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Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Signal Transduction: Overview01:26

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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.
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Overview of Cell Signaling01:23

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Despite the protective membrane that separates a cell from the environment, cells need the ability to detect and respond to environmental changes. Additionally, cells often need to communicate with one another. Unicellular and multicellular organisms use a variety of cell signaling mechanisms to communicate with the environment.
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The JAK-STAT Signaling Pathway01:20

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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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Amplifying Signals via Enzymatic Cascade01:22

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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...
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Updated: Jun 11, 2025

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Signaling pathways and targeted therapy for rosacea.

Fengjuan Yang1,2, Lian Wang1,2, Deyu Song1,2

  • 1Department of Dermatology, West China Hospital, Sichuan University, Chengdu, China.

Frontiers in Immunology
|October 1, 2024
PubMed
Summary

Rosacea, a chronic inflammatory skin disease, involves complex signaling pathways like TLR2 and LL37. Understanding these molecular mechanisms offers new targeted therapies for rosacea.

Keywords:
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Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • Rosacea is a prevalent chronic inflammatory skin condition affecting 1-20% globally.
  • Characterized by facial redness, visible blood vessels, papules, pustules, and eye issues.
  • Pathogenesis is multifactorial, involving genetics, environment, immunity, microbes, and neurovascular elements.

Purpose of the Study:

  • To review current knowledge on molecular signaling pathways in rosacea.
  • To explore the role of specific pathways like TLR2, LL37, mTOR, IL-17, TRPV, and JAK-STAT.
  • To discuss potential targeted therapeutic strategies based on these pathways.

Main Methods:

  • Literature review of recent studies on rosacea molecular pathogenesis.
  • Analysis of signaling pathways including toll-like receptor 2 (TLR2), LL37, mammalian target of rapamycin (mTOR), interleukin-17 (IL-17), transient receptor potential vanilloid (TRPV), and Janus kinase-signal transducer and activator of transcription (JAK-STAT).
  • Examination of molecular interactions and downstream effects on immune cells and vascular factors.

Main Results:

  • LL37-associated pathways, particularly TLR2 and mTORC1, are central to rosacea pathogenesis.
  • Interactions involve ERK1/2, NF-κB, inflammasomes, CXCL8, MRGPRX2-TRPV4, and VEGF, activating immune cells and leading to cytokine release (TNF-α, IL-6, IL-1β, CCL5, CXCL9, CXCL10).
  • IL-17 and JAK/STAT pathways significantly contribute to inflammation and angiogenesis in rosacea.

Conclusions:

  • Understanding these signaling pathways is crucial for elucidating rosacea pathophysiology.
  • Targeted therapies, including cytokine inhibitors, IL-17 inhibitors, JAK inhibitors, and VEGF antagonists, show promise for improved rosacea treatment.
  • Future therapies aim for greater efficacy and reduced side effects by targeting specific molecular pathways.