PI3K/AKT/mTOR Signaling Pathway Research Reagents

PIK3CA (p110α) — The catalytic subunit of class IA PI3K and one of the most commonly mutated oncogenes in solid tumors. Hotspot mutations (E545K, H1047R) constitutively activate lipid kinase activity independently of upstream RTK input. PIK3CA mutations are frequent in breast cancer (~35%), endometrial cancer (~40%), and colorectal cancer (~15–20%). The PI3Kα-selective inhibitor alpelisib is approved for PIK3CA-mutant HR+/HER2− breast cancer.
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Insulin / IGF-1 — Insulin and insulin-like growth factor 1 are major physiological activators of the PI3K/AKT axis via the insulin receptor (IR) and IGF-1R. Recombinant insulin and IGF-1 are widely used to stimulate AKT phosphorylation, study metabolic signaling, and maintain cell culture and differentiation protocols.
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PTEN — A dual-specificity lipid and protein phosphatase that dephosphorylates PIP3 to PIP2, directly opposing PI3K activity. PTEN is the second most frequently inactivated tumor suppressor after TP53 and is lost across prostate, endometrial, glioblastoma, and breast cancers. PTEN loss results in constitutive AKT activation and is a widely used biomarker for PI3K pathway dependency. Anti-PTEN antibodies are essential tools for IHC-based loss-of-expression screening.
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AKT1/2/3 (PKB) — A family of three serine/threonine kinases that serve as the central signaling node of the pathway. Full AKT activation requires dual phosphorylation: Thr308 by PDK1 and Ser473 by mTORC2. AKT isoforms have partially overlapping but distinct roles — AKT1 primarily drives cell survival and growth, AKT2 regulates glucose uptake and metabolism, and AKT3 is predominantly expressed in the brain. Phospho-AKT (Ser473 and Thr308) antibodies are widely used readouts for pathway activation across Western blot, IHC, and flow cytometry.
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PDK1 (PDPK1) — A constitutively active serine/threonine kinase that phosphorylates AKT at Thr308 and activates multiple AGC family kinases including S6K, SGK, and PKC. PDK1 membrane recruitment via its PH domain is PIP3-dependent, linking PI3K lipid output to AKT activation.
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FOXO3A — A forkhead box transcription factor that promotes apoptosis (BIM, FasL), cell cycle arrest (p27^Kip1), and oxidative stress resistance. AKT phosphorylation of FOXO3A triggers its nuclear exclusion and 14-3-3-mediated cytoplasmic sequestration, effectively suppressing its tumor-suppressive transcriptional program. Nuclear FOXO3A staining by IHC correlates with favorable prognosis in several tumor types.
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mTOR (FRAP1) — A serine/threonine kinase that functions as the catalytic core of two structurally and functionally distinct complexes. mTORC1 (mTOR–Raptor–mLST8) integrates growth factor and nutrient signals to drive protein synthesis, lipid biogenesis, and autophagy suppression; it is sensitive to rapamycin. mTORC2 (mTOR–Rictor–mLST8–mSIN1) phosphorylates AKT at Ser473 and regulates cytoskeletal organization; it is relatively rapamycin-insensitive in acute treatment but can be disrupted by prolonged rapamycin exposure in some cell types.
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S6K1 (RPS6KB1) — A direct mTORC1 substrate that phosphorylates ribosomal protein S6 and eIF4B to promote cap-dependent translation initiation. Phospho-S6K1 (Thr389) is a widely used pharmacodynamic marker for mTORC1 activity in preclinical and clinical studies of rapalogs and mTOR kinase inhibitors.
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4E-BP1 (EIF4EBP1) — An mTORC1 substrate that, in its hypophosphorylated state, binds and sequesters the cap-binding protein eIF4E, blocking cap-dependent translation. mTORC1-mediated hyperphosphorylation of 4E-BP1 releases eIF4E to initiate translation of pro-growth and pro-survival mRNAs (MYC, Cyclin D1, VEGF). The phosphorylation status of 4E-BP1 is a sensitive readout for mTORC1 activity.
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TSC1/TSC2 (Hamartin/Tuberin) — A heterodimeric GAP complex that inactivates the small GTPase RHEB, thereby suppressing mTORC1 signaling. AKT phosphorylation of TSC2 relieves this inhibition, linking PI3K/AKT activation to mTORC1-driven growth. Loss-of-function mutations in TSC1 or TSC2 cause tuberous sclerosis complex, characterized by mTORC1-hyperactive hamartomas in multiple organs. mTORC1 inhibitors (everolimus) are an approved treatment for TSC-associated tumors.
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1. Fruman DA, et al. The PI3K pathway in human disease. Cell. 2017;170(4):605-635. DOI

2. Saxton RA, Sabatini DM. mTOR signaling in growth, metabolism, and disease. Cell. 2017;168(6):960-976. DOI

3. Manning BD, Toker A. AKT/PKB signaling: navigating the network. Cell. 2017;169(3):381-405. DOI

4. Song MS, Salmena L, Bhatt DK, et al. The functions and regulation of the PTEN tumour suppressor. Nat Rev Mol Cell Biol. 2012;13(5):283-296. DOI