Interactions between oncostatin M and the IL-6 signal transducer, gp130
Cytokine, ISSN: 1043-4666, Vol: 6, Issue: 3, Page: 272-278
1994
- 28Citations
- 12Captures
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Metrics Details
- Citations28
- Citation Indexes27
- 27
- CrossRef18
- Patent Family Citations1
- Patent Families1
- Captures12
- Readers12
- 12
Article Description
Recently, gp130, the signal transducer for interleukin 6 (IL-6), leukemia inhibitory factor (LIF), and ciliary neurotrophice factor (CNTF), was identified as the low-affinity receptor for oncostatin M (OM). However, it is not yet clear if OM binding to gp130 requires accessory factor(s) and if gp130 alone can mediate OM signalling. Here we report that: (a) expressing murine gp130 in BAF-B03 cells (BAF-m130) resulted in the appearance of a single class of low-affinity OM binding sites; (b) chemical cross-linking studies with 125 I-OM identified a 180 kDa labelled complex on BAF-m130 cells; (c) OM cross-linking to the H2981 cell line which expresses both low- and high-affinity OM receptor, identified a 180 kDa and an additional 280 kDa species; (d) 125 I-OM was specifically cross-linked to soluble recombinant gp130 (sgp 130-Rg) in solution; and (e) the cellular proliferation of BAF-m130 was unaffected by OM treatment. These data indicate that gp130 can act as the low-affinity receptor for OM, however, gp130-OM interactions alone are unable to elicit cellular proliferation. This suggests that an additional factor(s) are required to interact with the OM/gp130 complex to form the high-affinity functional receptor. We propose that the 280 kDa species detected on H2981 cells is likely a complex of OM, gp130, and the putative β chain of the functional OM high-affinity receptor. Recently, OM has been shown to be the major growth factor for Kaposi's sarcoma derived cells. Since sgp130-Rg can inhibit OM binding to its receptor, it may be useful as a growth inhibitor of Kaposi's sarcoma cells in vitro and in vivo.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/104346669490023X; http://dx.doi.org/10.1016/1043-4666(94)90023-x; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0028085950&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/8054483; http://linkinghub.elsevier.com/retrieve/pii/104346669490023X; http://api.elsevier.com/content/article/PII:104346669490023X?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:104346669490023X?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/104346669490023X; http://dx.doi.org/10.1016/1043-4666%2894%2990023-x; https://dx.doi.org/10.1016/1043-4666%2894%2990023-x
Elsevier BV
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