Serine/threonine-protein phosphatase 2A catalytic subunit beta isoform · UniProt P62714
PPP2CB encodes the β catalytic subunit of protein phosphatase 2A (PP2A), a serine/threonine phosphatase with substrate-specific roles distinct from its α isoform PPP2CA. PPP2CB dephosphorylates G9a/EHMT2 at Thr1045 during late mitosis to restore H3K9me2 and permit normal mitotic exit (PMID:37661576), dephosphorylates LC3B to suppress PINK1/Parkin-mediated mitophagy (PMID:41059761), and dephosphorylates TBK1 to dampen IFN-β antiviral signaling until PPP2CB is itself degraded by the REGγ-proteasome pathway (PMID:40736577). In T cells, PPP2CB negatively regulates PI3K/Akt signaling and Ca²⁺ flux to restrain activation (PMID:35068054), while in vascular smooth muscle cells it is transcriptionally upregulated by the YAP1/TEAD1 axis to inhibit AMPK and activate mTORC1-driven proliferation (PMID:41797917).
Chromosomal mapping of PPP2CB to 8p12 and identification of a chromosome 16 pseudogene established the gene's genomic identity and distinguished it from PPP2CA.
Evidence Somatic cell hybrid PCR, FISH, and Southern blot in human cells
Demonstration that PPP2CA knockdown, but not PPP2CB knockdown, causes mitotic arrest established that the two catalytic isoforms are non-redundant in cell division, raising the question of what PPP2CB-specific roles exist.
Evidence Isoform-specific siRNA and antisense in cultured cells with flow cytometry and live imaging
Conditional Ppp2cb knockout mice were phenotypically normal, confirming in vivo that PPP2CA can compensate for PPP2CB loss in organismal development and establishing genetic tools for tissue-specific studies.
Evidence Cre-loxP conditional KO mouse with comprehensive phenotyping
Identification of PPP2CB upregulation as the proximate cause of meiotic arrest in MARF1-deficient oocytes placed PPP2CB downstream of an RNA-binding protein in female meiotic control.
Evidence Genetic epistasis in Marf1-mutant mouse oocytes with protein expression analysis
Discovery that PPP2CB interacts with adenylyl cyclase 5 and that its knockdown reduces cAMP accumulation in striatal neurons revealed a role for PP2A-β in regulating neuronal cAMP signaling.
Evidence BiFC interaction screen followed by genetic knockdown with cAMP assays in medium spiny neuron models
Structural and biochemical characterization of LB-100 as a catalytic-site inhibitor of PP2A (PPP2CA/PPP2CB) provided atomic-resolution understanding of the phosphatase active site, with metal-coordinating pharmacophore resolved at 1.65 Å.
Evidence In vitro inhibition assays with purified enzymes plus X-ray co-crystal structure of the related PPP5C active site
T cell-specific PPP2CB knockout showed the enzyme is dispensable for development but suppresses PI3K/Akt-dependent T cell activation, identifying a tissue-context in which PPP2CB has a non-redundant immunoregulatory function.
Evidence Conditional KO (Lck-Cre), flow cytometry, PI3K inhibitor rescue, phospho-proteomics
Identification of G9a/EHMT2-pThr1045 as a direct PPP2CB substrate during late mitosis linked PPP2CB to re-establishment of repressive H3K9me2 chromatin after mitotic exit, providing the first specific mitotic substrate for this isoform.
Evidence In vitro phosphatase assay, phosphomimic mutagenesis, ChIP-seq, co-IP, mass spectrometry, PPP2CB knockdown
REGγ-mediated proteasomal degradation of PPP2CB was shown to sustain TBK1 phosphorylation and IFN-β antiviral signaling, establishing PPP2CB as a negative regulator of innate immunity that is itself counter-regulated by a positive feedback loop.
Evidence Co-IP, REGγ KO mice, viral infection survival, IFN-β assays, genetic rescue
PPP2CB was identified as the phosphatase that dephosphorylates LC3B, reducing its interaction with the mitophagy receptor OPTN and impairing PINK1/Parkin mitophagy — connecting the SCA12-associated regulatory subunit PPP2R2Bβ2 to neuronal toxicity through enhanced PPP2CB activity.
Evidence Co-IP, proximity ligation assay, PPP2CB manipulation, mitophagy assays, pharmacological rescue, neuronal survival
Transcriptional activation of PPP2CB by YAP1/TEAD1 in vascular smooth muscle cells established a signaling axis in which PPP2CB inhibits AMPK to relieve mTORC1 suppression and drive proliferation and neointima formation.
Evidence TEAD1 ChIP, YAP1 overexpression/knockdown, AMPK phosphorylation, mTORC1 activity, PPP2CB rescue, VSMC proliferation assays
| Year | Finding | Method | Journal | Conf | PMIDs |
|---|---|---|---|---|---|
| 1993 | PPP2CB (the β isoform of the PP2A catalytic subunit) was chromosomally mapped to human chromosome 8p12→p11.2 using somatic cell hybrids and fluorescence in situ hybridization, and a pseudogene (PPP2CBP) was identified on chromosome 16 by Southern blot analysis. | Somatic cell hybrid PCR mapping, fluorescence in situ hybridization (FISH), Southern blot | Cytogenetics and cell genetics | High | 8383590 |
| 1998 | PP2A-β (PPP2CB) mRNA is intensely expressed in cerebellar floccular Purkinje cells and is upregulated within 2 days after unilateral labyrinthectomy in rats. Continuous infusion of the PP2A inhibitor okadaic acid into the flocculus prolonged UL-induced nystagmus, implicating PPP2CB upregulation in lesion-induced vestibular plasticity. | In situ hybridization, Northern blot, differential display PCR, pharmacological inhibition (okadaic acid infusion) with behavioral readout | Acta oto-laryngologica | Medium | 9840505 |
| 2006 | Suppression of PP2Aα (PPP2CA), but not PP2Aβ (PPP2CB), by antisense oligonucleotides or siRNA was sufficient to induce metaphase arrest with lagging chromosomes and aberrant mitotic spindles, demonstrating that the two catalytic subunit isoforms have non-redundant roles in mitotic progression. | siRNA knockdown, antisense oligonucleotides, flow cytometry, immunostaining, live cell time-lapse microscopy | Molecular cancer therapeutics | High | 17121919 |
| 2008 | PPP2CB transcript is significantly reduced in prostate carcinoma compared to benign prostate tissue, supporting its candidate role as a tumor suppressor on chromosome 8p, though no tumor-specific mutations were found in the coding exons. | Quantitative RT-PCR across 45 prostate carcinomas and 13 benign tissues | Cancer genomics & proteomics | Low | 18460741 |
| 2011 | Conditional knockout of Ppp2cb (exon 3 deleted via Cre-loxP) in mice produces no obvious morphological or physiological defects, demonstrating that PPP2CB is dispensable for normal development when PPP2CA is present, and establishing a mouse genetic tool for spatiotemporal studies. | Conditional knockout mouse generation (Cre-loxP), phenotypic analysis | Genesis | High | 21998041 |
| 2012 | Up-regulation of PPP2CB protein is identified as a key driver of the meiotic arrest phenotype in MARF1-deficient mouse oocytes; elevated PPP2CB levels correlate with failure to complete meiosis, placing PPP2CB downstream of MARF1 in the control of meiotic progression. | Genetic mouse model (Marf1 mutation), protein expression analysis, epistasis | Science | High | 22442484 |
| 2017 | miR-1246 directly targets PPP2CB (and PRKAR1A) in mesenchymal stem/stromal cells, suppressing its expression and thereby promoting NF-κB-dependent transcription and release of pro-inflammatory mediators (IL-6, CCL2, CCL5), linking PPP2CB to regulation of inflammatory signaling in the tumor microenvironment. | miRNA overexpression, luciferase reporter assay (direct targeting), Western blot, cytokine measurement | Oncotarget | Medium | 28159925 |
| 2018 | Co-immunoprecipitation demonstrated that PPP2CB (PP2A catalytic subunit β) directly interacts with GADD45α, and this interaction is associated with GADD45α-mediated promotion of AMPK activation and protection against acetaminophen-induced hepatotoxicity. | Co-immunoprecipitation (LC-MS and Western blot confirmation), in vivo APAP injury model, GADD45α overexpression/knockout | Cellular and molecular life sciences | Medium | 30151693 |
| 2019 | PPP2CB was identified as a novel interactor of adenylyl cyclase type 5 (AC5) in striatal medium spiny neurons using bimolecular fluorescence complementation screening; PPP2CB knockdown reduced both acute and sensitized adenylyl cyclase activity, demonstrating that PP2A is an important persistent regulator of AC5/cAMP signaling in D1 and D2 MSNs. | BiFC protein-protein interaction screen, genetic knockdown, cAMP accumulation assays in MSN cell lines and CAMPER mice | Cells | Medium | 31752385 |
| 2019 | PPP2CB was identified as a binding partner of JEV NS3 protein in a yeast two-hybrid screen of a human brain cDNA library, suggesting PPP2CB may be co-opted by Japanese encephalitis virus through its interaction with the viral NS3 helicase/protease. | Yeast two-hybrid screen | International journal of molecular sciences | Low | 31739611 |
| 2019 | LB-100 was demonstrated to be a catalytic inhibitor of both PP2AC (PPP2CA/PPP2CB) and PPP5C in vitro using purified enzymes; the crystal structure of PPP5C co-crystallized with LB-100 (1.65 Å) revealed that the drug's 7-oxabicyclo[2.2.1]heptane-2,3-dicarbonyl moiety coordinates with active-site metal ions and conserved residues shared between PP2AC and PPP5C. | In vitro phosphatase inhibition assays with purified enzymes, X-ray crystallography (1.65 Å), cell-based genetic disruption studies | Molecular cancer therapeutics | High | 30679389 |
| 2022 | T cell-specific knockout of PPP2CB (PPP2CBfl/fl Lck-Cre+) showed it is dispensable for T cell development and TCR-induced activation, but PPP2CB specifically suppresses PMA/ionomycin-induced T cell activation by negatively regulating the PI3K/Akt signaling pathway and Ca2+ flux; mass spectrometry-based phospho-peptide analysis identified potential substrates of PPP2CB during this activation. | Conditional T cell-specific knockout mouse, flow cytometry (CD69, CD25, cytokines), PI3K inhibitor rescue, phospho-proteomics by MS | The FEBS journal | High | 35068054 |
| 2023 | PPP2CB dephosphorylates G9a/EHMT2 at Thr1045 (phosphorylated by Plk1 kinase during early mitosis) during late mitosis, thereby reactivating G9a catalytic activity and restoring H3K9me2 levels; this PPP2CB-mediated dephosphorylation is correlated with decreased H3S10 phosphorylation and is required for normal mitotic progression. | In vitro kinase/phosphatase assays, site-directed mutagenesis (T1045E phosphomimic), ChIP-seq (chromatin accessibility), co-immunoprecipitation, mass spectrometry, PPP2CB knockdown | Advanced science | High | 37661576 |
| 2023 | Quantum-based ONIOM hybrid calculations on PP2A heterotrimers (containing PPP2CB/PPP2CA catalytic subunit) indicate that bidentate Arg89-substrate binding substantially lowers the activation barrier for phosphoserine hydrolysis (ΔH‡ ≈ +15.5 vs +18.8 kcal/mol), suggesting that Arg89 engagement with substrate phosphate—rather than with B-subunit Glu198—is critical for optimal PP2A catalytic function. | Quantum mechanics/molecular mechanics (ONIOM UB3LYP/6-31G(d):UPM7) computational modeling of catalytic mechanism | Frontiers in cell and developmental biology | Low | 37377738 |
| 2025 | REGγ (a proteasome activator) directly interacts with PPP2CB and promotes its proteasomal degradation in macrophages during viral infection; this degradation prevents PPP2CB from dephosphorylating TBK1, thereby sustaining TBK1-IRF3 interaction and IFNβ-mediated antiviral signaling. IFNβ in turn upregulates REGγ, forming a positive feedback loop. | Co-immunoprecipitation, REGγ knockout mice, viral infection models (in vivo mortality), Western blot, IFNβ production assays, genetic rescue | Cellular and molecular life sciences | High | 40736577 |
| 2025 | PPP2CB (PP2A-β) dephosphorylates LC3B, and this dephosphorylation reduces LC3B interaction with the mitophagy receptor OPTN, thereby impairing mitochondrial recruitment of phagophores during PINK1-PRKN-mediated mitophagy; overexpression of PPP2R2Bβ2 (the SCA12-associated isoform) enhances this PPP2CB-mediated LC3B dephosphorylation and causes neuronal toxicity. | Co-immunoprecipitation, proximity ligation assay, PPP2CB genetic manipulation, mitophagy assays, pharmacological rescue (deferiprone), neuronal survival assays | Autophagy | High | 41059761 |
| 2025 | PPP2CB overexpression in hepatic cells exacerbates lipid accumulation and LDL-C uptake, while PPP2CB silencing mitigates these effects; co-immunoprecipitation and immunofluorescence co-localization confirmed a direct interaction between PPP2CB and LOX-1 (lectin-like oxidized LDL receptor-1), and PPP2CB-mediated lipid dysregulation operates through the LOX-1/MAPK/ERK signaling cascade in atherosclerosis. | Overexpression and siRNA knockdown, co-immunoprecipitation, immunofluorescence co-localization, LDL-C uptake assay, Western blot, ApoE-/- mouse model | Lipids in health and disease | Medium | 40611318 |
| 2026 | YAP1 transcriptionally activates PPP2CB expression via the TEAD1 transcription factor in vascular smooth muscle cells (VSMCs); elevated PPP2CB inhibits AMPK (requiring upstream kinase CAMKK2), thereby relieving AMPK-mediated suppression of mTORC1 and driving VSMC proliferation and neointima formation. | YAP1 siRNA knockdown and overexpression, TEAD1 ChIP, mTORC1 activity assays, AMPK phosphorylation, PPP2CB knockdown rescue, proliferation assays in human VSMCs | iScience | High | 41797917 |
| Year | Title | Journal | Citations | PMID |
|---|---|---|---|---|
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| 2011 | Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. | Briefings in bioinformatics | 656 | 21873635 |
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| 2004 | 14-3-3-affinity purification of over 200 human phosphoproteins reveals new links to regulation of cellular metabolism, proliferation and trafficking. | The Biochemical journal | 372 | 14744259 |
| 2008 | A PP2A phosphatase high density interaction network identifies a novel striatin-interacting phosphatase and kinase complex linked to the cerebral cavernous malformation 3 (CCM3) protein. | Molecular & cellular proteomics : MCP | 302 | 18782753 |
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| 2018 | Coding mutations in NUS1 contribute to Parkinson's disease. | Proceedings of the National Academy of Sciences of the United States of America | 79 | 30348779 |
| 2017 | miRNA-1246 induces pro-inflammatory responses in mesenchymal stem/stromal cells by regulating PKA and PP2A. | Oncotarget | 63 | 28159925 |
| 2006 | Expression analysis of imbalanced genes in prostate carcinoma using tissue microarrays. | British journal of cancer | 57 | 17146477 |
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| 2019 | The Antitumor Drug LB-100 Is a Catalytic Inhibitor of Protein Phosphatase 2A (PPP2CA) and 5 (PPP5C) Coordinating with the Active-Site Catalytic Metals in PPP5C. | Molecular cancer therapeutics | 47 | 30679389 |
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| 2006 | Cantharidin-induced mitotic arrest is associated with the formation of aberrant mitotic spindles and lagging chromosomes resulting, in part, from the suppression of PP2Aalpha. | Molecular cancer therapeutics | 45 | 17121919 |
| 2019 | Plasma-derived exosomal miR-183 associates with protein kinase activity and may serve as a novel predictive biomarker of myocardial ischemic injury. | Experimental and therapeutic medicine | 39 | 31258652 |
| 2019 | Identification of Novel Adenylyl Cyclase 5 (AC5) Signaling Networks in D1 and D2 Medium Spiny Neurons using Bimolecular Fluorescence Complementation Screening. | Cells | 35 | 31752385 |
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| 2008 | Differential IL-4/Stat6 activities correlate with differential expression of regulatory genes SOCS-1, SHP-1, and PP2A in colon cancer cells. | Journal of cancer research and clinical oncology | 12 | 18536936 |
| 2016 | Serine/threonine phosphatases and aquaporin-2 regulation in renal collecting duct. | American journal of physiology. Renal physiology | 11 | 27784696 |
| 2023 | Secreted miR-210-3p, miR-183-5p and miR-96-5p reduce sensitivity to docetaxel in prostate cancer cells. | Cell death discovery | 10 | 38065937 |
| 2022 | Protein phosphatase 2A catalytic subunit β suppresses PMA/ionomycin-induced T-cell activation by negatively regulating PI3K/Akt signaling. | The FEBS journal | 9 | 35068054 |
| 2021 | The association of immunosurveillance and distant metastases in colorectal cancer. | Journal of cancer research and clinical oncology | 9 | 34476575 |
| 2023 | Striatins and STRIPAK complex partners in clinical outcomes of patients with breast cancer and responses to drug treatment. | Chinese journal of cancer research = Chung-kuo yen cheng yen chiu | 8 | 37691891 |
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| 2025 | PPP2CB aggravates atherosclerosis-related dyslipidemia via LOX-1/MAPK/ERK signaling pathway. | Lipids in health and disease | 2 | 40611318 |
| 2024 | Proteomic analysis of plasma and duodenal tissue in celiac disease patients reveals potential noninvasive diagnostic biomarkers. | Scientific reports | 2 | 39622892 |
| 2023 | Quantum-based modeling implies that bidentate Arg89-substrate binding enhances serine/threonine protein phosphatase-2A(PPP2R5D/PPP2R1A/PPP2CA)-mediated dephosphorylation. | Frontiers in cell and developmental biology | 2 | 37377738 |
| 2025 | Adaptation of Diqing Tibetan pigs to hypoxic and cold environments through extramedullary hematopoiesis and uncoupled thermogenesis in the liver. | BMC biology | 1 | 40598433 |
| 2025 | PPP2/PP2A-mediated dephosphorylation of LC3B links PINK1-PRKN/Parkin-mediated mitophagy to SCA12 pathogenesis. | Autophagy | 1 | 41059761 |
| 2024 | Identification of reproduction-related genes in the hypothalamus of sheep (Ovis aries) using the nanopore full-length transcriptome sequencing technology. | Scientific reports | 1 | 39537852 |
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| 2026 | PP2A dysfunction mediated by PPP2R1A deficiency drives cGAS-STING-dependent hyperinflammation in SLE CD14+ monocytes. | Clinical rheumatology | 0 | 41582267 |
| 2026 | Transcriptional control of PPP2CB by YAP1 and TEAD1 mediates AMPK inhibition and mTORC1 activation in vascular smooth muscle cells. | iScience | 0 | 41797917 |
| 2026 | Glycolytic-Cholesterol Subtypes of Severe Asthma Reveal Distinct Immune-Inflammatory and Metabolic Phenotypes. | Journal of inflammation research | 0 | 41940036 |
| 2025 | REGγ regulates antiviral response by activating TBK1-IFNβ signaling through degradation of PPP2CB. | Cellular and molecular life sciences : CMLS | 0 | 40736577 |
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