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An interferon-stimulated gene (ISG) is a gene that can be expressed in response to stimulation by interferon. [1] [2] Interferons bind to receptors on the surface of a cell, initiating protein signaling pathways within the cell. This interaction leads to the expression of a subset of genes involved in the innate immune system response. [1]
Interferome is an online bioinformatics database of interferon-regulated genes (IRGs). [1] These Interferon Regulated Genes are also known as Interferon Stimulated Genes (ISGs). The database contains information on type I (IFN alpha, beta), type II (IFN gamma) and type III (IFN lambda) regulated genes and is regularly updated.
Stimulator of interferon genes (STING), also known as transmembrane protein 173 (TMEM173) and MPYS/MITA/ERIS is a protein that in humans is encoded by the STING1 gene. [ 5 ] STING plays an important role in innate immunity .
ISG15 was originally identified in the late 1970s as a 15-kDa protein produced in response to type I interferon, a potent class of antiviral cytokines. [19] Given the molecular weight, it was originally termed "a 15-kDa protein", but later renamed interferon-stimulated-gene-15 when the cassette of interferon-stimulated genes were recognized.
STAT molecules form dimers and bind to ISGF3G/IRF-9, which is Interferon stimulated gene factor 3 complex with Interferon regulatory Factor 9. [7] This allows STAT1 to enter the nucleus. [8] STAT1 has a key role in many gene expressions that cause survival of the cell, viability or pathogen response.
IRF7 encodes interferon regulatory factor 7, a member of the interferon regulatory transcription factor (IRF) family. IRF7 has been shown to play a role in the transcriptional activation of virus-inducible cellular genes, including the type I interferon genes. In particular, IRF7 regulates many interferon-alpha genes. [5]
Interferon regulatory factor 1 was the first member of the interferon regulatory transcription factor (IRF) family identified. Initially described as a transcription factor able to activate expression of the cytokine Interferon beta, [6] IRF-1 was subsequently shown to function as a transcriptional activator or repressor of a variety of target genes.
Later, the results showed that siblings were homozygous for absent expression of gene for STAT2. Patients with AR STAT2 deficiency have mutations which bring substitutions at important splice sites what leads to defected splicing and premature stop codons leading to a loss of expression of an interferon-stimulated gene.