Cellular mechanism of action of steroid hormones

A preliminary analysis of the implications of the Zheng et al. data has been submitted as formal paper to a refereed journal by Steele and Lindley. [30] The Zheng et al. [29] data strongly imply that the RNA moiety would need to be first A-to-I RNA edited then reverse transcribed and integrated to generate the strong A>>>T strand biased mutation signatures at A:T base pairs observed in all SHM and cancer hypermutation data sets. [8] [9] [20] [25] Editing (A-to-I) of the DNA moiety at RNA:DNA hybrids in vivo cannot explain the A>>T strand bias because such direct DNA modifications would result in T>>>A strand bias which is not observed in any SHM or cancer data set in vivo. [8] [9] [20] [25] In this regard Robyn Lindley has also recently discovered that the Ig-SHM-like strand-biased mutations in cancer genome protein-coding genes are also in "codon-context". Lindley has termed this process targeted somatic mutation (TSM) to highlight that somatic mutations are far more targeted than previously thought in somatic tissues associated with disease. [31] [32] The TSM process implies an "in-frame DNA reader" whereby DNA and RNA deaminases at transcribed regions are guided in their mutagenic action, by the codon reading frame of the DNA. [31] [32]

Cellular mechanism of action of steroid hormones

cellular mechanism of action of steroid hormones

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