PI3K/Akt/mTOR · target hub
Phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma (p110γ)
PIK3CG encodes class IB PI3K p110γ, commonly partnered with PIK3R5/PIK3R6-encoded regulatory subunits (p101/p84-like modules), preferentially coupling GPCR–Ras inputs to PIP3 production with prominent roles in leukocyte chemotaxis, innate immunity, and inflammatory amplification—often co-shaping PI3K dependence with PIK3CD.
| Type / example | Domain / context (brief) |
|---|---|
| p101 / p84 调节亚基 | Partner levels tune membrane recruitment and Gβγ sensitivity—co-assay PIK3R5/R6 |
| Rare PIK3CG variants | Scattered reports—require functional validation |
| WT + GPCR 轴 | Classic modeling around chemokine receptors and G-protein inputs |
| 与 PIK3CD 重叠 | In myeloid cells δ/γ often co-shape chemotaxis/ROS readouts |
p110γ is class IB, commonly assembled with PIK3R5/PIK3R6 (p101/p84-like partners)—its lesion spectrum differs from class IA. Annotate with COSMIC, literature, and holoenzyme expression.
Class IB work must co-track regulatory subunits and G-protein inputs—examples below come from inflammation, allergy, and TAM literature; pilot before large campaigns.
Primary myeloid work needs ethics/biosafety; murine peritoneal macrophages are convenient but differ in receptor profiles from human cells.
p110γ activity depends on Gβγ and regulatory partners—catalytic overexpression alone can overestimate output; human vs murine chemokine receptor profiles differ.
Adds PIK3CG keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.
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
See the PI3K/Akt/mTOR hub for neighboring nodes and assay guidance—cross-check MAPK, RTK, metabolism, and autophagy pages as needed.