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Macrophage Differentiation and Growth Inhibition by METS

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Description

Cell differentiation begins only when the cell proliferation mechanism is seized, and the macrophage differentiation system is a good example, as the macrophages start to differentiate only when they stop proliferating. Molecular mechanisms which act coordinately in order to regulate cell proliferation and differentiation are vital in development. Induction of Ets (v-Ets Avian Erythroblastosis Virus E26 Oncogene Homolog) repressor that is METS (Mitogenic Ets Transcriptional Suppressor) leads to terminal differentiation and cell cycle arrest (Ref.1). Macrophages are models, which provide evidence that METS blocks HRas (v-Ha-Ras Harvey Rat Sarcoma Viral Oncogene Homolog)-dependent proliferation without inhibiting HRas-dependent expression of cell type-specific genes by selectively replacing Ets activators on the promoters of cell cycle control genes. Anti-proliferative effects of METS require its interaction [...]

References:

1.An induced Ets repressor complex regulates growth arrest during terminal macrophage differentiation.
Klappacher GW, Lunyak VV, Sykes DB, Sawka-Verhelle D, Sage J, Brard G, Ngo SD, Gangadharan D, Jacks T, Kamps MP, Rose DW, Rosenfeld MG, Glass CK.
Cell 2002 Apr 19;109(2):169-80.
2.Differential utilization of Ras signaling pathways by macrophage colony-stimulating factor (CSF) and granulocyte-macrophage CSF receptors during macrophage differentiation.
Guidez F, Li AC, Horvai A, Welch JS, Glass CK.
Mol. Cell Biol. 1998 Jul; 18(7):3851-61.
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