Hormonal regulation of sRNA methylase activity in regional brain areas in Peromyscus maniculatus bairdii.
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Biomedical subjects
Publications and source records attributed to R L Hancock.
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An hypothesis of carcinogenesis is derived which suggests that carcinogens initially induce derepressions of structional genes of post-translational modifying enzymes. Although the resulting cascade of changes in genic activity would be measureable because of the large number of differentiated cells present in a tissue, only stem cells are vulnerable to the neoplastic array of genic expression by virtue of their repressors being more vulnerable to conformational modification. Furthermore it is derived that there are at least three major classes of repressors and the repressors that are synthesized during embryogenesis are particularly susceptible to derepression mechanisms.
It is contended that redundant repressed tRed) with carcinogens in adult cells. Supportive evidence, especially from molecular model building, is presented for a mechanism of tRNA methylation. In this mechanism the adenine moiety of S-adenosyl-L-methionine base-pairs with uracil for all tRNA methylations. Furthermore it is proposed that such methylations are required during the transcription of a tRNA molecule in order to limit the number of possible conformers that can occur before further development of the molecule takes place. This theory of the function for methyl groups is discussed in the light of the properties found for hypomethylated tRNAs.