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 Differential functions of Ras for malignant phenotypic conversion Moon AArch Pharm Res  2006[Feb]; 29 (2): 113-22Among the effector molecules connected with the group of cell surface receptors,  Ras proteins have essential roles in transducing extracellular signals to diverse  intracellular events, by controlling the activities of multiple signaling  pathways. For over 20 years since the discovery of Ras proteins, an enormous  amount of knowledge has been accumulated as to how the proteins function in  overlapping or distinct fashions. The signaling networks they regulate are very  complex due to their multiple functions and cross-talks. Much attention has been  paid to the pathological role of Ras in tumorigenesis. In particular, human  tumors very frequently express Ras proteins constitutively activated by point  mutations. Up to date, three members of the Ras family have been identified,  namely H-Ras, K-Ras (A and B), and N-Ras. Although these Ras isoforms function in  similar ways, many evidences also support the distinct molecular function of each  Ras protein. This review summarizes differential functions of Ras and highlights  the current view of the distinct signaling network regulated by each Ras for its  contribution to the malignant phenotypic conversion of breast epithelial cells.  Four issues are addressed in this review: (1) Ras proteins, (2) membrane  localization of Ras, (3) effector molecules downstream of Ras, (4) Ras signaling  in invasion. In spite of the accumulation of information on the differential  functions of Ras, much more remains to be elucidated to understand the  Ras-mediated molecular events of malignant phenotypic conversion of cells in a  greater detail.|*Signal Transduction[MESH]|Amino Acid Sequence[MESH]|Animals[MESH]|Breast Neoplasms/genetics/metabolism/pathology[MESH]|Breast/metabolism/pathology[MESH]|Cell Membrane/metabolism[MESH]|Cell Transformation, Neoplastic/genetics/*metabolism[MESH]|Complementarity Determining Regions/genetics[MESH]|Epithelial Cells/metabolism/pathology[MESH]|Humans[MESH]|Matrix Metalloproteinase 2/metabolism[MESH]|Matrix Metalloproteinase 9/metabolism[MESH]|Molecular Sequence Data[MESH]|Neoplasm Invasiveness[MESH]|Protein Isoforms/genetics/metabolism[MESH]|ras Proteins/genetics/*metabolism[MESH]
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