Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

10.1K
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...
10.1K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

5.1K
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...
5.1K
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

12.4K
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...
12.4K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

15.1K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
15.1K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

7.1K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.1K
Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

7.6K
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...
7.6K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

BACH1 orchestrates macrophage state transitions to coordinate regenerative inflammation.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

Capturing Cardiomyocyte Cell-to-Cell Heterogeneity via Shotgun Single Cell Top-Down Proteomics.

bioRxiv : the preprint server for biology·2026
Same author

Pharmacological Inhibition of SLC33A1 Promotes Endoplasmic Reticulum Hyperoxidation and Induces Adaptive IRE1/XBP1s Signaling.

bioRxiv : the preprint server for biology·2026
Same author

Identification of a Selective Pharmacologic IRE1/XBP1s Activator with Enhanced Tissue Exposure.

ACS chemical biology·2025
Same author

Covalent Targeting As a Common Mechanism for Inhibiting NLRP3 Inflammasome Assembly.

ACS chemical biology·2024
Same author

Covalent targeting as a common mechanism for inhibiting NLRP3 inflammasome assembly.

bioRxiv : the preprint server for biology·2023

Related Experiment Video

Updated: Apr 25, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K

Activating PI3-kinase to dampen inflammation.

Bernard P Kok1, Enrique Saez1

  • 1Department of Chemical Physiology, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.

Chemistry & Biology
|August 16, 2014
PubMed
Summary

Diterpenes from acanthoic acid activate PI3-kinase signaling in macrophages. This molecular mechanism inhibits nuclear factor-kappa B (NF-κB) activation, suppressing inflammatory gene expression in vivo.

Area of Science:

  • Immunology
  • Molecular Biology
  • Natural Products Chemistry

Background:

  • Diterpene derivatives of acanthoic acid exhibit significant anti-inflammatory properties in living organisms.
  • Understanding the precise molecular pathways underlying these effects is crucial for therapeutic development.

Purpose of the Study:

  • To elucidate the primary molecular mechanism of action for diterpenes related to acanthoic acid.
  • To investigate the role of PI3-kinase and NF-κB signaling in mediating the anti-inflammatory effects of these compounds.

Main Methods:

  • The study involved analyzing diterpenes structurally related to acanthoic acid.
  • Experiments were conducted on macrophages to assess signaling pathway activation.
  • Key signaling molecules including PI3-kinase and NF-κB were monitored.

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

8.9K
Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice

Published on: January 31, 2020

6.2K

Related Experiment Videos

Last Updated: Apr 25, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K
Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

8.9K
Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice

Published on: January 31, 2020

6.2K

Main Results:

  • Diterpenes directly activate phosphoinositide 3-kinase (PI3K) signaling pathways.
  • Activated PI3K signaling leads to the inhibition of nuclear factor-kappa B (NF-κB) activation.
  • This cascade ultimately suppresses the expression of pro-inflammatory genes.

Conclusions:

  • The direct activation of PI3-kinase signaling in macrophages is the principal molecular mechanism for the anti-inflammatory action of acanthoic acid-related diterpenes.
  • This pathway provides a novel target for developing new anti-inflammatory therapies.