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Transcription basal level

Phosphorylation of HSF substantially enhances the transcriptional activity of HS gene expression which may be up to 100-fold of basal levels after HSFl binds to the promoter element. Heat shock will increase the C-terminal-domain-kinase activity in cell extracts, and this action may enhance the activity of RNA polymerase II that is bound to HS genes (Legagneux et al., 1990). Whether this kinase activity also affects HSFl phosphorylation is not known, but increased HS gene expression appears to occur as long as HSFl is bound to the promoter region. The CTD kinase complex contains multiple proteins, and it is quite possible that one or more of these proteins is also regulated by stress. [Pg.422]

We can conclude that our results are compatible with a model for the control of PG synthesis at transcriptional level in response to the inducer but with certain levels of protein, apparently similar to that showing PG activity, and its corresponding mRNA in non-inducing conditions. Further studies in order to quantify the relative amount of these basal levels are on a course. [Pg.890]

When animals are fed experimental diets lacking copper or zinc, their copper or zinc status rapidly declines, suggesting that there is not a storage pool of these metals. Thus, while the small, cysteine-rich protein metallothionein (see below) can avidly bind zinc and copper, this may reflect its role in detoxification rather than as a specific storage form. This is reflected by the fact that metallothionein genes are typically expressed at a basal level, but their transcription is strongly induced by heavy metal load. [Pg.148]

Fragmented, biotinylated RNA prepared in this manner was hybridized to the array and the signal developed using streptavidin-R-phycoerytherin. A confocal laser scanner was used for detection. The researchers estimated that they could detect two transcripts per cell based upon labeling efficiency and an estimated 4% mRNA content in total bacterial RNA. Thus, chip detection of labeled transcripts was found to be more sensitive than detection by Northern blot. Specific genes (e.g., basal levels of cinA) undetectable on Northern blots were quantifiable on the microarray. In addition, it was... [Pg.157]

Extensive studies on the reconstitution of a regulated transcription initiation in in vitro systems have shown that most of the specific transcription factors are not capable of stimulating transcription above the basal level without the assistance of further proteins. Further coactivators are required for this task. The coactivators can be subdivided into three classes (Fig. 1.34). [Pg.50]

The sequences of eukaryotic promoters are more variable than their prokaryotic counterparts (see Fig. 26-8). The three eukaryotic RNA polymerases usually require an array of general transcription factors in order to bind to a promoter. Yet, as with prokaryotic gene expression, the basal level of transcription is determined by the effect of promoter sequences on the function of RNA polymerase and its associated transcription factors. [Pg.1083]

Despite this elaborate binding complex, repression is not absolute. Binding of the Lac repressor reduces the rate of transcription initiation by a factor of 10s. If the 02 and 03 sites are eliminated by deletion or mutation, the binding of repressor to CL alone reduces transcription by a factor of about 102. Even in the repressed state, each cell has a few molecules of /3-galactosidase and galactoside permease, presumably synthesized on the rare occasions when the repressor transiently dissociates from the operators. This basal level of transcription is essential to operon regulation. [Pg.1087]

The TATA binding protein and general transcription initiation factors. A slow basal level of transcription can be observed when all but a small part of the control region at the 5 end of a gene is deleted.325 This minimum promoter, which includes the TATA sequence, is the binding site of both the RNA... [Pg.1628]

In healthy plants, the basal level of GUS expression remained unaffected when the promoter was deleted from -900 to —318. However, GUS activity decreased dramatically when the promoter was deleted to -222. GUS activity decreased to virtually undetectable levels when the promoter was deleted to -150. Further deletion to -75 slightly increased the level of constitutive expression to about the level of the —222 deletion. These results suggest that there may be an element in the —318 to —222 region which is important for non-specific transcription. Further, there may be a negative element that suppresses transcription around the —150 region that is lost when the promoter is deleted to —75. [Pg.219]

AK Jaiswal Fox Chase Cancer Center Elucidate the molecular mechanisms that control the basal level of expression in normal and tumor cells, induction and transcription due to xenobiotics such as 2,3,7,8-TCDD, and tissue-specific and developmental expression of NQOI and NQ02 genes in rat tissues ... [Pg.373]

Fig. 16. Basal ERp transcriptional activation by SRC-1 is AF-2 independent. (A) Dose-dependent activation of ERa and ERP by SRC-1 in absence of Eg. Cos-1 cells were transfected with ERETKLuc reporter along with ERa or ERP and increasing amounts of SRC-1 expression plasmids. Luciferase activities were normalized with P-Gal expression and results are expressed as factor by which response exceeds basal levels (-) and represent the mean SEM of three independent experiments. (B) Pure antiestrogen EM-652 but not the mixed antagonist 4-hydroxytamoxifen (OHT) inhibits basal ERP transcriptional activation by SRC-1. Cos-1 cells were transfected with ERETKLuc along with equivalent amounts of ERP and SRC-1 expression plasmids and incubated with increasing amounts of OHT or EM-652 prior to being assayed for luciferase activity. The maximal induction by SRC-1 alone (solid bar) was defined as 100%. Basal level in absence of SRC-1 is indicated by an open bar. (C) Basal activity of an ERP AF-2 mutant is induced by SRC-1. Cos-1 cells were transfected with ERETKLuc reporter and equivalent amounts of ERP or ERP L509A AF-2 mutant and SRC-1 (solid bars) expression plasmids. Cells were then treated with 10 nM Eg (striated bars) or left untreated (open and solid bars) for 16 hours prior to harvest. Results are plotted as factor by which induction exceeds basal levels (Tremblay et al, 1999). Fig. 16. Basal ERp transcriptional activation by SRC-1 is AF-2 independent. (A) Dose-dependent activation of ERa and ERP by SRC-1 in absence of Eg. Cos-1 cells were transfected with ERETKLuc reporter along with ERa or ERP and increasing amounts of SRC-1 expression plasmids. Luciferase activities were normalized with P-Gal expression and results are expressed as factor by which response exceeds basal levels (-) and represent the mean SEM of three independent experiments. (B) Pure antiestrogen EM-652 but not the mixed antagonist 4-hydroxytamoxifen (OHT) inhibits basal ERP transcriptional activation by SRC-1. Cos-1 cells were transfected with ERETKLuc along with equivalent amounts of ERP and SRC-1 expression plasmids and incubated with increasing amounts of OHT or EM-652 prior to being assayed for luciferase activity. The maximal induction by SRC-1 alone (solid bar) was defined as 100%. Basal level in absence of SRC-1 is indicated by an open bar. (C) Basal activity of an ERP AF-2 mutant is induced by SRC-1. Cos-1 cells were transfected with ERETKLuc reporter and equivalent amounts of ERP or ERP L509A AF-2 mutant and SRC-1 (solid bars) expression plasmids. Cells were then treated with 10 nM Eg (striated bars) or left untreated (open and solid bars) for 16 hours prior to harvest. Results are plotted as factor by which induction exceeds basal levels (Tremblay et al, 1999).
Zhao, X., Martin, M. M., and Elton, T. S. 2000. Basal level transcriptional regulation of the human angiotensin II type 1 receptor gene. Biochim Biophys Acta 1494 181-184. [Pg.116]

Favreau, L.V. and Pickett, C.B., Transcriptional regulation of the rat NAD(P)H quinone reductase gene. Identification of regulatory elements controlling basal level expression and inducible expression by planar aromatic compounds and phenolic antioxidants, J. Biol. Chem., 266, 4556 561, 1991. [Pg.119]


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See also in sourсe #XX -- [ Pg.309 ]




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