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Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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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
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Enzyme-linked Receptors01:00

Enzyme-linked Receptors

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Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
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Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

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Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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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...
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Signal Transduction: Overview01:26

Signal Transduction: Overview

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Cells respond to many types of information, often through receptor proteins positioned on the membrane. They respond to chemical signals, such as hormones, neurotransmitters, and other signaling molecules, initiating a series of molecular reactions to produce an appropriate response. This is called signal transduction. Cells also coordinate different responses elicited by the same signaling molecule via mediators, allowing molecular cross-talk.
Typically, signal transduction involves three...
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Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

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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.
Major types that are helpful drug targets include:
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Related Experiment Video

Updated: Nov 12, 2025

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

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TNFR signalling and its clinical implications.

Wen-Yi Tseng1, Yi-Shu Huang2, Hsi-Hsien Lin3

  • 1Kennedy Institute of Rheumatology, University of Oxford, OX3 7FY Oxford, UK; Division of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital-Keelung, Keelung, Taiwan.

Cytokine
|March 18, 2021
PubMed
Summary
This summary is machine-generated.

Tumour necrosis factor-α (TNF-α) is a key cytokine. Targeting its receptors (TNFR1/TNFR2) offers therapeutic benefits but can cause paradoxical effects, possibly via TNFR2 inhibition.

Keywords:
Anti-TNF-α therapyAutoimmune diseaseTNFTNFR1TNFR2

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SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
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SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Tumour necrosis factor-alpha (TNF-α) is a pleiotropic cytokine influencing numerous physiological and pathological processes.
  • TNF-α exerts its functions through two receptors: TNFR1, primarily mediating pro-inflammatory actions, and TNFR2, implicated in immunoregulation and tissue protection.

Purpose of the Study:

  • To review the biology and pathophysiologic role of TNF-α.
  • To explore the therapeutic implications of targeting TNF-α receptor signaling, particularly the paradoxical effects of anti-TNF biologics.

Main Methods:

  • Literature review of TNF-α biology, receptor signaling pathways, and clinical outcomes of anti-TNF therapies.
  • Analysis of hypothesized mechanisms behind paradoxical side effects of anti-TNF treatments.

Main Results:

  • Anti-TNF biologics are effective for immune-mediated diseases like rheumatoid arthritis and inflammatory bowel disease.
  • Paradoxical effects, including induction of lupus and psoriasis, and adverse outcomes in multiple sclerosis, have been observed with anti-TNF therapy.

Conclusions:

  • Inhibition of TNFR2 signaling is hypothesized to underlie the paradoxical adverse effects of anti-TNF therapies.
  • Understanding the distinct roles of TNFR1 and TNFR2 is crucial for optimizing anti-TNF therapeutic strategies and mitigating side effects.