Differential ability of SOCS proteins to regulate IL-6 and CSF-1 induced macrophage differentiation
- Author(s)
- Novak, U; Marks, D; Nicholson, SE; Hilton, D; Paradiso, L;
- Details
- Publication Year 1999,Volume 16,Issue #4,Page 305-314
- Journal Title
- GROWTH FACTORS
- Publication Type
- Journal Article
- Abstract
- M1/WT4 cells, derived from the murine myeloid leukemic M1 cells by over-expression of the receptor for CSP-I, were transfected with expression vectors encoding SOCS-1, SOCS-2, SOCS3 or Cis-l, The differentiation response to CSF-1 and IL-6 was analyzed in the resulting cell lines, Myeloid differentiation in response to CSF-1 was not affected by any of the SOCS proteins, whereas the IL-6-mediated differentiation was inhibited by SOCS-1 and SOCS3 and slightly delayed by SOCS-2 expression. In Il M1/WT4 cells IL-6 causes strong tyrosine phosphorylation of STAT3, whereas the response to CSF-1 is weaker, The expression of the SOCS proteins had no effect on CSF-1 mediated STAT3 tyrosine phosphorylation; however, SOCS-1 and SOCS3 reduced the tyrosine phosphorylation of STAT3 in response to IL-6 but did not abolish it. It appears, therefore, that SOCS-1, -2 and -3 and Cis-l do not inhibit tyrosine kinase activity involved in CSF-1 mediated cell differentiation, whereas SOCS-1 and -3 are inhibiting kinase activity required for IL-6-mediated differentiation.
- Publisher
- HARWOOD ACAD PUBL GMBH
- Keywords
- INDUCED STAT INHIBITOR; STIMULATING FACTOR-I; TYROSINE KINASE; GROWTH ARREST; FDC-P1 CELLS; BINDING-SITE; ACTIVATION; RECEPTOR; MURINE; FAMILY
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- Refer to copyright notice on published article.
Creation Date: 1999-01-01 12:00:00