期刊
JOURNAL OF CELL COMMUNICATION AND SIGNALING
卷 10, 期 1, 页码 61-67出版社
SPRINGER
DOI: 10.1007/s12079-015-0302-x
关键词
Co-stimulatory molecules; Interferon-gamma (IFN-gamma); Lipopolysaccharides; Pro-inflammatory cytokines; Protein-protein interactions; Translocation; NetSlim; Systems biology markup language
类别
资金
- Department of Biotechnology (DBT), Government of India
- Infosys Foundation
- University Grants Commission (UGC), Government of India
- Indian Council of Medical Research (ICMR), Government of India
- Council of Scientific & Industrial Research (CSIR), Government of India
- DST-IDP research grant on Development of epitope based diagnostic gadget for detection of Mycobacterium tuberculosis in the Indian population from the Department of Science Technology, Government of India [IDP/MED/2011/23]
Interleukin-10 (IL-10) is an anti-inflammatory cytokine with important immunoregulatory functions. It is primarily secreted by antigen-presenting cells such as activated T-cells, monocytes, B-cells and macrophages. In biologically functional form, it exists as a homodimer that binds to tetrameric heterodimer IL-10 receptor and induces downstream signaling. IL-10 is associated with survival, proliferation and anti-apoptotic activities of various cancers such as Burkitt lymphoma, non-Hodgkins lymphoma and non-small scell lung cancer. In addition, it plays a central role in survival and persistence of intracellular pathogens such as Leishmania donovani, Mycobacterium tuberculosis and Trypanosoma cruzi inside the host. The signaling mechanisms of IL-10 cytokine are not well explored and a well annotated pathway map has been lacking. To this end, we developed a pathway resource by manually annotating the IL-10 induced signaling molecules derived from literature. The reactions were categorized under molecular associations, activation/inhibition, catalysis, transport and gene regulation. In all, 37 molecules and 76 reactions were annotated. The IL-10 signaling pathway can be freely accessed through NetPath, a resource of signal transduction pathways previously developed by our group.
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