By Jeffery C. Hall
Advances in Genetics raises its concentrate on glossy human genetics and its relation to medication with the merger of this long-standing serial with Molecular Genetic medication . This merger affirms theAcademic Press dedication to post vital studies of the broadest curiosity to geneticists and their colleagues in affiliated disciplines.
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The degeneration of axons observed in some cases could be partially explained by this mechanism. Different connexins can be coexpressed in cells, as demonstrated by Nicholson and colleagues (1987), and can form heterotypic pairs, with each connexon being made of one subunit. Alternatively, the connexon can be made of different subunits. Given the general role of connexins, it is easy to understand why Cx32 should be detected in nonneural tissues. Transcriptional control and, ultimately, translational control in the different cell types could be interpreted as a need for expression at a higher level or, constitutively, in one or other cell.
Garcia, C. , Davis, S. , Patel, P. , and Lupski, J. R. (1993). Molecular analyses of unrelated Charcot-Marie-Tooth (CMT) disease patients suggest a high frequency of the C M T l A duplication. Am. J. Hum. Genet. 53:853-863. , Dyck, P. , and Chance, P. E (1996). Genetic heterogeneity in Charcot-Marie-Tooth neuropathy type 2. Neurology 46569-571. Tumor Suppressor Genes and Human Cancer Melissa A. Brown Somatic Cell Genetics Laboratory Imperial Cancer Research Fund London WCZA 3PX, England I. Introduction 46 11.
Conclusions References 105 107 Ideas contributing to our understanding of tumorigenic mechanisms date from the 1700s, when early records of cancer families suggested that cancer was a genetic disease. Most of our present knowledge, however, is built on the contributions of researchers in this century (reviewed in Witkowski, 1990). In 1911 Peyton Rous demonstrated that cell-free extracts from chickens could transmit tumors, suggesting the existence of tumor viruses. Subsequent studies on these viruses ultimately led to identification of the first dominantly acting oncogene, src, in 1976.