As a member of the Interleukine (IL-6) cytotkine superfamily, Oncostatin M (OSM) besides, contributing to the normal physiology of repair, remodeling and hematopoiesis, also plays an important role in pathological conditions such as oncogenesis and inflammation (add ref). The activation of OSM receptors (LIFR and OSMR beta) by OSM, causes the formation of heterodimeric complex of LIFR-gp130 or OSMR-gp130 .
OSM mediated stimulation of its receptors, causes the activation of downstream signaling cascades. JAK/STAT, Ras/Raf/MAPK and PI 3-kinase through phosphorylation . On phosphorylation the STATs undergo homo- or hetero-dimerization, followed by their nuclear translocation and subsequent regulation of target gene expression . The dual effects of OSM, is mediated through the variation in phosphorylation of residues at selected sites, in different cell types or conditions. The OSM stimulation of JAK/STAT/PI 3 K leads to the increased expression of SOCS3 mRNA . The increased SOCS3 expression in turn effects the inactivation of JAK1, upon OSM stimulation.
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