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Gene expression, inhibitors

Asada S, Choi Y, Uesugi M. A gene-expression inhibitor that targets an alpha-helix-mediated protein interaction. J. Am. Chem. Soc. 2003 125 4992-1993. [Pg.1870]

Experiments with gene expression inhibitors have demonstrated that the secondary metabolic enzymes, which are present in chloroplasts are synthesized in the cytoplasm (A 2.1). Hence those enzymes must penetrate the plastid envelope, which shows maximum permeability at early stages of greening. During this period the precursors of secondary products, such as oxalacetate, succinate or mevalonate, and even the CoA-esters of cinnamic acid derivatives may also be transported across the plastid envelope. [Pg.43]

With respect to targeting viral gene products expressed in virus-infected cells, it should be considered that infectious mammalian viruses may express inhibitors of RNAi similar to plant viruses. [Pg.1093]

The inhibitors of RNA polymerase, which generates RNA from DNA, inhibit a crucial step in gene expression. Inhibition of the eukaryotic form of RNA polymerase is used in cancer chemotherapy and is also an important experimental tool. For example, actinomy-cin D binds to the guanine residues in DNA and blocks the movement of the eukaryotic RNA polymerase. Specific inhibitors of bacterial RNA polymerase can be used as antibacterial agents. Most of these inhibitors like rifamycin bind to the prokaryotic enzyme. [Pg.1094]

Monia BP, Lesnik EA, Gonzalez C, Lima WF, McGee D, Guinosso CJ, Kawasaki AM, Cook PD, Freier SM (1993) Evaluation of 2 -modified oligonucleotides containing 2 -deoxy gaps as antisense inhibitors of gene expression, J Biol Chem 268 14514-14522... [Pg.260]

Fig. 1 Antiviral genes inhibit virus replication at different stages of the viral life cycle. Early inhibitors prevent the establishment of the viral genome in the target cell (class I, e.g., entry inhibitors, RT inhibitors for HIV). Intermediate inhibitors prevent viral gene expression or amplification of the viral genome (class II, e.g., siRNAs, antisense RNAs). Late inhibitors prevent virion assembly or release, or inactivate the mature virions (class III, e.g., transdominant core proteins, capsid-targeted virion inactivation, CTVI). A list of antiviral genes in each class is found in Table 1... Fig. 1 Antiviral genes inhibit virus replication at different stages of the viral life cycle. Early inhibitors prevent the establishment of the viral genome in the target cell (class I, e.g., entry inhibitors, RT inhibitors for HIV). Intermediate inhibitors prevent viral gene expression or amplification of the viral genome (class II, e.g., siRNAs, antisense RNAs). Late inhibitors prevent virion assembly or release, or inactivate the mature virions (class III, e.g., transdominant core proteins, capsid-targeted virion inactivation, CTVI). A list of antiviral genes in each class is found in Table 1...
Sopchik AE, Jiao X-Y, Bentrude WG (1999) Phosphorus, Sulfur and Silicon 144-146 373 Cohen JS (ed) (1989) Oligonucleotides, antisense inhibitors of gene expression. CRC, Boca Raton FI... [Pg.75]

There is evidence that protease inhibitors selectively regulate the activity of specific digestive enzymes at the level of gene expression (Rosewicz et al., 1989). Specifically, soybean trypsin inhibitor increases secretion of proteases, including a form of trypsin that is resistant to inhibition but does not cause an increase in amylase secretion. Although the relationships between protease inhibitors and exocrine pancreatic secretion have received the most attention, pancreatic secretion is increased when potato fiber is added to the diet (Jacob et al., 2000), although the mechanism and signaling pathway have not been elucidated. [Pg.166]

ROSEWicz s, LEWIS L D, WANG X Y, LiDDLE R A, LOGSDON c D (1989) Pancreatic digestive enzyme gene expression effects of CCK and soybean trypsin inhibitor. dm J Physiol. 256 G733-8. [Pg.183]

The carotenoid pathway may also be regulated by feedback inhibition from the end products. Inhibition of lycopene cyclisation in leaves of tomato causes increase in the expression of Pds and Psy-1 (Giuliano et al, 1993 Corona et al, 1996). This hypothesis is supported by other studies using carotenoid biosynthesis inhibitors where treated photosynthetic tissues accumulated higher concentrations of carotenoids than untreated tissues (reviewed by Bramley, 1993). The mechanism of this regulation is unknown. A contrary view, however, comes from studies on the phytoene-accumulating immutans mutant of Arabidopsis, where there is no feedback inhibition of phytoene desaturase gene expression (Wetzel and Rodermel, 1998). [Pg.266]

Caco-2 cells and ezetimibe, a potent inhibitor of chloresterol absorption in humans, it was reported that (1) carotenoid transport was inhibited by ezetimibe up to 50% and the extent of that inhibition diminished with increasing polarity of the carotenoid molecule, (2) the inhibitory effects of ezetimibe and the antibody against SR-BI on P-carotene transport were additive, and (3) ezetimibe may interact physically with cholesterol transporters as previously suggested - and also down-regulate the gene expression of three surface receptors, SR-BI, NPCILI, and ABCAl. [Pg.163]

Caruthers, M. H., Synthesis of oligonucleotides and oligonucleotide analogues, in Oligodeoxynucleotides — Antisense Inhibitors of Gene Expression, Cohen, J. S., Ed., CRC Press, Boca Raton, FL, 1989, 7. [Pg.126]

Dervan PB, Poulin-Kerstien AT, Fechter EJ, Edelson BS (2005) Regulation of Gene Expression by Synthetic DNA-Binding Ligands. 253 1-31 Dias N, Vezin H, Lansiaux A, Badly C (2005) Topoisomerase Inhibitors of Marine Origin and Their Potential Use as Anticancer Agents. 253 89-108 DiMauro E, see Saladino R (2005) 259 29-68... [Pg.258]

Another type of intestinal peptide transporter, hPTl, which is significantly different in sequence from PEPT1, was identified using a functionally inhibitory monoclonal antibody [99]. This transporter is widely expressed in the human GI tract and facilitates the oral absorption of pdactam antibiotics and ACE inhibitors from the intestine [18, 99]. Interestingly, we recently reported that hPTl gene expression is approximately 4-fold higher than PEPT1 in the human duodenum [4] (Fig. 11.1). [Pg.253]

LSD1. A recent study identified LSD2 inhibitors that exhibited a 10-55-fold selectivity for LSD2 over LSD1, but that also potently inhibited MAO A and MAO B [109]. As specific inhibitors for individual demethylases and their isoforms are identified, it will be possible to elucidate the role that each enzyme plays in the epigenetic control of gene expression. [Pg.256]


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See also in sourсe #XX -- [ Pg.23 , Pg.295 ]




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