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ISRE

Last updated on: 29.04.2022

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DefinitionThis section has been translated automatically.

ISRE is the acronym for IFN-stimulated response elements. The ISRE element serves as a binding site for a family of transcription factors called IFN regulatory factors (IRFs) (Heim MH 1999).

General informationThis section has been translated automatically.

Type I and type II interferons induce IFN-stimulated gene (ISG) expression through Janus kinase (JAK)-dependent phosphorylation of Signal Transducer and Activator of Transcription (STAT) STAT1 and STAT2. The evolutionarily highly conserved interferon-stimulated genes (Levraud JP et al. 2019) are the effectors of interferon (IFN) actions and play an important role in innate immune defense against microbial infections (Green R et al. 2018).

STAT1 homodimers, known as gamma-activated factor (GAF), activate transcription in response to all types of interferons by directly binding GEne containing the one IFN-II activation site.

The association of interferon regulatory factor 9 (IRF-9) with STAT1-STAT2 heterodimers (known as interferon-stimulated gene factor 3 - ISGF3) or with STAT2 homodimers(STAT2/IRF9) in response to IFN-I directs these complexes to a specific group of target genes containing the interferon-stimulated response element (ISRE) to which they can bind (Michalska A et al. 2018).

Clinical pictureThis section has been translated automatically.

Studies with knockout mice showed that IRF-4 plays a critical role in controlling the activation and homeostasis of immune responses and is crucial for the maturation of B cells. IRF-8\ICSBP is essential for myeloid cell differentiation into mature macrophages.

Note(s)This section has been translated automatically.

To date, nine cellular IFN regulatory factors have been identified. Some of the IRFs, such as IRF-1, IRF-2, IRF-3, and IRF-7, bind directly to ISRE elements, whereas others, such as IRF-4 and IRF-8, bind only indirectly. Thus, IRF8/ICSBP can associate with either IRF-1 or IRF-2 and form heterocomplexes that then bind to DNA. These protein-protein interactions are mediated by a conserved domain. This domain is referred to as the IRF association domain (IAD). This IAD motif can be detected in all seven IRFs except IRF-1 and IRF-2.

LiteratureThis section has been translated automatically.

  1. Green R et al (2018) Interferon-stimulated genes: new platforms and computational approaches. Mamm Genome 29:593-602
  2. Heim MH (1999) The Jak-STAT pathway: cytokine signalling from the receptor to the nucleus. J Recept Signal Transduct Res 19: 75-120.
  3. Levraud JP et al (2019) IFN-stimulated genes in zebrafish and humans Define an Ancient Arsenal of Antiviral Immunity. J Immunol 203:3361-3373.
  4. Manry J et al (2011) Evolutionary genetic dissection of human interferons. J Exp Med 208:2747-2759.
  5. Michalska A et al. (2018) A Positive Feedback Amplifier Circuit That Regulates Interferon (IFN)-Stimulated Gene Expression and Controls Type I and Type II IFN Responses. Front Immunol 9:1135.
  6. Sheikh SZ et al (2011) Characterization of an interferon-stimulated response element (ISRE) in the Il23a promoter. J Biol Chem. 286:1174-1180.

Last updated on: 29.04.2022