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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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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 are of three kinds RI, RII, and RIII. The RI...

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Related Experiment Video

Updated: Jun 13, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
12:40

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

Multiomic Analysis Reveals an IFN-driven Cellular Landscape Effectively Targeted by Ruxolitinib in Hailey-Hailey

Sara Ceccacci, Hoang Duc Minh Pham, Marion Dessaignes

    Biorxiv : the Preprint Server for Biology
    |June 12, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Hailey-Hailey disease involves skin blistering driven by interferon (IFN) signaling. Topical JAK inhibitors like ruxolitinib offer a new, effective treatment for this rare genetic skin condition.

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    Published on: December 7, 2014

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    11:06

    Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

    Published on: September 20, 2017

    Area of Science:

    • Dermatology
    • Genetics
    • Immunology

    Background:

    • Hailey-Hailey disease (HHD) is a rare autosomal dominant genodermatosis causing debilitating skin blistering and erosions.
    • Current treatments for HHD lack targeted mechanisms and often fail to provide lasting relief.

    Purpose of the Study:

    • To elucidate the molecular and cellular mechanisms underlying HHD pathogenesis.
    • To identify potential targeted therapies for HHD.

    Main Methods:

    • Multiomics approach including bulk, single-cell, and spatial transcriptomics, alongside proteomics.
    • Analysis of skin lesions from HHD patients.
    • Clinical trial of topical ruxolitinib in patients with refractory HHD.

    Main Results:

    • A significant interferon (IFN) signature was identified in HHD skin lesions.
    • Inflammatory niches involving multiple cell types were characterized, forming an IFN-driven amplification loop.
    • Topical ruxolitinib treatment resulted in rapid re-epithelialization, reduced symptoms, and improved quality of life in HHD patients.

    Conclusions:

    • Interferon signaling is a key pathogenic driver in Hailey-Hailey disease.
    • Topical JAK inhibition with ruxolitinib represents a promising and effective therapeutic strategy for HHD.
    • This study redefines the standard of care for HHD management.