Theoretical mechanism for synthesis of carcinogen induced embryonic proteins: VIII. Transcriptional theory.
In this paper an extension of prior writings on the mechanism by which changes in genic expression is presented. The previous development of these ideas led to a unifying concept of alterations in heterochromatin due to a variety of carcinogenic agents as a pivital process leading to potential re-expressions of genes (1). The following deals just with structural features of chromatin before continuing to finer control levels of gene expression, especially in reference to cancer cells. The DNA methylation status is presented as being an important step in an intermediate stage of chromatin expression along with protein acetylation, phosphorylation and methylation as other means of modifying chromatin status.
D000818:Animals; D002272:Carcinoembryonic Antigen / Q000235:genetics*; D002843:Chromatin / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D005786:Gene Expression Regulation; D006570:Heterochromatin / Q000378:metabolism; D006801:Humans; D008745:Methylation; D009369:Neoplasms / Q000235:genetics*; D010641:Phenotype; D014158:Transcription, Genetic
D002272:Carcinoembryonic Antigen; D002843:Chromatin; D006570:Heterochromatin; D004247:DNA