Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

MAPK Signaling Cascades

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...

Interactions Between Signaling Pathways

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...

NF-κB-dependent Signaling Pathway

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...

The JAK-STAT Signaling Pathway

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...

cAMP-dependent Protein Kinase Pathways

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,...

Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Absolute Eczema Area and Severity Index Responses with Lebrikizumab in Patients with Moderate-to-severe Atopic Dermatitis: A Secondary Analysis of Two Phase 3 Trials.

Acta dermato-venereologica·2026

Same author

p75NTR and psoriasis: a new inflammatory pathway?

The British journal of dermatology·2026

Same author

Correction to: Real-World Evidence of Effectiveness and Safety of Abrocitinib, Baricitinib and Upadacitinib in Atopic Dermatitis: A Systematic Review and Meta-Analysis.

American journal of clinical dermatology·2026

Same author

A safety checklist before initiating second-generation immunomodulating drugs for inflammatory dermatoses: a systematic review.

The Journal of dermatological treatment·2026

Same author

Atopic Dermatitis and Academic Performance.

JAMA dermatology·2026

Same author

International development of Investigator Global Assessment scores for pemphigus.

Journal of the European Academy of Dermatology and Venereology : JEADV·2026

Search research articles

Related Experiment Video

Updated: May 28, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

CCL27 expression is regulated by both p38 MAPK and IKKβ signalling pathways.

Jette Lindorff Riis¹, Claus Johansen, Christian Vestergaard

¹Department of Dermatology, Aarhus Sygehus, Aarhus University Hospital, Aarhus C, Denmark. jette.lindorff.riis@ki.au.dk

|October 14, 2011

Summary

Interleukin-1 beta (IL-1β) induces skin chemokine CCL27 expression in keratinocytes via p38 MAPK and IKK/NF-κB pathways. This regulation is crucial for inflammatory skin disease pathogenesis.

More Related Videos

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

Published on: January 6, 2017

Related Experiment Videos

Last Updated: May 28, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

Published on: January 6, 2017

Area of Science:

Immunodermatology
Molecular Biology
Cell Signaling

Background:

CCL27, a skin-specific chemokine, promotes lymphocyte migration to the skin via CCR10 binding, contributing to inflammatory skin diseases.
The precise regulatory mechanisms of CCL27 gene expression remain largely unelucidated.

Purpose of the Study:

To investigate the regulation of IL-1β-induced CCL27 gene expression in normal human keratinocytes (NHEK).

Main Methods:

Utilized inhibitors of IκB kinase (IKK) and p38 mitogen-activated protein kinase (MAPK).
Assessed the impact of downstream kinases MSK1 and Mnk1+2 inhibitors on CCL27 expression.
Employed electrophoretic mobility shift assay (EMSA) and supershift analyses to identify NF-κB involvement.

Main Results:

Inhibition of IKK and p38 MAPK significantly reduced CCL27 mRNA and protein expression.
Downstream kinases MSK1 and Mnk1+2 were implicated in CCL27 regulation.
EMSA and supershift assays confirmed the binding of p50/p65 NF-κB heterodimers to the CCL27 gene promoter.

Conclusions:

IL-1β-induced CCL27 gene expression in NHEK is regulated by both the p38 MAPK/MSK1/Mnk1+2 and IKKβ/NF-κB signaling pathways.
These findings elucidate key molecular mechanisms underlying CCL27 regulation in skin inflammation.