Titlebook: c-Myc Function in Neoplasia; Chi V. Dang,Linda A. Lee Book 1995 Springer-Verlag Berlin Heidelberg 1995 biology.cancer.cell.cell death.gene

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Max Association with Myc,spected that Myc partner proteins were necessary for Myc function because Myc possesses a dimerization domain that appears necessary for cell transformation. Although early studies indicated that Myc could homodimerize, it became rapidly apparent that homodimerization of c-Myc only occurs at high pr

觀察

DNA Binding Properties of Myc,uence CANNTG that is recognized by all basic regions of members of the bHLHZip family.. Studies using pools of random oligonucleotides, the polymerase chain reaction, and recombinant fusion Myc protein along with electrophoretic mobility gel shift assay indicate that the preferred core binding site

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Myc Target Genes in Cell Proliferation and Programmed Cell Death, function is regulated by a complicated network of proteins that developed through millions of years of evolution and is likely to include a large repertoire of interacting proteins. Yet, the mechanism by which c-Myc or its retroviral counterpart v-Myc transforms cells remains largely unknown. Clues

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https://doi.org/10.1007/978-981-19-1166-8an to posttranslational modification.. Hence this protein is termed p62Myc. From the same c-. mRNAs, an alternative form of c-Myc polypeptide is translationally initiated at a CUG, 14 codons upstream from the canonical AUG (Fig. 6.1).. This alternative form is termed p64Myc. These two forms of c-Myc appear as a doublet of polypeptides on SDS-PAGE.

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1080-3645 gy of human cancers. Much of this progress can be attributed to our abil- ity to dissect many biological processes at the molecular level. Most spectacular is the technology of molecular biology that allows identi- fication and characterization of genes that participate in the genesis of human cance