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Interferons (IFNs, / ˌ ɪ n t ər ˈ f ɪər ɒ n / IN-tər-FEER-on [1]) are a group of signaling proteins [2] made and released by host cells in response to the presence of several viruses. In a typical scenario, a virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.
The type-I interferons (IFN) are cytokines which play essential roles in inflammation, immunoregulation, tumor cells recognition, and T-cell responses. In the human genome, a cluster of thirteen functional IFN genes is located at the 9p21.3 cytoband over approximately 400 kb including coding genes for IFNα (IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16 ...
3456 15977 Ensembl ENSG00000171855 ENSMUSG00000048806 UniProt P01574 P01575 RefSeq (mRNA) NM_002176 NM_010510 RefSeq (protein) NP_002167 NP_034640 Location (UCSC) Chr 9: 21.08 – 21.08 Mb Chr 4: 88.44 – 88.44 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Interferon beta is a protein that in humans is encoded by the IFNB1 gene. The natural and recombinant protein forms have ...
Interferon gamma (IFNG or IFN-γ) is a dimerized soluble cytokine that is the only member of the type II class of interferons. [5] The existence of this interferon, which early in its history was known as immune interferon, was described by E. F. Wheelock as a product of human leukocytes stimulated with phytohemagglutinin, and by others as a product of antigen-stimulated lymphocytes. [6]
Interferon beta-1a (also interferon beta 1-alpha) is a cytokine in the interferon family used to treat multiple sclerosis (MS). [5] It is produced by mammalian cells, while interferon beta-1b is produced in modified E. coli. [6] Some research indicates that interferon injections may result in an 18–38% reduction in the rate of MS relapses. [7]
The type III interferon group is a group of anti-viral cytokines, that consists of four IFN-λ (lambda) molecules called IFN-λ1, IFN-λ2, IFN-λ3 (also known as IL29, IL28A and IL28B respectively), and IFN-λ4. [1]
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[21] [22] Perforation of the phagosome membrane mediated by ESX1 secretion system allows extracellular mycobacterial DNA to access host cytosolic DNA sensors, thus inducing the production of type I interferon in macrophages. High type I interferon signature leads to the M. tuberculosis pathogenesis and prolonged infection. [22]