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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...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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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...

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Related Experiment Video

Updated: Jun 28, 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

DAPK-ZIPK-L13a axis constitutes a negative-feedback module regulating inflammatory gene expression.

Rupak Mukhopadhyay1, Partho Sarothi Ray, Abul Arif

  • 1Department of Cell Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.

Molecular Cell
|November 11, 2008
PubMed
Summary
This summary is machine-generated.

Interferon-gamma triggers a kinase cascade that phosphorylates ribosomal protein L13a, inhibiting inflammatory gene translation. This pathway also represses the kinases themselves, forming a regulatory module for inflammation resolution.

Related Experiment Videos

Last Updated: Jun 28, 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

Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Biology

Background:

  • The interferon-gamma-activated inhibitor of translation (GAIT) complex represses inflammatory gene expression.
  • Phosphorylation of ribosomal protein L13a is critical for GAIT complex function.

Purpose of the Study:

  • To elucidate the kinase cascade regulating L13a phosphorylation and GAIT complex activity.
  • To investigate the role of this pathway in controlling inflammatory gene expression and resolution.

Main Methods:

  • Kinase assays to identify upstream activators of DAPK and ZIPK.
  • Analysis of L13a phosphorylation and ribosomal association.
  • mRNA and protein expression analysis of GAIT target genes.

Main Results:

  • IFN-gamma activates DAPK, which in turn activates ZIPK, leading to L13a phosphorylation at Ser(77).
  • Phosphorylated L13a is released from the ribosome, silencing translation of GAIT element-bearing mRNAs.
  • The mRNAs encoding DAPK and ZIPK are also targets of this inhibitory pathway.
  • Inhibition of DAPK and ZIPK allows for the re-induction of inflammatory gene expression.

Conclusions:

  • The DAPK-ZIPK-L13a axis is a novel regulatory module controlling inflammatory gene expression.
  • This pathway acts as a checkpoint in macrophage resolution of inflammation.
  • Defects in this axis may contribute to chronic inflammatory diseases.