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Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and produces two-second...
Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
Protein kinases
Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...

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The constitutive oncogenic and signaling activities of phosphatidylinositol 3-kinase (PI3K) isoforms p110β and p110δ.

bioRxiv : the preprint server for biology·2025
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Long Non-Coding RNAs as "MYC Facilitators".

Pathophysiology : the official journal of the International Society for Pathophysiology·2023
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Structural insights into the interaction of three Y-shaped ligands with PI3Kα.

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Structural and mechanistic insights provided by single particle cryo-EM analysis of phosphoinositide 3-kinase (PI3Kα).

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The MYC-regulated lncRNA LNROP (ENSG00000254887) enables MYC-driven cell proliferation by controlling the expression of OCT2.

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Cryo-EM structures of cancer-specific helical and kinase domain mutations of PI3Kα.

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Related Experiment Video

Updated: May 24, 2026

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts
11:19

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts

Published on: October 9, 2016

PI3K and STAT3: a new alliance.

Peter K Vogt1, Jonathan Ross Hart

  • 1The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. pkvogt@scripps.edu

Cancer Discovery
|February 21, 2012
PubMed
Summary

The PI3K and STAT3 pathways are linked, with BMX kinase mediating STAT3 activation in PI3K-driven cancers like glioblastoma. Targeting BMX may enhance PI3K inhibitor effectiveness.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Proteomic data reveal an interdependence between Phosphoinositide 3-kinase (PI3K) and Signal transducer and activator of transcription 3 (STAT3) signaling pathways.
  • STAT3 phosphorylation and activation are PI3K-dependent in transformed murine cells, suggesting a functional link between these pathways.

Purpose of the Study:

  • To investigate the role of STAT3 and the TEC kinase BMX in PI3K-driven oncogenesis.
  • To explore BMX as a potential therapeutic target in cancers involving PI3K and STAT3 signaling.

Main Methods:

  • Analysis of PI3K-transformed murine cells to assess STAT3 phosphorylation and activation.
  • Utilizing dominant-negative STAT3 to evaluate its role in PI3K-induced transformation.
  • Investigating the involvement of the TEC kinase BMX in STAT3 phosphorylation.
Keywords:
BMXPH domainSILACTEC kinaseTOR

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  • Examining the roles of STAT3 and BMX in glioblastoma stem cells.

    • Main Results:

    • STAT3 is phosphorylated on Y705 and activated in a PI3K-dependent manner in transformed murine cells.
    • STAT3 plays a critical role in PI3K-induced oncogenic transformation.
    • The TEC kinase BMX mediates STAT3 phosphorylation in PI3K-transformed cells.
    • STAT3 and BMX exhibit similar critical roles in glioblastoma stem cells.

    Conclusions:

    • A functional link exists between the PI3K–TOR and STAT3 signaling pathways.
    • STAT3 is crucial for PI3K-driven oncogenic transformation.
    • The TEC kinase BMX is identified as a novel therapeutic target for enhancing PI3K inhibitor efficacy in cancer treatment.