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Related Concept Videos

Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
Intracellular Signaling Cascades01:24

Intracellular Signaling Cascades

Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
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...
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

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 the...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
cAMP-dependent Protein Kinase Pathways01:25

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...

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Imaging Spatial Reorganization of a MAPK Signaling Pathway Using the Tobacco Transient Expression System
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Transactivation joins multiple tracks to the ERK/MAPK cascade.

Reinhard Wetzker1, Frank-D Böhmer

  • 1Institute for Molecular Cell Biology, Jena University Hospital, Drackendorfer Strasse 1, D-07747 JENA, Germany. i5rewe@rz.uni-jena.de

Nature Reviews. Molecular Cell Biology
|August 19, 2003
PubMed
Summary

G-protein-coupled receptors (GPCRs) can activate the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway. A multi-track model may explain the complex signaling puzzles observed in GPCR transactivation studies.

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Area of Science:

  • Cellular signaling
  • Molecular biology
  • Biochemistry

Background:

  • G-protein-coupled receptors (GPCRs) are key cellular regulators.
  • GPCR activation can influence other signaling pathways, including receptor tyrosine kinases (RTKs).
  • The extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway is a critical downstream signaling cascade.

Purpose of the Study:

  • To investigate the signaling mechanisms linking GPCRs to the ERK/MAPK pathway.
  • To address the complexities and unresolved questions arising from the 'transactivation' model.
  • To propose an alternative model for understanding GPCR-ERK/MAPK signaling.

Main Methods:

  • Review and analysis of existing literature on GPCR signaling.
  • Examination of experimental data supporting transactivation mechanisms.
  • Conceptual development of a multi-track signaling model.

Main Results:

  • Observed cross-talk between GPCRs and RTKs leading to ERK/MAPK activation.
  • Identified limitations and inconsistencies with a simple linear transactivation model.
  • Proposed a 'multi-track' model to accommodate diverse signaling outcomes.

Conclusions:

  • The 'transactivation' model alone may not fully explain GPCR-mediated ERK/MAPK pathway activation.
  • A 'multi-track' model offers a more comprehensive framework for understanding GPCR signaling to ERK/MAPK.
  • This revised model may resolve existing puzzles in the field of GPCR signaling.