TY - JOUR
T1 - Transactivation of gp130 in myeloma cells
AU - French, Jena D.
AU - Walters, Denise K.
AU - Jelinek, Diane F.
PY - 2003/4/1
Y1 - 2003/4/1
N2 - Receptor transactivation, i.e., interaction between unrelated receptor systems, is a growing theme in cytokine and growth factor signaling. In this study we reveal for the first time the ability of IFN-α to transactivate gp130 in myeloma cells. An epidermal growth factor receptor/gp130 chimeric receptor previously shown by us to transactivate endogenous gp130, provided a complementary tool to study the underlying mechanisms of receptor cross-talk. Further analysis revealed that transactivation of gp130 by IFN-α did not require the extracellular or trans-membrane domain of gp130. Moreover, transactivation of gp130 was critically dependent upon Janus kinase activation by the initiating receptor and correlated with rapid and sustained Janus kinase 1 and tyrosine kinase (Tyk) 2 tyrosine phosphorylation. Finally, transactivation of gp130 may be a common theme in myeloma cells, perhaps providing a mechanism for enhanced or qualitatively distinct cellular responses to specific stimuli.
AB - Receptor transactivation, i.e., interaction between unrelated receptor systems, is a growing theme in cytokine and growth factor signaling. In this study we reveal for the first time the ability of IFN-α to transactivate gp130 in myeloma cells. An epidermal growth factor receptor/gp130 chimeric receptor previously shown by us to transactivate endogenous gp130, provided a complementary tool to study the underlying mechanisms of receptor cross-talk. Further analysis revealed that transactivation of gp130 by IFN-α did not require the extracellular or trans-membrane domain of gp130. Moreover, transactivation of gp130 was critically dependent upon Janus kinase activation by the initiating receptor and correlated with rapid and sustained Janus kinase 1 and tyrosine kinase (Tyk) 2 tyrosine phosphorylation. Finally, transactivation of gp130 may be a common theme in myeloma cells, perhaps providing a mechanism for enhanced or qualitatively distinct cellular responses to specific stimuli.
UR - http://www.scopus.com/inward/record.url?scp=0037379269&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037379269&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.170.7.3717
DO - 10.4049/jimmunol.170.7.3717
M3 - Article
C2 - 12646637
AN - SCOPUS:0037379269
SN - 0022-1767
VL - 170
SP - 3717
EP - 3723
JO - Journal of Immunology
JF - Journal of Immunology
IS - 7
ER -