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Schematic model, transcriptional activation

Figure 9.2 Schematic model for transcriptional activation. The TATA box-binding protein, which bends the DNA upon binding to the TATA box, binds to RNA polymerase and a number of associated proteins to form the preinitiation complex. This complex interacts with different specific transcription factors that bind to promoter proximal elements and enhancer elements. Figure 9.2 Schematic model for transcriptional activation. The TATA box-binding protein, which bends the DNA upon binding to the TATA box, binds to RNA polymerase and a number of associated proteins to form the preinitiation complex. This complex interacts with different specific transcription factors that bind to promoter proximal elements and enhancer elements.
Fig. 10.2 Schematic model for the regulation of Mn-SOD in co//.33 36) RG, regulatory gene RP, apo-repressor protein (inactive) RP-Fe3+, ferric repressor (inactive) RP-Fe2, ferrous repressor (active). Mn-SOD, nucleotide sequence of the 5 regulatory region oisodA (nucleotides —59 to +1 are shown). The +1 nucleotide designates the start point of transcription. The —35 and —10 (Pribnow box) regions for RNA polymerase binding are boxed. Fur-, and Fnr-binding sites are bracketed. Fig. 10.2 Schematic model for the regulation of Mn-SOD in co//.33 36) RG, regulatory gene RP, apo-repressor protein (inactive) RP-Fe3+, ferric repressor (inactive) RP-Fe2, ferrous repressor (active). Mn-SOD, nucleotide sequence of the 5 regulatory region oisodA (nucleotides —59 to +1 are shown). The +1 nucleotide designates the start point of transcription. The —35 and —10 (Pribnow box) regions for RNA polymerase binding are boxed. Fur-, and Fnr-binding sites are bracketed.
Fig. 4. Schematic model of the mechanisms of oestrogen control of cell proliferation. Three different mechanisms are illustrated. In (1) the interaction of oestrogen (E) with ER leads to increased transcription of genes whose products are directly involved in the control of cell replication. The mechanism illustrated in (2) postulates that oestrogens modulate the production of autocrine growth factors which in turn bind to growth factor receptors at the cell surface and mitogenesis occurs as a consequence of growth factor-activated metabolic pathways. The underlying hypothesis in (3) is that cells are under inhibitory (I) control by undefined molecules in the extracellular fluid and that oestrogens block the effects of these inhibitory molecules. Fig. 4. Schematic model of the mechanisms of oestrogen control of cell proliferation. Three different mechanisms are illustrated. In (1) the interaction of oestrogen (E) with ER leads to increased transcription of genes whose products are directly involved in the control of cell replication. The mechanism illustrated in (2) postulates that oestrogens modulate the production of autocrine growth factors which in turn bind to growth factor receptors at the cell surface and mitogenesis occurs as a consequence of growth factor-activated metabolic pathways. The underlying hypothesis in (3) is that cells are under inhibitory (I) control by undefined molecules in the extracellular fluid and that oestrogens block the effects of these inhibitory molecules.
In prokaryotes, the effector could be cAMP or some small metabolic product, whereas the activity of eukaryotic transcription factors is often modulated by phosphorylation (Chapter 29). It can be seen from the schematic models in Figure 28.2 that there are at least... [Pg.787]


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