Current theories of oncogenesis suggest that tumors develop as a result of sequential alterations, which activate or inactivate tumor suppressor genes involved in the regulation of the cell cycle, and ultimately over express or suppress the proteins derived from those genes. Mutation is an obvious way of constitutive activation of a kinase. Owing to the importance of ERBB proteins in both development and cellular transformation, a lot of attention has been drawn to characterize the functions of this family of receptor tyrosine kinases. ERBB2 alterations are frequent in human tumors and result from translocation, mutation or amplification. The ERBB2 (Her2) proto-oncogene encodes a receptor tyrosine kinase, which is frequently amplified and over expressed in human tumors. The protein sequence of ERBB2, containing 1255 residues obtained from Swiss-Prot, was induced with a mutation to be characterized by using Insilico tools and compared with the wild type.
Key words: Oncogenesis, inactive - tumor suppressor genes, mutation, proto-oncogene.
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