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Related Concept Videos

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...
General Transcription Factors01:30

General Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
NF-kB-dependent Signaling Pathway02:26

NF-kB-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...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...

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Related Experiment Video

Updated: Jun 27, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
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Published on: March 24, 2015

Integrative Transcriptomics Uncovers IFN-β Signature and IFITM3 as Putative Molecular Mediator in MS.

Alessandro Maglione1,2, Rachele Rosso2, Simona Rolla2

  • 1Department of Computer Science, University of Turin, 10124 Torino, Italy.

International Journal of Molecular Sciences
|June 26, 2026
PubMed
Summary

Interferon-beta (IFN-β) treatment for multiple sclerosis (MS) induces a 43-gene signature. This signature, linked to MS risk variants and IFITM3, offers insights into IFN-β

Keywords:
EBVbiomarkersinterferon-betamultiple sclerosistranscriptomics

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Area of Science:

  • Neuroimmunology
  • Genomics
  • Pharmacogenomics

Background:

  • Multiple sclerosis (MS) neuroinflammation involves myelin-reactive T cells infiltrating the central nervous system (CNS).
  • Interferon-beta (IFN-β) is an early disease-modifying treatment (DMT) for MS, favored in special populations due to its safety profile.
  • The precise mechanism of action and reliable biomarkers for IFN-β treatment response in MS remain incompletely understood.

Purpose of the Study:

  • To characterize IFN-β-induced gene expression changes in MS patients using integrative transcriptomic analysis.
  • To identify a consistent transcriptional signature associated with IFN-β treatment across different MS stages.
  • To explore the functional relevance of the identified gene signature by linking it to MS-associated genetic risk variants.

Main Methods:

  • Integrative analysis of publicly available transcriptomic datasets from MS patients.
  • Identification of a robust 43-gene transcriptional signature associated with IFN-β treatment.
  • Cross-referencing the gene signature with expression quantitative trait loci (eQTL) datasets to assess the influence of MS risk variants.

Main Results:

  • A consistent 43-gene transcriptional signature associated with IFN-β treatment was identified across independent MS cohorts and disease stages.
  • The identified gene signature was cross-referenced with eQTL data, revealing potential links to known MS-associated risk variants.
  • Interferon-Induced Transmembrane Protein 3 (IFITM3) emerged as a candidate molecular mediator influenced by IFN-β treatment and MS risk.

Conclusions:

  • The study identified a robust IFN-β-induced transcriptional signature in MS patients, providing insights into treatment response.
  • The findings suggest a role for IFITM3 as a potential molecular mediator in IFN-β therapy and MS pathogenesis.
  • This integrative approach enhances understanding of IFN-β's immunomodulatory effects and supports the development of novel therapeutic strategies for MS.