Raf induces TGF(beta) production while blocking its apoptotic but not invasive responses: a mechanism leading to increased malignancy in epithelial cells

Article Abstract:

A mechanism leading to increased malignancy in epithelial cells is discussed based on looking at interactions between the Ras-MAP kinase pathway and TFG(beta) signaling. Whether activation of Raf brings a global inhibition of TBF(beta) signals, through Smads at least, or whether the effects are more selective, acting on the tumor-suppressive aspects of the TGF(beta) response only, was investigated. Raf was found to induce TGF(beta) production, at the same time blocking its apoptotic, not invasive, responses. Raf promotes invasive growth in collagen gels, dependent on operation of an autocrine loop involving TGF(beta). Its secretion was brought on by Raf. An inducible form of Raf was used in MDCK cells.

United Kingdom, Austria, Statistical Data Included, Physiological aspects, Cell death, Cellular signal transduction, Epithelial cells, Cytochemistry, Protein kinases, Skin cancer, Oncogenes, Ras genes

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SOCS1 deficiency causes a lymphocyte-dependent perinatal lethality

Article Abstract:

Suppressor of cytokine signaling (SOCS1) protein deficiency, which causes a lymphocyte-dependent perinatal lethality, is discussed. SOCS1 is an SH2-containing protein mainly expressed in thymocytes in a way that is independent of cytokines and T cell receptors. Delection of SOCS1 brings perinatal lethality with thymic changes, including loss of cellularity and a switch from predominantly CD4+CD8+ to single positive cells.

Japan, Proteins, T cell antigen receptors, Cell differentiation, Cell receptors, T cells, Stem cells, Cytokines, Lymphocytes, Thymus, Thymus gland, Lethal mutation

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