Affinage

PIK3R2

Phosphatidylinositol 3-kinase regulatory subunit beta · UniProt O00459

Length
728 aa
Mass
81.5 kDa
Annotated
2026-06-10
100 papers in source corpus 34 papers cited in narrative 34 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PIK3R2/p85β is a non-catalytic regulatory subunit of Class IA PI3K that heterodimerizes with p110 catalytic subunits and constrains their basal lipid kinase activity through coordinated contacts from its nSH2, iSH2, and cSH2 domains, with RTK-derived pYXXM phosphopeptides relieving this inhibition by distinct mechanisms at the nSH2 and cSH2 (PMID:21362552, PMID:1334406). Receptor engagement couples p85β to PI3K activation: phosphorylated IRS proteins and adaptor scaffolds recruit p85β via its SH2 domains—for example FER-phosphorylated IRS4 Tyr779 and EPHA2 Ser897 (PMID:35550247, PMID:34484860)—while genetic loss-of-function studies establish that excess p110-free p85β is itself a negative regulator of insulin signaling, competing for IRS proteins and dampening downstream AKT activation (PMID:11752399, PMID:14504291). The free p85β pool is set by FBXL2/PTPL1-controlled ubiquitin-proteasomal degradation gated by Tyr655 phosphorylation (PMID:23604317), and p85β is further regulated post-translationally by threonine phosphorylation during T-cell activation and dephosphorylation by PTEN (PMID:8388374, PMID:20515662). Beyond catalytic regulation, p85β acquires distinct activating and oncogenic properties: it is a less effective inhibitor of p110 than p85α and is sufficient to transform fibroblasts via PI3K-TOR signaling, and its cSH2 domain is activating rather than inhibitory (PMID:25385636, PMID:28915558); cancer-associated mutations confer gain-of-function phenocopying PTEN loss (PMID:21984976). p85β supports a nuclear oncogenic program—following FAK-mediated Y464 phosphorylation and KPNA1-dependent import, or dissociation from helical-domain-mutant p110α, nuclear p85β recruits USP7 to stabilize EZH1/EZH2, drives H3K27 trimethylation, represses tumor suppressors including RB1, and acts as a transcriptional cofactor with BCLAF1 (PMID:35418124, PMID:36857183, PMID:40016211). p85β also has PI3K-independent roles in cell motility, focal adhesion dynamics, and clathrin/dynamin-mediated endocytosis through AP-2 binding motifs in its iSH2 region (PMID:25217619, PMID:38521786), and it regulates AXL stability by altering autophagic degradation (PMID:32385243). Influenza A NS1 hijacks p85β by binding its iSH2 domain at Val573 to activate PI3K and promote viral replication (PMID:16963558, PMID:18534979).

Mechanistic history

Synthesis pass · year-by-year structured walk · 27 steps
  1. 1992 High

    Establishing that p85β is a regulatory, not catalytic, subunit defined its core identity as an adaptor coupling PI3K to activated receptor tyrosine kinases.

    Evidence Baculovirus co-expression, co-immunoprecipitation and in vitro kinase assays in insect cells

    PMID:1334406

    Open questions at the time
    • Did not resolve which domains mediate inhibition vs. recruitment
    • Functional difference from p85α not yet defined
  2. 1993 Medium

    Differential threonine phosphorylation of p85β upon TCR/CD3 stimulation revealed isoform-specific regulation of PI3K during immune signaling.

    Evidence Isoform-specific immunoprecipitation and phosphoamino acid analysis in T cells

    PMID:8388374

    Open questions at the time
    • Kinase responsible for threonine phosphorylation not identified
    • Functional consequence of the modification untested
  3. 2001 High

    Knockout of p85β demonstrated that, contrary to a purely activating adaptor, p85β is a negative regulator of insulin signaling in vivo, distinct from p85α.

    Evidence Pik3r2−/− mice with metabolic phenotyping, PI3K activity and AKT immunoblots

    PMID:11752399

    Open questions at the time
    • Mechanism of negative regulation not yet defined at this stage
    • Tissue-specific contributions not dissected
  4. 2003 High

    Reconstitution in isogenic KO cells localized the negative regulatory activity to excess free p85, clarifying that monomeric p85β competes with the active heterodimer for IRS proteins.

    Evidence Genetic KO brown adipose cell lines with p85 reconstitution and signaling assays

    PMID:14504291

    Open questions at the time
    • Stoichiometry of free vs. heterodimeric pools in vivo not quantified
    • Direct IRS-competition not structurally shown
  5. 2006 High

    Influenza NS1 was found to bind p85β specifically (not p85α) and activate PI3K, identifying a viral mechanism of subunit hijacking.

    Evidence Co-IP, NS1 Y89F mutagenesis, recombinant virus rescue and PI3K assays

    PMID:16963558

    Open questions at the time
    • Binding interface on p85β not mapped in this study
    • Why isoform specificity exists unresolved here
  6. 2008 High

    Mapping the NS1 interaction to iSH2 Val573 explained the isoform specificity and showed a trimeric NS1–p85β–p110 complex drives PI3K activation.

    Evidence Reciprocal mutagenesis with gain-of-function p85α, competition and PI3K activity assays

    PMID:18534979

    Open questions at the time
    • Structural basis of how NS1 binding activates p110 not fully resolved
    • In vivo viral fitness consequence in animals not addressed here
  7. 2009 Medium

    p85β was shown to bind CD28 and CBL preferentially over p85α, linking it to receptor downregulation and T-cell differentiation.

    Evidence Co-IP, p85β KO mice and T-cell differentiation assays

    PMID:19190244

    Open questions at the time
    • Interaction interfaces with CD28/CBL not mapped
    • Catalytic vs. adaptor contribution not separated
  8. 2009 Medium

    B cell studies revealed partial redundancy with p85α alongside a unique inhibitory role for p85β in opposing BCR responses.

    Evidence p85β KO mice, BCR stimulation and ERK/AKT immunoblots

    PMID:19811262

    Open questions at the time
    • Molecular basis of BCR inhibition unresolved
    • Single-lab observation
  9. 2010 High

    p85 monomers were found to bind XBP-1s and promote its nuclear translocation, expanding p85β function into ER stress resolution.

    Evidence Co-IP, adenoviral overexpression and ob/ob mouse rescue

    PMID:20348926

    Open questions at the time
    • Relative roles of p85α vs. p85β monomers not separated
    • Interaction interface with XBP-1s undefined
  10. 2010 Medium

    PTEN was identified as a phosphatase acting on p85β, adding a counter-regulatory layer to p85β phosphorylation.

    Evidence Co-IP, phosphatase assay and phospho-specific immunoblot with siRNA

    PMID:20515662

    Open questions at the time
    • Functional consequence of dephosphorylation not established
    • Single-study, single-lab finding
  11. 2010 Medium

    Structures of the p85β iSH2 coiled-coil and SH3 domains provided atomic detail and revealed subtle ligand-specificity differences from p85α.

    Evidence X-ray crystallography of iSH2 and SH3 domains with peptide binding assays

    PMID:21139197 PMID:22102226

    Open questions at the time
    • Limited functional validation of conformational plasticity
    • Full-length p85β architecture not determined
  12. 2011 High

    The p110β/p85β crystal structure defined the multi-domain inhibitory mechanism and how distinct pYXXM-engagement at nSH2 and cSH2 relieves inhibition.

    Evidence X-ray crystallography, in vitro lipid kinase assays, mutagenesis and cell signaling

    PMID:21362552

    Open questions at the time
    • Dynamics of activation in cells not visualized
    • Does not address nuclear or non-catalytic functions
  13. 2011 High

    Cancer genome analysis showed PIK3R2 mutations are gain-of-function and phenocopy PTEN loss, establishing p85β as an oncogenic driver.

    Evidence Tumor sequencing, functional mutation and PTEN stability assays

    PMID:21984976

    Open questions at the time
    • Whether p85β mutants directly destabilize PTEN like p85α not fully resolved
    • Mechanism of individual mutations varies
  14. 2012 Medium

    Elevated p85β was shown to drive PIP3 production, invasion and tumor progression, linking expression level to oncogenicity.

    Evidence IHC, PIP3 and invasion assays, xenograft models

    PMID:22733740

    Open questions at the time
    • Mechanism of enhanced PIP3 generation by excess p85β unclear
    • Single-lab in vivo data
  15. 2012 Medium

    p85β was found to restrain KIT signaling by promoting receptor internalization and CBL binding, defining a tumor-suppressive role in mast cells/leukemia.

    Evidence KO mice, overexpression, internalization and Co-IP assays, bone marrow transplantation

    PMID:22378847

    Open questions at the time
    • Reconciliation with oncogenic roles in other contexts unresolved
    • Direct internalization machinery not identified
  16. 2013 High

    FBXL2/PTPL1-mediated, Tyr655-gated degradation of the p110-free pool defined how p85β abundance is set, controlling PI3K output and autophagy.

    Evidence AP-MS, in vitro ubiquitylation, phospho-mutant analysis, proteasome inhibition

    PMID:23604317

    Open questions at the time
    • Kinase phosphorylating Tyr655 not identified
    • How free vs. bound pools are sensed in cells unresolved
  17. 2014 Medium

    p85β alone was shown sufficient to transform fibroblasts via PI3K-TOR, attributing oncogenicity to its weaker inhibition of p110 relative to p85α.

    Evidence Avian fibroblast transformation assay with pathway reporters and inhibitors

    PMID:25385636

    Open questions at the time
    • Structural basis of weaker inhibition not detailed here
    • Single-lab assay system
  18. 2014 Medium

    Imaging revealed a PI3K-context role at adhesions where p85β recruits FAK and active Cdc42/Rac to build invadopodia and promote invasion.

    Evidence Fluorescence microscopy, Co-IP, siRNA and invasion/F-actin assays

    PMID:25217619

    Open questions at the time
    • Whether adhesion role requires PI3K catalysis not separated here
    • GAP/GEF link to Cdc42/Rac undefined
  19. 2017 Medium

    Domain-swap analysis reversed the canonical view by showing the p85β cSH2 is activating and the SH3 domain modulates oncogenic signaling.

    Evidence Domain deletion/substitution mutants with transformation and signaling assays

    PMID:28915558

    Open questions at the time
    • Structural mechanism of cSH2 activation not resolved
    • Single-lab finding
  20. 2020 High

    p85β was found to stabilize the RTK AXL by blocking its autophagic degradation via TRIM2/optineurin phosphorylation, activating AKT-independent PDK1/SGK3 signaling.

    Evidence Co-IP, phosphoproteomics, autophagy flux and kinase assays with AXL inhibition rescue

    PMID:32385243

    Open questions at the time
    • Direct kinase target of p85β regulation of TRIM2/optineurin unclear
    • Generality across cell types untested
  21. 2022 High

    Dissociation from helical-domain-mutant p110α was shown to drive nuclear p85β that stabilizes EZH1/2 via USP7 and reprograms H3K27me3.

    Evidence Fractionation, Co-IP with USP7/EZH1/2, ChIP-seq, NLS mutagenesis and xenografts

    PMID:35418124

    Open questions at the time
    • Trigger for dissociation beyond the specific mutation unclear
    • Direct USP7 binding interface not mapped
  22. 2022 High

    FER-phosphorylated IRS4 Tyr779 was shown to recruit p85β to activate PI3K-AKT, defining a receptor-adaptor route to PI3K activation in tumors.

    Evidence MS, proximity tagging, Co-IP, phospho-mutant rescue and in vivo tumor model

    PMID:35550247

    Open questions at the time
    • Whether p85β isoform selectivity over p85α exists here untested
    • Generalizability beyond ovarian tumors unclear
  23. 2023 High

    FAK-mediated Y464 phosphorylation and KPNA1 import were identified as the route for cytoplasm-to-nucleus translocation of oncogenic p85β repressing RB1.

    Evidence Phospho-site mutagenesis, Co-IP with importin, fractionation, xenografts and FAK inhibitor

    PMID:36857183

    Open questions at the time
    • Whether this pathway operates outside ccRCC unclear
    • How nuclear vs. cytoplasmic balance is set physiologically unresolved
  24. 2024 High

    AP-2 binding motifs in the iSH2 disordered region were shown to drive clathrin/dynamin endocytosis and constrain migration independently of PI3K catalysis.

    Evidence Motif mutagenesis, live imaging, clathrin/dynamin inhibitors and adhesion microscopy

    PMID:38521786

    Open questions at the time
    • In vivo relevance of this non-catalytic role untested
    • Cargo selectivity of p85β-AP-2 endocytosis undefined
  25. 2024 Medium

    NSUN2-mediated m5C methylation was shown to stabilize PIK3R2 mRNA, identifying epitranscriptomic control of p85β abundance.

    Evidence m5C-RIP-qPCR, mRNA stability, siRNA and xenograft

    PMID:38411298

    Open questions at the time
    • m5C sites on PIK3R2 not precisely mapped
    • Single-lab study
  26. 2025 High

    Nuclear p85β was shown to act as a transcriptional cofactor with BCLAF1, assembling TRIM28/ZNF263 for positive autoregulation, extending its non-catalytic oncogenic program.

    Evidence ChIP-seq, RNA-seq, reciprocal Co-IP and loss-of-function

    PMID:40016211

    Open questions at the time
    • Direct DNA vs. cofactor binding mode of p85β unresolved
    • Generality across tumor types not established
  27. 2025 Medium

    YTHDF2 was shown to bind m6A-modified PIK3R2 mRNA and undergo LLPS to degrade it, adding an opposing epitranscriptomic regulator of p85β.

    Evidence m6A-RIP, YTHDF2 knockdown, phase separation and mRNA stability assays

    PMID:40473165

    Open questions at the time
    • Physiological contexts balancing NSUN2 vs. YTHDF2 control unclear
    • Single-lab study

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple, sometimes opposing, p85β activities—catalytic inhibition, free-pool competition, nuclear epigenetic/transcriptional roles, and non-catalytic endocytic/adhesion functions—are integrated and switched within a single cell remains unresolved.
  • No unified model linking cytoplasmic and nuclear pools quantitatively
  • Triggers that partition p85β between functions not defined
  • Structural basis of nuclear cofactor activity unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0042393 histone binding 2 GO:0060089 molecular transducer activity 2 GO:0060090 molecular adaptor activity 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-4839726 Chromatin organization 2 R-HSA-8953854 Metabolism of RNA 2 R-HSA-9612973 Autophagy 2 R-HSA-5653656 Vesicle-mediated transport 1
Partners
BCLAF1EZH2FBXL2KPNA1PIK3CAPIK3CBPTENUSP7
Complex memberships
Class IA PI3K (p85β–p110α/p110β heterodimer)NS1–p85β–p110 trimeric complex

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 Crystal structure of p110β/p85β complex reveals that the C-terminal SH2 domain (cSH2) of p85β exerts an inhibitory function by tying up the C-terminal region of the p110β catalytic subunit essential for lipid kinase activity. In vitro, p110β basal activity is restrained by contacts with three p85β domains (cSH2, nSH2, iSH2). RTK phosphopeptides relieve inhibition by nSH2 and cSH2 through distinct mechanisms: the cSH2 requires an extended pYXXM motif to disrupt its inhibitory contact with p110β, whereas the nSH2 pY-binding site itself forms the inhibitory contact. Mutagenesis of a cSH2 contact residue activates downstream signaling in cells. X-ray crystallography, in vitro lipid kinase assay, mutagenesis, cell-based signaling assay Molecular cell High 21362552
1992 p85β associates with p110 (PI3K catalytic subunit) and with activated receptor tyrosine kinases (EGF receptor, CSF-1 receptor, c-erbB2, p59c-fyn) in co-expression studies in insect cells. Both p85α and p85β are substrates for these protein-tyrosine kinases. p85β lacks intrinsic enzymatic activity, indicating it is a regulatory subunit. Free p85β shows less restricted binding specificity than p85 within the active p85-p110 heterodimer. Baculovirus expression, co-immunoprecipitation, in vitro kinase assay The Biochemical journal High 1334406
2006 Influenza A virus NS1 protein binds directly and specifically to p85β (but not p85α) regulatory subunit of PI3K. This interaction activates PI3K signaling and AKT phosphorylation; a Y89F mutation in NS1 disrupts both the interaction and PI3K activation, and the mutant virus shows a small-plaque phenotype and slower growth. Co-immunoprecipitation, in vitro binding assay, site-directed mutagenesis, recombinant virus rescue, PI3K activity assay Proceedings of the National Academy of Sciences of the United States of America High 16963558
2008 NS1 binds specifically to the inter-SH2 (iSH2) domain of p85β; Val-573 in p85β iSH2 is the critical residue mediating the interaction. Substitution of the corresponding Met-582 in p85α to Val confers NS1 binding (gain-of-function). NS1, p85β, and p110 form a trimeric complex in cells. Mutant virus with NS1 unable to bind p85β fails to upregulate p85β-associated PI3K activity. Co-immunoprecipitation, mutagenesis, gain-of-function p85α mutant, PI3K activity assay, competition experiments The Journal of biological chemistry High 18534979
2001 Genetic deletion of p85β (Pik3r2−/− mice) results in hypoglycemia, hypoinsulinemia, and improved insulin sensitivity. PI3K activity associated with phosphotyrosine complexes is preserved despite ~20–30% reduction in total regulatory subunit protein. Insulin-induced AKT activation is significantly upregulated in muscle from p85β−/− mice, and insulin-dependent IRS-2 tyrosine phosphorylation is specifically enhanced—a phenotype not observed in p85α−/− mice. This demonstrates a negative regulatory role of p85β in insulin signaling beyond its role in PI3K recruitment. Germline gene knockout (mice), PI3K activity assay, immunoblot for AKT phosphorylation, glucose/insulin tolerance tests Proceedings of the National Academy of Sciences of the United States of America High 11752399
2003 In brown adipose cell lines, Pik3r2−/− (p85β−/−) cells show 25% reduction in p85 protein but normal PI3K activity, yet significantly increased insulin-induced AKT activation and glycogen synthase activation. Reconstitution experiments indicate that the excess free p85 (including p85β) negatively regulates downstream PI3K signaling independently of its role in catalytic subunit recruitment. Additionally, a p85-dependent, PI3K-independent signaling pathway for JNK activation was identified that is specific to p85α. Genetic KO cell lines, reconstitution with p85 constructs, PI3K activity assay, immunoblot, glucose uptake assay The Journal of biological chemistry High 14504291
2010 p85α and p85β form heterodimers that are disrupted by insulin treatment. The resulting monomers of p85 interact with the spliced form of XBP-1 (XBP-1s) and increase its nuclear translocation. In ob/ob mice, the p85–XBP-1s interaction is lost, impairing XBP-1s nuclear translocation and ER stress resolution; overexpression of p85α and p85β in ob/ob mouse liver ameliorates these defects. Co-immunoprecipitation, adenoviral overexpression in liver, immunofluorescence/subcellular fractionation, ob/ob mouse model Nature medicine High 20348926
2011 PIK3R2 (p85β) is frequently mutated in endometrial cancer. Multiple PIK3R1 and PIK3R2 mutations demonstrate gain-of-function activity. A novel regulatory mechanism is identified: p85α dimers bind and stabilize PTEN protein; mutations disrupting this interaction reduce PTEN stability. p85β mutations phenocopy PTEN loss by activating PI3K pathway signaling. Sequencing of tumor samples, functional mutation assays, PTEN stability assay, PI3K pathway activation readout Cancer discovery High 21984976
2013 The F-box protein FBXL2 specifically interacts with the pool of p85β that is free of p110 PI3K catalytic subunits and targets this pool for ubiquitylation and proteasomal degradation. FBXL2-mediated degradation requires integrity of the p85β CaaX motif. Phosphorylation of p85β on Tyr655 (by an unspecified kinase) inhibits its binding to FBXL2; dephosphorylation of pTyr655 by the tyrosine phosphatase PTPL1 promotes p85β binding to FBXL2 and its subsequent degradation. Defects in FBXL2-mediated degradation of p85β inhibit binding of p110 subunits to IRS1, attenuate the PI3K signaling cascade, and promote autophagy. Affinity purification/MS of FBXL2 complex, Co-IP, ubiquitylation assay, proteasome inhibitor experiments, phospho-mutant analysis Nature cell biology High 23604317
1993 T cells express both p85α and p85β, both of which associate with p110 and PI3K activity. Upon TCR/CD3 stimulation or PKC activation, p85β undergoes rapid and marked phosphorylation on threonine residues, whereas the p110 complexed with p85α becomes phosphorylated on serine residues. This differential phosphorylation reveals divergent regulation of the two PI3K isoforms during T cell activation. Immunoprecipitation with isoform-specific antibodies, phosphopeptide affinity isolation, phosphoamino acid analysis, kinase assay The Journal of biological chemistry Medium 8388374
2010 PTEN protein phosphatase activity acts on p85β as a substrate: insulin stimulates phosphorylation of tyrosine and threonine/proline residues on p85β in Huh-7 and HEK293 cells, and PTEN specifically binds and dephosphorylates p85β. PTEN does not show the same activity on p85α. Co-immunoprecipitation, phosphatase assay, phospho-specific immunoblot, siRNA knockdown Biochemical and biophysical research communications Medium 20515662
2009 p85β binds to CD28 and to CBL ubiquitin ligase with greater affinity than p85α. Deletion of p85β impairs CD28-induced PI3K pathway activation and c-CBL/CBL-b downregulation, resulting in defective T cell differentiation and impaired secondary immune response. Co-immunoprecipitation, p85β knockout mice, T cell proliferation and differentiation assays, immunoblot Blood Medium 19190244
2012 p85β expression is elevated in breast and colon carcinomas; increased p85β induces moderate PIP3 generation at the plasma membrane and enhanced cell invasion. Genetic alteration of Pik3r2 expression modulates tumor progression in vivo in xenograft models. Immunohistochemistry, PIP3 production assay, invasion assay, in vivo xenograft model Proceedings of the National Academy of Sciences of the United States of America Medium 22733740
2014 Expression of p85β alone is sufficient to induce oncogenic transformation of primary avian fibroblasts, dependent on an active PI3K-TOR signaling cascade and mediated through p110α and p110β isoforms. p85β is a less effective inhibitor of the PI3K catalytic subunit than p85α, and this reduced inhibition accounts for its oncogenic activity. Oncogenic transformation assay in primary avian fibroblasts, PI3K pathway reporter, pharmacological inhibitors Proceedings of the National Academy of Sciences of the United States of America Medium 25385636
2017 Domain swap and deletion analysis reveals that in p85β the cSH2 domain exerts an activating effect on PI3K/oncogenic signaling (opposite to p85α where cSH2 is inhibitory). Deletion of the SH3 domain increases oncogenic and PI3K signaling activity of p85β; deletion of SH3-RhoGAP domains abolishes this activity. Domain exchanges confirm that p85β cSH2 exerts activating effects even in the p85α context. Domain deletion/substitution mutants, oncogenic transformation assay, PI3K signaling readouts Oncotarget Medium 28915558
2014 p85β localizes at cell adhesions in complex with focal adhesion kinase (FAK) and enhances stability/maturation of cell adhesions. p85β induces F-actin polymerization at cell adhesions by recruiting active Cdc42/Rac, leading to formation of invadopodium-like structures. p85β depletion reduces invadopodium formation and invasion; p85β levels increase in metastatic melanoma. Fluorescence microscopy, co-immunoprecipitation, siRNA knockdown, invasion assay, F-actin staining Biology open Medium 25217619
2020 p85β upregulates the protein level of the receptor tyrosine kinase AXL by disrupting autophagic degradation of AXL. Mechanistically, p85β alters phosphorylation of TRIM2 (E3 ligase) and optineurin (autophagy receptor), preventing selective autophagic degradation of AXL. p85β activates p110 activity and AKT-independent PDK1/SGK3 signaling; all of these are abolished upon AXL inhibition. Co-immunoprecipitation, phosphoproteomics, autophagy flux assay, knockdown/overexpression, kinase activity assay Nature communications High 32385243
2022 p85β dissociates from p110α carrying a PIK3CA helical domain mutation and translocates into the nucleus via a nuclear localization sequence (NLS). Nuclear p85β recruits deubiquitinase USP7 to stabilize EZH1 and EZH2, enhancing H3K27 trimethylation. Knockout of p85β or NLS mutation reduces growth of helical-domain-mutant tumors. Subcellular fractionation, Co-immunoprecipitation, ChIP-seq, xenograft tumor model, NLS mutagenesis Nature communications High 35418124
2023 FAK phosphorylates p85β at Y464, which enhances the binding of p85β to importin KPNA1 and facilitates its nuclear translocation in kidney cells. Nuclear (but not cytoplasmic) p85β promotes ccRCC tumorigenesis by repressing RB1 expression through stabilization of EZH1/EZH2, regulating G1/S cell cycle transition. FAK inhibitor defactinib suppresses ccRCC tumor growth in models with high p85β Y464 levels. Phospho-site mutagenesis, Co-immunoprecipitation, subcellular fractionation, xenograft model, FAK inhibitor treatment Cell reports High 36857183
2025 Nuclear p85β physically interacts with transcription factor BCLAF1 and acts as a transcriptional co-factor. Multi-omics (ChIP-seq, RNA-seq) shows genome-wide co-occupancy of p85β and BCLAF1 at gene targets. BCLAF1 recruits p85β to its own locus; p85β facilitates assembly of BCLAF1, TRIM28, and ZNF263 to activate BCLAF1 transcription (positive autoregulation). This nuclear transcriptional activity contributes to oncogenic potential. ChIP-seq, RNA-seq, Co-immunoprecipitation, multi-omics, loss-of-function experiments Nature communications High 40016211
2022 FER tyrosine kinase phosphorylates IRS4 at Tyr779, enabling IRS4 to recruit PIK3R2/p85β (the PI3K regulatory subunit) via its SH2 domain, thereby activating the PI3K-AKT pathway. Phosphorylation-defective IRS4 mutant (Y779F) fails to recruit p85β and delays ovarian tumor cell proliferation in vitro and in vivo. Mass spectrometry, proximity-based tagging, Co-immunoprecipitation, kinase assay, phospho-mutant rescue, in vivo tumor model eLife High 35550247
2024 The disordered region of the p85β iSH2 domain contains AP-2 binding motifs that trigger clathrin- and dynamin-mediated endocytosis independently of PI3K catalytic activity. AP-2 binding motif mutants of p85β aberrantly accumulate at focal adhesions and increase both velocity and persistence in fibroblast migration, demonstrating a non-catalytic role for p85β/PI3K in cell motility. Mutagenesis of AP-2 binding motifs, live cell imaging, clathrin/dynamin inhibitors, focal adhesion microscopy Nature communications High 38521786
2012 Loss of p85β enhances KIT-induced proliferation and reduces IL-3-mediated mast cell maturation. Overexpression of p85β represses these processes partly by impaired ligand-induced KIT receptor internalization and increased binding of c-Cbl to p85β relative to p85α. In vivo, overexpression of p85β suppresses growth of oncogenic KIT-expressing cells and prolongs survival of leukemic mice. p85β KO mice, retroviral overexpression, proliferation assay, receptor internalization assay, Co-IP, bone marrow transplantation Blood Medium 22378847
2010 Crystal structure of the human p85β iSH2 domain (coiled-coil motif) determined at 3.3 Å resolution. Comparison with the bovine p85β iSH2/NS1 complex shows little structural change upon NS1 binding. The domain exhibits conformational plasticity in the interhelical turn region, which may regulate its functional and molecular-recognition properties. X-ray crystallography Acta crystallographica. Section F Medium 21139197
2011 X-ray structure of the SH3 domain of human p85β determined at 2.0 Å resolution reveals a compact β-barrel fold similar to p85α SH3. Binding studies with proline-rich ligand peptides show slightly different ligand-binding specificity between p85β and p85α SH3 domains despite high structural similarity. X-ray crystallography, ligand peptide binding assay Acta crystallographica. Section F Medium 22102226
1998 A fusion oncogene was isolated comprising the p85β subunit of PI3K and HUMORF8 (a putative deubiquitinating enzyme), generated during DNA transfection. Tumorigenicity assays in nude mice showed that the recombination of both p85β and HUMORF8, rather than truncation of either alone, confers tumorigenic activity. Additionally, p85β has an Ala at a position that is Ser in p85α, corresponding to a residue important for regulation of PI3K lipid kinase activity. Nude mouse tumorigenicity assay, genomic cloning, cDNA sequencing Oncogene Low 9582025
2004 T cells lacking p85β show a marked increase in proliferation and decreased death upon anti-CD3 + IL-2 stimulation. Transcriptional profiling revealed reduced caspase-6 mRNA in p85β-deficient T cells, paralleled by reduced caspase-6 enzyme activity. Increased T cell accumulation was also observed in vivo after viral infection of p85β-deficient mice. p85β KO mice, in vitro T cell stimulation, proliferation assay, gene expression profiling, caspase activity assay, in vivo viral infection model Journal of immunology Medium 15153476
2009 In B cells, loss of p85β alone does not impair B cell development but loss of both p85β and p85α causes greater defects in B cell development and peripheral survival than loss of p85α alone, indicating partial functional redundancy. Unexpectedly, loss of p85β results in increased BCR-mediated proliferation and ERK phosphorylation, indicating a unique inhibitory role for p85β in opposing BCR responses. p85β KO mice, B cell development analysis, BCR stimulation assay, AKT/ERK phosphorylation immunoblot, proliferation assay Autoimmunity Medium 19811262
2019 A C-SH2 point mutation in p85β (p85β mutant) activates the longevity protein FOXO in response to NGF and confers resistance to oxidative stress. Mutant p85β alters downstream PI3K signaling in response to NGF and PDGF but not insulin. Mutant transgenic mice show increased serum insulin and low blood glucose. Point mutant p85β transgenic mice, FOXO reporter, oxidative stress assay, immunoblot Scientific reports Low 31481652
2024 NSUN2-mediated m5C methylation stabilizes PIK3R2 mRNA, increasing PIK3R2 protein and activating PI3K-AKT signaling. Silencing NSUN2 decreases m5C levels, reduces PIK3R2 mRNA stability, and suppresses PI3K-AKT signaling and lung adenocarcinoma cell proliferation and invasion. m5C-RIP-qPCR, mRNA stability assay, siRNA knockdown, RNA-seq, xenograft model Molecular carcinogenesis Medium 38411298
2025 YTHDF2 binds m6A-modified PIK3R2 mRNA and undergoes liquid-liquid phase separation (LLPS) driven by m6A, promoting YTHDF2-mediated degradation of PIK3R2 mRNA. This suppresses PI3K-AKT signaling activity and promotes arsenite-induced oxidative stress in keratinocytes. m6A-RIP, YTHDF2 knockdown, phase separation assay, mRNA stability assay, PI3K-AKT immunoblot International journal of biological macromolecules Medium 40473165
2022 YWHAB (14-3-3β) physically interacts with PIK3R2 (p85β) as demonstrated by co-immunoprecipitation; YWHAB knockdown decreases PIK3R2 expression and suppresses PI3K/AKT pathway activation. PIK3R2 overexpression reverses the antiproliferative effects of YWHAB knockdown in colon cancer cells. Co-immunoprecipitation, siRNA knockdown, overexpression rescue, PI3K/AKT immunoblot, cell cycle analysis Experimental and therapeutic medicine Low 37090079
2021 EFNA4 interacts directly with EPHA2 and promotes its phosphorylation at Ser897, which then recruits PIK3R2 and activates GSK3β/β-catenin signaling. Overexpression of β-catenin further promotes PIK3R2 expression, forming a positive feedback loop driving HCC proliferation and migration. Co-immunoprecipitation, phosphorylation assay, siRNA knockdown, in vivo tumor model Molecular therapy. Nucleic acids Low 34484860
2022 SPTBN1 binds directly to PIK3R2 in fibroblast-like synoviocytes (confirmed by immunoprecipitation). SPTBN1 overexpression inhibits PI3K/AKT signaling through this interaction; PIK3R2 depletion reverses the anti-inflammatory and pro-apoptotic effects of SPTBN1 overexpression, placing PIK3R2 downstream of SPTBN1 in this pathway. Immunoprecipitation, siRNA knockdown, PI3K/AKT immunoblot, cell functional assays Immunity, inflammation and disease Low 36444616

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 De novo germline and postzygotic mutations in AKT3, PIK3R2 and PIK3CA cause a spectrum of related megalencephaly syndromes. Nature genetics 557 22729224
2011 High frequency of PIK3R1 and PIK3R2 mutations in endometrial cancer elucidates a novel mechanism for regulation of PTEN protein stability. Cancer discovery 398 21984976
2006 Influenza A virus NS1 protein binds p85beta and activates phosphatidylinositol-3-kinase signaling. Proceedings of the National Academy of Sciences of the United States of America 257 16963558
2010 The regulatory subunits of PI3K, p85alpha and p85beta, interact with XBP-1 and increase its nuclear translocation. Nature medicine 245 20348926
2001 Increased insulin sensitivity in mice lacking p85beta subunit of phosphoinositide 3-kinase. Proceedings of the National Academy of Sciences of the United States of America 193 11752399
2011 Endothelial-specific intron-derived miR-126 is down-regulated in human breast cancer and targets both VEGFA and PIK3R2. Molecular and cellular biochemistry 175 21249429
2011 Structure of lipid kinase p110β/p85β elucidates an unusual SH2-domain-mediated inhibitory mechanism. Molecular cell 167 21362552
2003 Positive and negative roles of p85 alpha and p85 beta regulatory subunits of phosphoinositide 3-kinase in insulin signaling. The Journal of biological chemistry 165 14504291
2019 The Opposing Roles of PIK3R1/p85α and PIK3R2/p85β in Cancer. Trends in cancer 113 30961830
2002 Phosphorylation of p85 beta PIX, a Rac/Cdc42-specific guanine nucleotide exchange factor, via the Ras/ERK/PAK2 pathway is required for basic fibroblast growth factor-induced neurite outgrowth. The Journal of biological chemistry 112 12226077
2013 FBXL2- and PTPL1-mediated degradation of p110-free p85β regulatory subunit controls the PI(3)K signalling cascade. Nature cell biology 109 23604317
2014 MiR-126-3p suppresses tumor metastasis and angiogenesis of hepatocellular carcinoma by targeting LRP6 and PIK3R2. Journal of translational medicine 100 25240815
2020 Exosomes from microRNA-126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2-mediated PI3K/Akt signalling pathway. Journal of cellular and molecular medicine 90 33350092
1993 Divergent regulation of phosphatidylinositol 3-kinase P85 alpha and P85 beta isoforms upon T cell activation. The Journal of biological chemistry 86 8388374
2022 Pan-cancer analysis on the role of PIK3R1 and PIK3R2 in human tumors. Scientific reports 85 35395865
2017 MicroRNA-126-3p attenuates blood-brain barrier disruption, cerebral edema and neuronal injury following intracerebral hemorrhage by regulating PIK3R2 and Akt. Biochemical and biophysical research communications 84 29042193
2013 microRNA 126 inhibits the transition of endothelial progenitor cells to mesenchymal cells via the PIK3R2-PI3K/Akt signalling pathway. PloS one 76 24349482
2016 MicroRNA-126 Targeting PIK3R2 Inhibits NSCLC A549 Cell Proliferation, Migration, and Invasion by Regulation of PTEN/PI3K/AKT Pathway. Clinical lung cancer 74 27236384
2019 Megalencephaly syndromes associated with mutations of core components of the PI3K-AKT-MTOR pathway: PIK3CA, PIK3R2, AKT3, and MTOR. American journal of medical genetics. Part C, Seminars in medical genetics 73 31441589
2012 The miR-126 regulates angiopoietin-1 signaling and vessel maturation by targeting p85β. Biochimica et biophysica acta 73 22867989
1992 Expression and characterization of the p85 subunit of the phosphatidylinositol 3-kinase complex and a related p85 beta protein by using the baculovirus expression system. The Biochemical journal 67 1334406
2012 p85β phosphoinositide 3-kinase subunit regulates tumor progression. Proceedings of the National Academy of Sciences of the United States of America 65 22733740
2016 MicroRNA-126 affects rheumatoid arthritis synovial fibroblast proliferation and apoptosis by targeting PIK3R2 and regulating PI3K-AKT signal pathway. Oncotarget 61 27729613
2015 Upregulation of MicroRNA-126 Contributes to Endothelial Progenitor Cell Function in Deep Vein Thrombosis via Its Target PIK3R2. Journal of cellular biochemistry 61 25652288
2015 Characterisation of mutations of the phosphoinositide-3-kinase regulatory subunit, PIK3R2, in perisylvian polymicrogyria: a next-generation sequencing study. The Lancet. Neurology 59 26520804
2015 microRNA-126 targeting PIK3R2 promotes rheumatoid arthritis synovial fibro-blasts proliferation and resistance to apoptosis by regulating PI3K/AKT pathway. Experimental and molecular pathology 59 26723864
2008 Mechanism of influenza A virus NS1 protein interaction with the p85beta, but not the p85alpha, subunit of phosphatidylinositol 3-kinase (PI3K) and up-regulation of PI3K activity. The Journal of biological chemistry 59 18534979
2004 Enhanced T cell proliferation in mice lacking the p85beta subunit of phosphoinositide 3-kinase. Journal of immunology (Baltimore, Md. : 1950) 57 15153476
2013 Synergistic effect of the PDZ and p85β-binding domains of the NS1 protein on virulence of an avian H5N1 influenza A virus. Journal of virology 49 23408626
2005 p85 beta-PIX is required for cell motility through phosphorylations of focal adhesion kinase and p38 MAP kinase. Experimental cell research 44 15893751
2022 lncRNA XLOC013218 promotes cell proliferation and TMZ resistance by targeting the PIK3R2-mediated PI3K/AKT pathway in glioma. Cancer science 41 35637600
2020 miR-126 reduces trastuzumab resistance by targeting PIK3R2 and regulating AKT/mTOR pathway in breast cancer cells. Journal of cellular and molecular medicine 41 32410348
2016 MiR-126 regulates proliferation and invasion in the bladder cancer BLS cell line by targeting the PIK3R2-mediated PI3K/Akt signaling pathway. OncoTargets and therapy 38 27578985
2014 Oncogenic activity of the regulatory subunit p85β of phosphatidylinositol 3-kinase (PI3K). Proceedings of the National Academy of Sciences of the United States of America 38 25385636
2003 Protein profiling of the human epidermis from the elderly reveals up-regulation of a signature of interferon-gamma-induced polypeptides that includes manganese-superoxide dismutase and the p85beta subunit of phosphatidylinositol 3-kinase. Molecular & cellular proteomics : MCP 37 12644569
1998 An oncogenic fusion product of the phosphatidylinositol 3-kinase p85beta subunit and HUMORF8, a putative deubiquitinating enzyme. Oncogene 36 9582025
2016 MiR-126 overexpression inhibits high glucose-induced migration and tube formation of rhesus macaque choroid-retinal endothelial cells by obstructing VEGFA and PIK3R2. Journal of diabetes and its complications 33 28131600
2009 p85beta phosphoinositide 3-kinase regulates CD28 coreceptor function. Blood 33 19190244
2021 Cotargeting of miR-126-3p and miR-221-3p inhibits PIK3R2 and PTEN, reducing lung cancer growth and metastasis by blocking AKT and CXCR4 signalling. Molecular oncology 31 34107168
2022 Nuclear translocation of p85β promotes tumorigenesis of PIK3CA helical domain mutant cancer. Nature communications 30 35418124
2007 Genetic and pharmacologic evidence implicating the p85 alpha, but not p85 beta, regulatory subunit of PI3K and Rac2 GTPase in regulating oncogenic KIT-induced transformation in acute myeloid leukemia and systemic mastocytosis. Blood 29 17483298
2020 p85β regulates autophagic degradation of AXL to activate oncogenic signaling. Nature communications 27 32385243
2017 Structure-Guided Functional Annotation of the Influenza A Virus NS1 Protein Reveals Dynamic Evolution of the p85β-Binding Site during Circulation in Humans. Journal of virology 25 28814525
2017 Domain analysis reveals striking functional differences between the regulatory subunits of phosphatidylinositol 3-kinase (PI3K), p85α and p85β. Oncotarget 25 28915558
2022 FER-mediated phosphorylation and PIK3R2 recruitment on IRS4 promotes AKT activation and tumorigenesis in ovarian cancer cells. eLife 24 35550247
2021 EFNA4 promotes cell proliferation and tumor metastasis in hepatocellular carcinoma through a PIK3R2/GSK3β/β-catenin positive feedback loop. Molecular therapy. Nucleic acids 24 34484860
2020 MiR-126-3p-Enriched Extracellular Vesicles from Hypoxia-Preconditioned VSC 4.1 Neurons Attenuate Ischaemia-Reperfusion-Induced Pain Hypersensitivity by Regulating the PIK3R2-Mediated Pathway. Molecular neurobiology 23 33029740
2014 Phosphoinositide 3-kinase p85beta regulates invadopodium formation. Biology open 23 25217619
2010 The p85beta regulatory subunit of PI3K serves as a substrate for PTEN protein phosphatase activity during insulin mediated signaling. Biochemical and biophysical research communications 23 20515662
2024 NSUN2 promotes lung adenocarcinoma progression through stabilizing PIK3R2 mRNA in an m5C-dependent manner. Molecular carcinogenesis 22 38411298
2020 CAPN1 promotes malignant behavior and erlotinib resistance mediated by phosphorylation of c-Met and PIK3R2 via degrading PTPN1 in lung adenocarcinoma. Thoracic cancer 22 32395869
2019 Candidate tumor suppressor gene IRF6 is involved in human breast cancer pathogenesis via modulating PI3K-regulatory subunit PIK3R2 expression. Cancer management and research 22 31417306
2015 Epigenetic silencing of tumor suppressor miR-3151 contributes to Chinese chronic lymphocytic leukemia by constitutive activation of MADD/ERK and PIK3R2/AKT signaling pathways. Oncotarget 22 26517243
2022 The ClinGen Brain Malformation Variant Curation Expert Panel: Rules for somatic variants in AKT3, MTOR, PIK3CA, and PIK3R2. Genetics in medicine : official journal of the American College of Medical Genetics 21 35997716
2016 De novo PIK3R2 variant causes polymicrogyria, corpus callosum hyperplasia and focal cortical dysplasia. European journal of human genetics : EJHG 21 26860062
2015 MicroRNA‑126 inhibits proliferation and metastasis by targeting pik3r2 in prostate cancer. Molecular medicine reports 21 26677064
2022 METTL3 contributes to slow transit constipation by regulating miR-30b-5p/PIK3R2/Akt/mTOR signaling cascade through DGCR8. Journal of gastroenterology and hepatology 20 36068012
2016 MicroRNA-126-3p suppresses cell proliferation by targeting PIK3R2 in Kaposi's sarcoma cells. Oncotarget 20 27191494
2015 MicroRNA-126 suppresses proliferation of undifferentiated (BRAF(V600E) and BRAF(WT)) thyroid carcinoma through targeting PIK3R2 gene and repressing PI3K-AKT proliferation-survival signalling pathway. Experimental cell research 19 26384552
2016 Targeted depletion of PIK3R2 induces regression of lung squamous cell carcinoma. Oncotarget 18 27835880
2009 The p85beta regulatory subunit of phosphoinositide 3-kinase has unique and redundant functions in B cells. Autoimmunity 17 19811262
2023 LncRNA HOTAIR regulates the PI3K/AKT pathway via the miR-126-3p/PIK3R2 axis to participate in synovial angiogenesis in rheumatoid arthritis. Immunity, inflammation and disease 15 37904709
2021 Cell specific tumor suppressor effect of Hsa-miR-1226-3p through downregulation of HER2, PIK3R2, and AKT1 genes. The international journal of biochemistry & cell biology 15 33675995
1992 Chromosomal localization of human p85 alpha, a subunit of phosphatidylinositol 3-kinase, and its homologue p85 beta. Oncogene 13 1314371
2024 Extracellular vesicles derived from endothelial progenitor cells modified by Houshiheisan promote angiogenesis and attenuate cerebral ischemic injury via miR-126/PIK3R2. Scientific reports 12 39548169
2024 SNAI1 promotes epithelial-mesenchymal transition and maintains cancer stem cell-like properties in thymic epithelial tumors through the PIK3R2/p-EphA2 Axis. Journal of experimental & clinical cancer research : CR 12 39702326
2023 FAK-mediated phosphorylation at Y464 regulates p85β nuclear translocation to promote tumorigenesis of ccRCC by repressing RB1 expression. Cell reports 12 36857183
2021 p85β alters response to EGFR inhibitor in ovarian cancer through p38 MAPK-mediated regulation of DNA repair. Neoplasia (New York, N.Y.) 12 34144267
2011 New routes to old places: PIK3R1 and PIK3R2 join PIK3CA and PTEN as endometrial cancer genes. Cancer discovery 12 22586352
2021 miR-126 Controls the Apoptosis and Proliferation of Immature Porcine Sertoli Cells by Targeting the PIK3R2 Gene through the PI3K/AKT Signaling Pathway. Animals : an open access journal from MDPI 11 34438716
2020 PIK3R2/Pik3r2 Activating Mutations Result in Brain Overgrowth and EEG Changes. Annals of neurology 10 32856318
2024 Non-catalytic role of phosphoinositide 3-kinase in mesenchymal cell migration through non-canonical induction of p85β/AP2-mediated endocytosis. Nature communications 9 38521786
2023 YWHAB knockdown inhibits cell proliferation whilst promoting cell cycle arrest and apoptosis in colon cancer cells through PIK3R2. Experimental and therapeutic medicine 9 37090079
2022 SPTBN1 attenuates rheumatoid arthritis synovial cell proliferation, invasion, migration and inflammatory response by binding to PIK3R2. Immunity, inflammation and disease 9 36444616
2021 A PIK3R2 Mutation in Familial Temporal Lobe Epilepsy as a Possible Pathogenic Variant. Frontiers in genetics 9 34040629
2016 PI3K p85 β regulatory subunit deficiency does not affect NK cell differentiation and increases NKG2D-mediated activation. Journal of leukocyte biology 9 27381007
2012 p85β regulatory subunit of class IA PI3 kinase negatively regulates mast cell growth, maturation, and leukemogenesis. Blood 9 22378847
2021 Asiatic acid alleviates Ang-II induced cardiac hypertrophy and fibrosis via miR-126/PIK3R2 signaling. Nutrition & metabolism 8 34256802
2010 Heterologous SH3-p85beta inhibits influenza A virus replication. Virology journal 8 20653952
2022 The regulatory subunits of PI3K, p85α and p85β, differentially affect BRD7-mediated regulation of insulin signaling. Journal of molecular cell biology 7 34751372
2021 Understanding the Binding Transition State After the Conformational Selection Step: The Second Half of the Molecular Recognition Process Between NS1 of the 1918 Influenza Virus and Host p85β. Frontiers in molecular biosciences 6 34307465
2010 Structure of the iSH2 domain of human phosphatidylinositol 3-kinase p85β subunit reveals conformational plasticity in the interhelical turn region. Acta crystallographica. Section F, Structural biology and crystallization communications 6 21139197
2024 Differential miRNA Profiling Reveals miR-4433a-5p as a Key Regulator of Chronic Obstructive Pulmonary Disease Progression via PIK3R2- mediated Phenotypic Modulation. Combinatorial chemistry & high throughput screening 5 38178680
2024 Ethoxy-erianin phosphate inhibits angiogenesis in colorectal cancer by regulating the TMPO-AS1/miR-126-3p/PIK3R2 axis and inactivating the PI3k/AKT signaling pathway. BMC cancer 5 39402462
2025 YTHDF2 phase separation promotes arsenite-induced oxidative stress by facilitating YTHDF2-mediated PIK3R2 mRNA degradation. International journal of biological macromolecules 4 40473165
2020 Generation of a human induced pluripotent stem cell line from an epilepsy patient carrying mutations in the PIK3R2 gene. Stem cell research 4 32155459
2025 Gestational diabetes mellitus-derived miR-7-19488 targets PIK3R2 mRNA to stimulate the abnormal development and maturation of offspring-islets. Life sciences 3 39778763
2023 Chitosan inhibits vascular intimal hyperplasia via LINC01615/MIR-185-5p/PIK3R2 signaling pathway. Gene 3 37778418
2023 MicroRNA-126-3P targets PIK3R2 to ameliorate autophagy and apoptosis of cortex in hypoxia-reoxygenation treated neonatal rats. Cellular and molecular biology (Noisy-le-Grand, France) 3 38063094
2019 C-SH2 point mutation converts p85β regulatory subunit of phosphoinositide 3-kinase to an anti-aging gene. Scientific reports 3 31481652
2020 Oncogenic pathway driven by p85β: upstream signals to activate p110. Molecular & cellular oncology 2 32944639
2025 Novel Small-Molecule miR-124 Inducer Acts as "a Physiological Brake" of Inflammation in Ulcerative Colitis by Targeting the PIK3R2/PI3K/Akt Axis. Journal of medicinal chemistry 1 40553443
2021 MiR-126 Regulates Proliferation and Invasion in the Bladder Cancer BLS Cell Line by Targeting the PIK3R2-Mediated PI3K/Akt Signaling Pathway [Retraction]. OncoTargets and therapy 1 33732003
2011 X-ray structure of the SH3 domain of the phosphoinositide 3-kinase p85β subunit. Acta crystallographica. Section F, Structural biology and crystallization communications 1 22102226
2026 Macrophage-Derived Ferritin Exacerbates Silica-Induced Pulmonary Fibrosis via PIK3R2-Mediated Fibroblast Differentiation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41566645
2026 ERβ-PIK3R2 axis promotes estrogen-driven gastric cancer progression. Biochemical and biophysical research communications 0 41633200
2025 Blocking p85β nuclear translocation by importazole enhances Alpelisib efficacy against PIK3CA-helical-domain-mutant tumors. Biochemical and biophysical research communications 0 39823894
2025 p85β acts as a transcription cofactor and cooperates with BCLAF1 in the nucleus. Nature communications 0 40016211
2023 Non-catalytic role of phosphoinositide 3-kinase in mesenchymal cell migration through non-canonical induction of p85β/AP-2-mediated endocytosis. Research square 0 36712095
2023 Non-catalytic role of phosphoinositide 3-kinase in mesenchymal cell migration through non-canonical induction of p85β/AP-2-mediated endocytosis. bioRxiv : the preprint server for biology 0 36712134

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