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Related Concept Videos

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...
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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...
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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...
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Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
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Published on: February 9, 2014

MAP Kinase Phosphatase-1 and Septic Shock.

Yusen Liu1, Thomas P Shanley

  • 1Center for Perinatal Research, Children's Research Institute, Columbus Children's Hospital, Department of Pediatrics, The Ohio State University College of Medicine, Columbus, OH, USA.

Journal of Organ Dysfunction
|September 28, 2011
PubMed
Summary

Mitogen-activated protein kinase phosphatase-1 (MKP-1) is vital for controlling inflammatory cytokine production. MKP-1 knockout mice show severe immune responses, highlighting its role in preventing septic shock.

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05:28

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

Area of Science:

  • Immunology
  • Cellular signaling

Background:

  • Mitogen-activated protein (MAP) kinase cascades are key in inflammatory cytokine biosynthesis.
  • MAP kinase phosphatase (MKP)-1 regulates p38 and JNK pathways, crucial for immune response.
  • In vitro studies suggest MKP-1 restrains pro-inflammatory cytokine production.

Purpose of the Study:

  • To verify the in vivo role of MKP-1 in regulating inflammatory cytokine synthesis.
  • To investigate the function of MKP-1 in the innate immune response and septic shock.

Main Methods:

  • Utilized MKP-1 knockout mouse models.
  • Administered lipopolysaccharide (LPS) challenge to mice.
  • Monitored cytokine production, organ function, and mortality rates.

Main Results:

  • MKP-1 knockout mice exhibited significantly elevated inflammatory cytokine levels post-LPS challenge.
  • These mice developed severe hypotension, multi-organ failure, and increased mortality.
  • MKP-1 deficiency led to an uncontrolled innate immune response.

Conclusions:

  • MKP-1 is an essential feedback regulator of the innate immune response.
  • MKP-1 plays a critical role in preventing septic shock and multi-organ dysfunction.
  • Targeting MKP-1 could be a strategy for managing severe infections.