Related Experiment Video

Updated: May 7, 2026

Time-resolved Förster Resonance Energy Transfer Assays for Measurement of Endogenous Phosphorylated STAT Proteins in Human Cells
07:12

Time-resolved Förster Resonance Energy Transfer Assays for Measurement of Endogenous Phosphorylated STAT Proteins in Human Cells

Published on: September 9, 2021

The JAK-STAT pathway in hypertrophic stress signaling and genomic stress response

Michael A Wagner1, M A Q Siddiqui

  • 1Department of Cell Biology; Center for Cardiovascular and Muscle Research; State University of New York Downstate Medical Center; Brooklyn, NY USA.

JAK-STAT
|September 24, 2013
PubMed

Insights

The Janus kinase- (JAK) and Signal transducer and activator of transcription- (STAT) pathway is key in heart stress signaling. This review explores its complex interactions and role in stress response genes.

Area of Science:

  • Molecular Biology
  • Cardiovascular Biology
  • Cell Signaling

Background:

  • The Janus kinase- (JAK) and Signal transducer and transcription (STAT) pathway is crucial for cellular responses to stress and growth factors in the heart.
  • JAK-STAT signaling exhibits unique versatility, operating through multiple mechanisms and interacting with other signaling cascades.

Purpose of the Study:

  • To review the multifaceted roles of the JAK-STAT pathway in cardiac hypertrophic signaling.
  • To elucidate the mechanisms of IL-6 trans-signaling and JAK-STAT interactions with GPCR-linked pathways.
  • To examine the intersection of JAK-STAT signaling with transcriptional regulation of stress response genes.

Main Methods:

  • Literature review of studies on JAK-STAT signaling in cardiac hypertrophy.
  • Analysis of IL-6 trans-signaling mechanisms.
  • Examination of cross-talk between JAK-STAT and GPCR-linked pathways.
  • Review of transcriptional regulation of STAT-dependent genes.

Main Results:

  • IL-6 activates cells lacking IL-6 receptors via trans-signaling.
  • JAK-STAT pathways interact with GPCR-linked pathways both intracellularly and intercellularly.
  • The JAK-STAT pathway integrates with transcriptional machinery to regulate stress response genes.

Conclusions:

  • The JAK-STAT pathway is a central regulator of cardiac stress and growth.
  • Its complex interactions with other pathways, including IL-6 trans-signaling and GPCR signaling, highlight its adaptability.
  • Understanding these intricate mechanisms is vital for deciphering cardiac stress responses and developing therapeutic strategies.

Keywords:
Il-6 trans-signalingJAK-STAT signaling pathwayangiotensin IIautocrine signalingcardiac hypertrophycardiac lineage protein-1endothelin-1paracrine signalingtranscription elongation factor bαB-crystallin

More Related Videos

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model08:15

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model

Published on: June 6, 2025

Related Concept Videos

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...
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...
Other Stress Responses in Bacteria01:30

Other Stress Responses in Bacteria

Bacteria have global regulatory systems that control several types of stress mechanisms. These include Pho regulon and the heat shock response, which are essential systems for environmental adaptation, such as nutrient limitation and proteotoxic stress. The Pho regulon and the heat shock response exemplify bacterial resilience, enabling rapid adaptation to fluctuating environmental conditions.Pho RegulonBacteria require phosphorus for essential cellular processes, including nucleic acid...
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...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

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,...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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 are of three kinds RI, RII, and RIII. The RI...