, linking its deficiency to radiosensitivity, chromatid aberrations, and G2/M arrest, implicating Arp2/3-dependent actin in double-strand break repair.

    Evidence Cytogenetic aberration assays, gammaH2AX foci, and cell cycle analysis after ionizing radiation/bleomycin in patient cells

    PMID:35967303

    Open questions at the time
    • Mechanistic link to DSB clustering inferred from phenotypic convergence, not direct
    • Single lab; no rescue
  10. 2026 Medium

    Identified post-translational control of ARPC1B abundance, showing NAA30-mediated N-terminal acetylation protects it from polyubiquitination and proteasomal degradation.

    Evidence Co-IP, IP-LC/MS, N-terminal acetylation omics, ubiquitination assay, and re-expression rescue in ovarian cancer cells

    PMID:41615304

    Open questions at the time
    • Single lab
    • Whether acetylation affects Arp2/3 assembly or only stability is untested
  11. 2024 Medium

    Defined non-canonical scaffolding roles in cancer whereby ARPC1B stabilizes partner proteins against ubiquitination to sustain oncogenic and immunosuppressive signaling.

    Evidence Reciprocal Co-IP with domain mapping, ubiquitination assays, RNA-IP, and in vivo tumor/macrophage models for IFI16/HuR, STAT1, and IGF2BP3

    PMID:36380368 PMID:39841088 PMID:41803983

    Open questions at the time
    • Each interaction shown by single lab
    • Whether these scaffolding roles require Arp2/3 complex incorporation is unknown
    • Generalizability beyond the specific tumor types not established
  12. 2025 Medium

    Demonstrated ARPC1B is directly druggable, with the Arp2/3 inhibitor CK-636 binding ARPC1B at high affinity, nominating it as a therapeutic target in cancer stem cells.

    Evidence Surface plasmon resonance, molecular docking, organoid cytotoxicity, and xenograft models in pancreatic cancer

    PMID:40903212

    Open questions at the time
    • Binding site not validated by mutagenesis
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single subunit reconciles its canonical Arp2/3 branched-actin role with the distinct centrosomal, DNA-repair, and ubiquitin-protective scaffolding functions, and whether the cancer scaffolding roles operate independently of the Arp2/3 complex.
  • No structural model distinguishing ARPC1B from ARPC1A function
  • Unknown whether scaffolding partners require Arp2/3 incorporation
  • Cross-talk between phosphorylation and acetylation control of ARPC1B undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140313 molecular sequestering activity 3 GO:0005198 structural molecule activity 2 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005856 cytoskeleton 2 GO:0005886 plasma membrane 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-168256 Immune System 4 R-HSA-109582 Hemostasis 1 R-HSA-1640170 Cell Cycle 1
Partners
AURKAIFI16IGF2BP3NAA30PAK1STAT1USP7WASP
Complex memberships
Arp2/3 complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 ARPC1B (p41-Arc) physically interacts with PAK1 both in vitro and in vivo, and PAK1 phosphorylates ARPC1B on threonine 21 within the first WD repeat. This phosphorylation regulates ARPC1B localization with the Arp2/3 complex at cortical nucleation regions and is required for both constitutive and growth-factor-induced cell motility. In vitro kinase assay, co-immunoprecipitation, site-directed mutagenesis (T21A), cell motility assays EMBO reports High 14749719
2010 ARPC1B colocalizes with gamma-tubulin at centrosomes and acts as both a physiological activator and substrate of Aurora A kinase. Aurora A phosphorylates ARPC1B on threonine 21; expression of wild-type but not non-phosphorylatable ARPC1B leads to Aurora A activation and abnormal centrosome amplification. Depletion of ARPC1B inhibits Aurora A activation at the centrosome and impairs mitotic entry. Immunofluorescence colocalization, in vitro kinase assay, Aurora A activity assay, siRNA depletion, overexpression of phosphomutant ARPC1B The Journal of cell biology High 20603326
2017 Loss of ARPC1B in platelets abolishes Arp2/3 complex assembly (greatly reduced Arp2/3 complex detected in platelet lysates), causes aberrant platelet spreading consistent with loss of Arp2/3-dependent actin branching, and leads to microthrombocytopenia. Knockout of ARPC1B in megakaryocytic cells decreases proplatelet formation. Loss of ARPC1B is accompanied by compensatory upregulation of ARPC1A, but the two isoforms are not functionally interchangeable. Western blot of patient platelet lysates, platelet spreading assay, ARPC1B knockout in megakaryocytic cell lines, patient genetics (homozygous frameshift) Nature communications High 28368018
2017 ARPC1B is required for T cell and thrombocyte development in zebrafish; loss-of-function ARPC1B defects are rescued by wild-type human ARPC1B but not by the patient frameshift variant p.V208VfsX20, establishing the causality of this variant. ARPC1B expression is restricted to hematopoietic cells. Zebrafish ARPC1B morpholino knockdown / genetic loss-of-function, rescue with human ARPC1B cDNA versus mutant variant, whole-exome sequencing Journal of immunology High 29127144
2018 ARPC1B deficiency in T cells impairs Arp2/3-dependent actin-rich lamellipodia extension upon TCR stimulation, prevents immunological synapse assembly, and causes defective TCR-mediated proliferation and SDF1-α-directed migration. Lentiviral gene transfer of ARPC1B into patient-derived T cells restored ARPC1B expression and T-cell proliferation, confirming direct causality. Confocal microscopy (lamellipodia/immunological synapse), proliferation assays, migration assays, lentiviral gene correction, flow cytometry Blood High 30254128
2019 ARPC1B is required for CTL lamellipodia formation, actin reorganization at the immune synapse, and polarized lytic granule secretion. Additionally, ARPC1B is indispensable for retromer/WASH-dependent recycling of TCR, CD8, and GLUT1 to the plasma membrane; loss of ARPC1B causes depletion of these surface proteins, impaired T cell signaling and proliferation, and progressive CD8+ T cell loss. ARPC1B-deficient patient CTL assays, cytotoxicity assays, imaging of immune synapse, flow cytometry of surface TCR/CD8/GLUT1, retromer/WASH complex functional assessment The Journal of clinical investigation High 31710310
2021 ARPC1B-containing Arp2/3 complexes are stimulated by WASP to nucleate branched actin networks. Despite ARPC1A upregulation, ARPC1B-deficient cells are incapable of WASP-mediated Arp2/3 nucleation, demonstrating that ARPC1B specifically mediates WASP-stimulated actin branching. Loss of this activity weakens the cortical F-actin cytoskeleton in B cells, increases BCR diffusion, and causes elevated tonic lipid signaling, oscillatory calcium release from the ER, and elevated phospho-Akt. Actin nucleation assay (WASP-stimulated), podosome formation assay in macrophages, lamellipodia assay in B cells, calcium imaging, BCR diffusion (single-molecule or FRAP), Akt phosphorylation, patient ARPC1B-deficient cells JCI insight High 34673575
2021 ARPC1B-deficient neutrophils show defective actin polymerization and are able to transmigrate through TNF-α-activated endothelium with decreased efficiency under physiological flow conditions but show severe impairment in subendothelial crawling, 3D collagen matrix migration, and vessel-on-a-chip locomotion, indicating that Arp2/3-dependent actin branching via ARPC1B is specifically required for post-transmigration migration modes. Flow-based neutrophil transmigration assay, subendothelial crawling assay, 3D collagen matrix migration, vessel-on-a-chip model, patient ARPC1B-deficient neutrophils Frontiers in immunology Medium 34135903
2021 EVA1A promotes endothelial cell migration partly through ARPC1B as a downstream effector; siRNA-mediated knockdown of ARPC1B downstream of EVA1A ablates EVA1A-promoted migration. Proteomics revealed reduced Arpc1b levels when EVA1A is absent, and Rac1/Cdc42 GTPase activation is regulated by EVA1A upstream of Arpc1b. Proteomics, siRNA knockdown, transwell/scratch migration assays, Rac1/Cdc42 activation assay, Eva1a-/- mouse model Cardiovascular research Medium 31977009
2011 Overexpression of ARPC1B (p41-Arc) in p53/Rb-deficient human osteosarcoma cells (SaOs-2) induces premature senescence, characterized by SA-β-galactosidase activity, irreversible cell cycle exit, and nuclear accumulation of actin filaments, demonstrating a p53/Rb-independent senescence-inducing role linked to actin cytoskeletal reorganization. ARPC1B overexpression in SaOs-2 cells, SA-β-gal assay, actin staining, cell cycle analysis Experimental & molecular medicine Low 21628992
2022 ARPC1B interacts with IFI16 (via IFI16 Pyrin domain) and HuR (via RRM2 domain) in glioma stem cells, protecting both proteins from TRIM21-mediated ubiquitination and degradation, thereby sustaining NF-κB (via IFI16) and STAT3 (via HuR) signaling and maintaining the mesenchymal GSC phenotype and radioresistance. Co-immunoprecipitation, mass spectrometry, ubiquitination assay, deletion mutant constructs, in vitro and in vivo knockdown/overexpression, intracranial xenograft model Journal of experimental & clinical cancer research Medium 36380368
2024 ARPC1B in GBM tumor cells inhibits NEDD4L-mediated ubiquitination of STAT1 and promotes the USP7–STAT1 deubiquitinase interaction, thereby stabilizing STAT1, increasing IL-10 production, and inducing protumorigenic macrophage polarization that contributes to immune checkpoint blockade resistance. Co-immunoprecipitation (ARPC1B-STAT1-NEDD4L-USP7), ubiquitination assay, ARPC1B knockdown, GBM mouse models, ICB combination treatment Cancer research Medium 39841088
2024 ARPC1B-deficient iPSC-derived neutrophils (iNeutrophils) show impaired migration and switch from pseudopod formation to elongated filopodia, indicating that ARPC1B/Arp2/3-dependent branched actin is specifically required for pseudopod-based motility. Additionally, ARPC1B deficiency in endothelium (blood vessel-on-a-chip) independently impairs neutrophil transmigration, with combined neutrophil+endothelial ARPC1B deficiency causing additive migration reduction. iPSC-derived ARPC1B-KO neutrophils, blood vessel-on-a-chip model, live-cell migration imaging, primary human ARPC1B-deficient endothelial cells Journal of cell science Medium 38224139
2022 ARPC1B deficiency in patients is associated with increased radiosensitivity, manifested as elevated chromatid-type chromosomal aberrations, increased γH2AX foci, and G2/M cell cycle arrest after ionizing radiation or bleomycin treatment, implicating ARPC1B/Arp2/3 in double-strand break clustering for homology-directed repair. Cytogenetic aberration assay, γH2AX immunofluorescence, cell cycle analysis (G2/M), radiomimetic bleomycin treatment in patient-derived cells Frontiers in immunology Medium 35967303
2025 CK-636, a known Arp2/3 complex inhibitor, directly binds ARPC1B protein with high affinity as determined by surface plasmon resonance and molecular docking, providing a mechanistic basis for CK-636 activity and identifying ARPC1B as a druggable target in pancreatic cancer stem cells. Surface plasmon resonance (SPR), molecular docking, in vitro cytotoxicity, organoid cultures, in vivo xenograft/orthotopic models Cell proliferation Medium 40903212
2026 ARPC1B binds IGF2BP3 and prevents its ubiquitination and degradation; IGF2BP3 in turn stabilizes HK2 mRNA, promoting glycolytic reprogramming in gastric cancer. Co-immunoprecipitation and RNA immunoprecipitation confirmed the ARPC1B–IGF2BP3 interaction and IGF2BP3–HK2 mRNA binding; HK2 overexpression rescued anti-glycolytic effects of ARPC1B knockdown. Co-immunoprecipitation, confocal microscopy, RNA immunoprecipitation, actinomycin D mRNA stability assay, ARPC1B KD/OE, in vivo xenograft European journal of medical research Medium 41803983
2026 NAA30, an N-alpha-acetyltransferase, directly binds ARPC1B and N-terminally acetylates it; NAA30 knockdown enhances polyubiquitination and proteasomal degradation of ARPC1B, and re-expression of ARPC1B in NAA30-silenced ovarian cancer cells rescues malignant phenotypes, placing ARPC1B as the critical downstream effector of the NR2C2–NAA30 axis. Co-immunoprecipitation, IP–LC/MS, N-terminal acetylation modification omics, ubiquitination assay, ARPC1B re-expression rescue, dual-luciferase assay (for upstream NR2C2) FASEB journal Medium 41615304

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Loss of the Arp2/3 complex component ARPC1B causes platelet abnormalities and predisposes to inflammatory disease. Nature communications 163 28368018
2004 p41-Arc subunit of human Arp2/3 complex is a p21-activated kinase-1-interacting substrate. EMBO reports 116 14749719
2018 T-cell defects in patients with ARPC1B germline mutations account for combined immunodeficiency. Blood 98 30254128
2019 Loss of ARPC1B impairs cytotoxic T lymphocyte maintenance and cytolytic activity. The Journal of clinical investigation 69 31710310
2017 Disruption of Thrombocyte and T Lymphocyte Development by a Mutation in ARPC1B. Journal of immunology (Baltimore, Md. : 1950) 68 29127144
2022 ARPC1B promotes mesenchymal phenotype maintenance and radiotherapy resistance by blocking TRIM21-mediated degradation of IFI16 and HuR in glioma stem cells. Journal of experimental & clinical cancer research : CR 55 36380368
2010 Arpc1b, a centrosomal protein, is both an activator and substrate of Aurora A. The Journal of cell biology 54 20603326
2021 Eva1a ameliorates atherosclerosis by promoting re-endothelialization of injured arteries via Rac1/Cdc42/Arpc1b. Cardiovascular research 25 31977009
2021 Case Report: A Novel Synonymous ARPC1B Gene Mutation Causes a Syndrome of Combined Immunodeficiency, Asthma, and Allergy With Significant Intrafamilial Clinical Heterogeneity. Frontiers in immunology 25 33679784
2021 ARPC1B binds WASP to control actin polymerization and curtail tonic signaling in B cells. JCI insight 25 34673575
2022 Dual role of ARPC1B in regulating the network between tumor-associated macrophages and tumor cells in glioblastoma. Oncoimmunology 22 35111386
2006 Arpc1b gene is a candidate prediction marker for choroidal malignant melanomas sensitive to radiotherapy. Investigative ophthalmology & visual science 22 16723437
2021 Estrogen Receptor Beta Prevents Signet Ring Cell Gastric Carcinoma Progression in Young Patients by Inhibiting Pseudopodia Formation via the mTOR-Arpc1b/EVL Signaling Pathway. Frontiers in cell and developmental biology 20 33553141
2022 ARPC1B Is Associated with Lethal Prostate Cancer and Its Inhibition Decreases Cell Invasion and Migration In Vitro. International journal of molecular sciences 19 35163398
2019 Flow Cytometric Determination of Actin Polymerization in Peripheral Blood Leukocytes Effectively Discriminate Patients With Homozygous Mutation in ARPC1B From Asymptomatic Carriers and Normal Controls. Frontiers in immunology 17 31379835
2025 Targeting ARPC1B Overcomes Immune Checkpoint Inhibitor Resistance in Glioblastoma by Reversing Protumorigenic Macrophage Polarization. Cancer research 13 39841088
2022 Hematopoietic Stem Cell Transplantation in ARPC1B Deficiency. Journal of clinical immunology 11 35767111
2023 The overexpression of actin related protein 2/3 complex subunit 1B(ARPC1B) promotes the ovarian cancer progression via activation of the Wnt/β-catenin signaling pathway. Frontiers in immunology 10 37304283
2022 Radiosensitivity in patients affected by ARPC1B deficiency: a new disease trait? Frontiers in immunology 10 35967303
2021 Defective Neutrophil Transendothelial Migration and Lateral Motility in ARPC1B Deficiency Under Flow Conditions. Frontiers in immunology 10 34135903
2024 Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1B. Journal of cell science 8 38224139
2024 Description of a Novel Pathogenic Variant in the ARPC1B and a Severe Allergy in Two Infants. Iranian journal of allergy, asthma, and immunology 5 38485907
2011 p41-Arc, a regulatory subunit of Arp2/3 complex, can induce premature senescence in the absence of p53 and Rb. Experimental & molecular medicine 5 21628992
2025 Targeting ARPC1B + Cancer Stem Cells to Sensitise Pancreatic Cancer to Gemcitabine Treatment. Cell proliferation 4 40903212
2020 DHX36, BAX, and ARPC1B May Be Critical for the Diagnosis and Treatment of Tuberculosis. Canadian respiratory journal 4 32774561
2024 Recurrent eosinophilia with a novel homozygous ARPC1B mutation. Frontiers of medicine 3 39609360
2021 ARPC1B Mutation Manifesting as Recurrent Hematemesis With Metaplasia. JPGN reports 2 37205964
2025 The c.64 + 2 T > A Founder Variant Hits Home: Report on 14 Patients Expands the Phenotypic Landscape of Inherited ARPC1B Deficiency - a Comparative Analysis. Clinical reviews in allergy & immunology 1 40668456
2025 ARPC1B Promotes Clear Cell Renal Cell Carcinoma Progression via the Wnt/β-Catenin Signaling Pathway. Oncology research 1 41050079
2026 N-Alpha-Acetyltransferase 30, Transcriptionally Regulated by NR2C2, Promotes Ovarian Cancer Progression by Mediating ARPC1B Acetylation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 41615304
2026 Characterisation of a Leaky Splice-Site Mutation Associated with Phenotypic Diversity in Two Unrelated Patients with ARPC1B Deficiency. Journal of clinical immunology 0 41793545
2026 ARPC1B promotes gastric cancer tumorigenesis via IGF2BP3-mediated stabilization of HK2 mRNA and glycolytic reprogramming. European journal of medical research 0 41803983
2025 Molecular analysis and immunological characterization of a founder mutation causing ARPC1B deficiency. Genes and immunity 0 41249596
2024 CircZMYM2 plays a pivotal role in osteosarcoma by regulating the translation of NACA and ARPC1B. Heliyon 0 39624324

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