PI3K/Akt/mTOR · target hub

PIK3CB

Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit beta (p110β)

PIK3CB encodes p110β, forming class IA PI3K complexes with p85-family regulatory subunits and catalyzing PIP2→PIP3. Compared with PIK3CA, p110β shows broad basal expression across tissues and can be selectively important for viability, platelet signaling, or pathway maintenance in certain PTEN-null contexts—tumor dependency is context-specific.

Back to pathway overviewSearch: PIK3CBUniProt (P42338)

Research notes

  • Overlaps with p110α function yet differs genetically and pharmacologically; combine isoform KD/KO to dissect contributions.
  • Pan-PI3K inhibitors hit multiple isoforms—interpret phenotypes with insulin/RTK stimulation and cell density controls.
  • Assess alongside PIK3CA/PTEN status in glioma, breast, prostate, and other models (literature/database-guided).

On the pathway hub (sections)

Genetic lesions & expression context (quick reference)

Type / exampleDomain / context (brief)
CN gain / amplificationCopy-number gain; reported in resistance/hormone-independent contexts (tumor-type dependent)
Rare missenseCase-report spectrum—validate with functional assays and cohort context
WT + PTEN lossCommon modeling context where p110β helps sustain PIP₃/viability signaling
Broad basal expressionBroad basal expression vs some p110α-biased contexts—pair isoform-selective probes

PIK3CB lacks a PIK3CA-like dominant hotspot spectrum—copy gains, rare missense lesions, and PTEN-null combinatorial contexts are more typical. Annotate with COSMIC, ClinVar, sequencing, and literature.

Assay readouts for p110β / PIK3CB

  • Overlap with p110α on PIP₃, membrane recruitment, and p-AKT/S6K/4E-BP outputs—partition with isoform-selective inhibitors or genetics.
  • Insulin/IGF–IRS and some GPCR inputs often amplify p110β dependence—pair starvation/stimulation titrations.
  • Platelet/hematopoietic contexts highlight p110β (species differences)—design humanized or immune-depleted models deliberately.
  • Annotate PTEN/PIK3CA status and p85 stoichiometry; CRISPR/siRNA titrations help dissect redundancy vs compensation.

PIK3CB experimental notes

Examples below are common literature/public-resource settings to parse p110β contribution—PIK3CB often redundantly overlaps PIK3CA; record both catalytic subunit genotypes and probe panels.

[1] Cell lines commonly used for PIK3CB studies (examples)

  • PTEN-null prostate models: PC-3, DU 145—common for p110β vs p110α compensation under insulin/serum stimulation.
  • Breast/endometrium: PTEN-null or PIK3CA-mutant lines where PIK3CB KD reveals non-redundant addiction (confirm via databases/sequencing).
  • Colorectal: HT-29, SW480 as matrix members; contrast with PIK3CA-mutant HCT116 to partition isoform roles.
  • Tooling: HEK293T co-transfection PIK3CB + PIK3R1/p85 for holoenzyme/pulldown; stable lines for rescue.
  • Isogenics: dual PIK3CA/CB KO, single KO + pharmacologic rescue—to test context-specific β dependence.
  • Megakaryoid/hematopoietic lines as literature-guided—mind species differences for platelet/immune toxicology angles.

[2] Cell samples commonly used for PIK3CB (p110β) Western blot

  • PTEN-null solid tumor lysates—mind higher p110β baseline; load in parallel with PIK3CA tracks.
  • Paired pre/post insulin or IGF stimulation to enrich β-biased engagement—pilot time courses.
  • Primary/short-term cultures—document donor/passage; concentrate lysates if input-limited.
  • Antibody QC: datasheet cross-reactivity; KD/KO to separate p110α/β bands (similar MW—use high-resolution gels or tagged lines).

[3] Tissue samples commonly used for PIK3CB (p110β) Western blot

  • Frozen tumor/adjacent tissues from prostate, breast, endometrium where PTEN lesions are frequent.
  • PDX/xenografts for post-drug p110β and downstream shifts—watch species specificity.
  • Platelet-rich preparations—project-specific; optimize lysis and inhibitors against degradation.
  • FFPE as on PIK3CA guidance—prefer frozen; validated extraction if FFPE is unavoidable.

[4] Cell samples commonly used for PIK3CB (p110β) immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-PIK3CB ± p85 for holoenzyme capture vs mutants.
  • Endogenous IP: PTEN-null prostate lines or high-expression screens—often higher input than PIK3CA-only workflows.
  • Co-IP/sequential IP with PIK3CA when dissecting holoenzyme competition—follow published matrices.
  • Controls: isotype IgG, PIK3CB or PIK3CA KD lines, pan-PI3K inhibitor pretreatment as applicable.

Human tissues/primaries require ethics approval; for blood/platelet-enriched samples, mind spin protocols and activation state for WB/IP.

Resistance & bypass (often with PIK3CB / PTEN contexts)

Models & genetics note

Broad p110β tissue distribution means systemic inhibition needs platelet/immune toxicity readouts; compensation with p110α is best parsed by KO titrations and inhibitor IC50 matrices.

Quick search presets

PIK3CBPI3K β antibodyp110βPI3K p110βPI3K inhibitorTGX-221

PIK3CB-related antibodies (keyword-biased)

Adds PIK3CB keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

PIK3CAPIK3CDPIK3CGPIK3R1PIK3R2PIK3R3PIK3R4PIK3AP1

External databases & resources

FAQ

This content supports research reagents and pathway education—not medical advice. Annotate mutations, drug indications, and protocols with authoritative databases, datasheets, and institutional oversight.

Last reviewed: 2026-05-03

Related on this site

See the PI3K/Akt/mTOR hub for neighboring nodes and assay guidance—cross-check MAPK, RTK, metabolism, and autophagy pages as needed.

PI3K/Akt/mTOR·MAPK/ERK·Receptor tyrosine kinase·Metabolism