Protein mRNA and

CYP2A6 (cytochrome P450 2A6) has been purified from human liver and CYP2A6 cDNA expression systems are available. Many studies have demonstrated marked interindividual variation in the levels of hepatic CYP2A6 protein, mRNA and associated microsomal coumarin 7-hydroxylase activity (reviewed in Pelkonen et al., 1997 Lake, 1999). The role of CYP2A6 in the metabolism of coumarin by human liver microsomes has been confirmed by Sai et al. (1999), who found that a monoclonal antibody to CYP2A6 inhibited coumarin 7-hydroxylation by more than 94%. 

Analogous rRNAs from many different species fold into quite similar three-dimensional structures containing numerous stem-loops and binding sites for proteins, mRNA, and tRNAs. Much smaller rlbosomal proteins are associated with the periphery of the rRNAs. 

Burgi B, Lichtensteiger W, Schlumpf M. Diazepam-binding inhibitory/acyl-Co-A-binding protein mRNA and peripheral benzodiazepine receptor mRNA in endocrine and immune tissues after prenatal diazepam exposure of male and female rats. J Endocrinol 2000 166 163-171. 

G. Shanker, A.T. Campagnoni and R.A. Pieringer, Investigations on myelinogenesis in vitro developmental expression of myelin basic protein mRNA and its regulation by thyroid hormone in primary cerebral cell cultures from embryonic mice. J. Neurosci. Res. 17 220 (1987). 

Rising, A., Johansson, J., Larson, G., Bongcam-Rudlofl) E., Engstrom, W., and Hjalm, G. (2007). Major ampullate spidroins from Euprosthenops australis Multiplicity at protein, mRNA and gene le cls. InsectMoL Biol. 16, 551-561. 

There is strong upregulation of cytokines, chemo-kines, and their receptors at the protein, mRNA, and gene levels. 

Ignotz et al. (1981), studying the selective inhibition of ribosomal protein synthesis in chick embryo fibroblasts deprived of insulin, concluded that it is due to less efficient initiation of translation on some ribosomal protein mRNAs, and suggested that these mRNAs compete less effectively in translation. Likewise, synthesis of proinsulin appears to occur on a weak mRNA template, and increases preferentially when overall translation is stimulated in whole cells by glucose (Lomedico and Saunders, 1977). 

From the foregoing analyses of data it seems safe to assume that a newly synthesized VSV product is the principal inhibitor of protein synthesis in infected cells. The fact that VSV transcription is required to inhibit cellular protein synthesis (McAllister and Wagner, 1976 Marvaldi et al., 1977) limited the search to newly synthesized viral RNAs and proteins. Circumstantial evidence obtained from very early studies with interferon and other inhibitors appeared to rule out viral proteins as primary inhibitors of cellular protein synthesis (Yamazaki and Wagner, 1970 Wertz and Youngner, 1970 reviewed by Bablan-ian, 1975). Careful studies by UV inactivation of selected VSV transcripts appear to rule out the mRNAs for the M, G, and L proteins (Marvaldi et al., 1977 Dunigan and Lucas-Lenard, 1983). This would seem to leave the VSV leader RNA, the N protein mRNA, and/or the NS protein mRNA as the principal candidates for inhibitors of cellular protein synthesis, or possibly one or all of these transcripts... 

Cellular protein biosynthesis involves the following steps. One strand of double-stranded DNA serves as a template strand for the synthesis of a complementary single-stranded messenger ribonucleic acid (mRNA) in a process called transcription. This mRNA in turn serves as a template to direct the synthesis of the protein in a process called translation. The codons of the mRNA are read sequentially by transfer RNA (tRNA) molecules, which bind specifically to the mRNA via triplets of nucleotides that are complementary to the particular codon, called an anticodon. Protein synthesis occurs on a ribosome, a complex consisting of more than 50 different proteins and several stmctural RNA molecules, which moves along the mRNA and mediates the binding of the tRNA molecules and the formation of the nascent peptide chain. The tRNA molecule carries an activated form of the specific amino acid to the ribosome where it is added to the end of the growing peptide chain. There is at least one tRNA for each amino acid. 

The antiviral activity of (5)-DHPA in vivo was assessed in mice inoculated intranasaHy with vesicular stomatitis vims ( 5)-DHPA significantly increased survival from the infection. (5)-DHPA did not significantly reduce DNA, RNA, or protein synthesis and is not a substrate for adenosine deaminase of either bacterial or mammalian origin. However, (5)-DHPA strongly inhibits deamination of adenosine and ara-A by adenosine deaminase. Its mode of action may be inhibition of Vadenosyl-L-homocysteine hydrolase (61). Inhibition of SAH hydrolase results in the accumulation of SAH, which is a product inhibitor of Vadenosylmethionine-dependent methylation reactions. Such methylations are required for the maturation of vital mRNA, and hence inhibitors of SAH hydrolase may be expected to block vims repHcation by interference with viral mRNA methylation. 

Anticodon (Section 28.5) A sequence of three bases on tRNA that reads the codons on mRNA and brings the correct amino acids into position for protein synthesis. 

A problem with employment of ASON in a larger clinical setting is their poor uptake and inappropriate intracellular compartmentalization, e.g., sequestration in endosomal or lysosomal complexes. In addition, there is a need for a very careful selection of the ASON-mRNA pair sequences that would most efficiently hybridize. To date, several computer programs are used to predict the secondary and tertiary structures of the target mRNA and, in turn, which of the mRNA sequences are most accessible to the ASON. However, even with this sophisticated techniques, the choice of base-pairing partners still usually includes a component of empiricism. Despite these principal limitations, it has become clear that ASON can penetrate into cells and mediate their specific inhibitory effect of the protein synthesis in various circumstances. 

A length of DNA in a gene that is transcribed into mRNA and translated into the final protein product. 

Tumor necrosis factor alpha (TNFa) is a negative regulator of FATP expression and downregulates FATP mRNA and protein levels in several tissues. 

A splice variant can arise when a gene contains at least two introns leading to the possibility that the DNA between them (an exon) may not be included in the final mRNA and protein product. Thus, the final protein product may exist in two forms one containing the amino-acid sequence encoded by the exon that is located between the introns in the original DNA, and another form in which the amino-acid sequence encoded by that exon has been spliced out . These two products are refened to as splice variants. 

Tachykinins and their Receptors. Table 3 Human TK and TK receptor genes (DNA), TK and TK receptor-encoding mRNAs, and TK peptides and TK receptor proteins... 

Fargnoli, J., Kunisada, T., Fomace, A.J.. Schneider, E.L., Holbrook, N.J. (1990). Decreased expression of heat shock protein 70 mRNA and protein after heat treatment in cells of aged rats. Proc. Natl. Acad. Sci. USA 87, 846-850. 

Mehta, H.B., Popovich, B.K., Dillman, W.H. (1988). Ischemia induces changes in the level of mRNAs coding for stress protein 71 and creatin kinase M. Circ. Res. 63,512—517. 

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