Activated schematic model

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. 5. The level of cdc2 activity determines whether a progenitor divides, divides symmetrically or divides asymmetrically. A schematic model is shown. 

FIGURE 1 2-2 Schematic diagram of the phosphorylation sites on each of the four 60kDa subunits of tyrosine hydroxylase (TOHase). Serine residues at the N-terminus of each of the four subunits of TOHase can be phosphorylated by at least five protein kinases. (J), Calcium/calmodulin-dependent protein kinase II (CaM KII) phosphorylates serine residue 19 and to a lesser extent serine 40. (2), cAMP-dependent protein kinase (PKA) phosphorylates serine residue 40. (3), Calcium/phosphatidylserine-activated protein kinase (PKC) phosphorylates serine 40. (4), Extracellular receptor-activated protein kinase (ERK) phosphorylates serine 31. (5), A cdc-like protein kinase phosphorylates serine 8. Phosphorylation on either serine 19 or 40 increases the activity of TOHase. Serine 19 phosphorylation requires the presence of an activator protein , also known as 14-3-3 protein, for the expression of increased activity. Phosphorylation of serines 8 and 31 has little effect on catalytic activity. The model shown includes the activation of ERK by an ERK kinase. The ERK kinase is activated by phosphorylation by PKC. (With permission from reference [72].)... 

Asymmetric diarylmethanes, hydrogenolytic behaviors, 29 229-270, 247-252 catalytic hydrogenolysis, 29 243-258 kinetics and scheme, 29 252-258 M0O3-AI2O3 catalyst, 29 259-269 relative reactivity, 29 255-257 schematic model, 29 254 Asymmetric hydrogenations, 42 490-491 Asymmetric synthesis, 25 82, 83 examples of, 25 82 Asymmetry factor, 42 123-124 Atom-by-species matrix, 32 302-303, 318-319 Atomic absorption, 27 317 Atomic catalytic activities of sites, 34 183 Atomic displacements, induced by adsorption, 21 212, 213 Atomic rate or reaction definition, 36 72-73 structure sensitivity and, 36 86-87 Atomic species, see also specific elements adsorbed... 

Figure 2.9 Schematic model of the (R)-enantiomer of a secondary glycerol-like substrate as its tetrahedral intermediate inside the active site cleft of hpase B from Candida antarctica (CALB). The large group (-CH2-0-Rj) and the acyl part is inserted hke a V-shape into the cleft while the small group (-CH2-R2) at the stereocentre is located in the stereospecificity pocket which is next to the site of reaction.

Some energy diagram models of simple enzymic reactions are shown in Figure 8.1. A schematic model for an advantageous binding of the substrate on the enzyme active center is illustrated in Figure 8.2. 

Fig. 27. Schematized model of activation of hydrogen on the metal catalyst.

Fig. 7.110. Schematic model for the active surface of the perovskite, in which transition metal B is electrochemically active. (Reprinted with permission from J. O M. Bockris and T. Ottagawa, J. Phys. Chem. 87 2964, copyright 1983 American Chemical Society.)...

Fig. 4. Schematic model showing the role of calcineurin in T-cell activation.

Fig. 9.1 Schematic model depicting the key events which mediate diabetes-associated vascular complications. Diabetes/hyperglycemia augments the levels of vasoactive peptides including Ang II/ET-1 that enhance the generation of reactive oxygen species (ROS). ROS-induced activation of growth-promoting signaling pathways, such as PKC and MAPK, contributes to aberrant vascular functions.

Fig. 9. Schematic model for laminin showing the 3-chain structure (A, Bl, and B2) and the projection of the three chains down the long arm of the molecule. The location of a pentapeptide (YIGSR) with cell attachment activity is indicated, as well as the region with neurite-promoting activity (Baron van Evercooren et al., 1982 Edgar et al., 1984).

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.

Schematic model of the glutamate synapse. Gly glycine o-Ser D-serine DAAO D-amino acid oxidase DAOA D-amino acid oxidase activator (aka, G72)...

Figure 10.8. Schematic model of metal ion uptake through a membrane of a phytoplankton cell, (a) The metal ion is bound to the outside surface of the cell either by biologically released ligands or by surface functional ligand groups subsequently to the surface complex formation. The metals are carried—usually by porter molecules—to the inside of the cell. If the transport into the cell is slow in comparison to the pre-equilibration process on the solution side, then the uptake of the metal ion of the cell depends on the free metal ion activity, (b) Solution variables outside and inside the cell.

Biochemists, medicinal chemists, and computer chemists have previously tried to identify the pharmacophore for KOR. Their efforts include the following schematic models based on structure-activity relationship (SAR) studies ligand-based... 

Figure 4.5 Schematic plot showing the general applicability of different activity coefficient models as a function of ionic strength for a divalent cation. The dashed tangent to the curve at its origin is a plot of the Debye-Hiickel limiting law for the ion.

FIGURE 3.6 Schematic model of the suggested mechanism for the wettability alteration induced by seawater, (a) represents the mechanism when Ca and SO/ are active at lower temperature and (b) represents the mechanism when Mg and S04 " are active at a higher temperature. Source Zhang et al. (2007a). 

Figure 1.10 Schematic model of a central serotonergic neurone indicating possible sites of drug action. Tryptophan is converted to 5-hydroxytryptophcm (5-HTP) by tryptophan hydroxylase (1) and this enzyme can be inhibited by parachlorophenylalanine (pCPA) but this compound has only experimental value. 5-HTP is then converted to 5-HT and stored in vesicles (2), a process disrupted by reserpine and tetrabenazine. 5-HT is released by a Ca -dependentprocess (3) parachloramfetamine andfenfluramine increase 5-HT release while activation of 5-HTib/d autoreceptors inhibits release (at the cell bodies this function is served by 5-HTia receptors). After release 5-HT activates a range of postsynaptic 5-HT receptors (4) to produce functional responses and...

FIGURE 1.13 Schematic model for the active surface of the perovskite with an electrochemically active metal, M , anion lanthanide , and the lattice oxide o ion with hydroxide ions in solution and OH adsorbates at M. This figure is a simplified scheme of that in [23]. 

Fig. 4. Schematic model illustrating the coordinated action of the UPR with other cellular systems. As misfoided proteins enter the endoplasmic reticulum, they either fold to their native states and are then moved through the rest of the secretory pathway, or fail to properly fold. In the event that a protein unrecoverably fails to fold, it can be degraded by the ERAD machinery. During cellular stress, an accumulation of misfoided proteins leads to activation of the UPR (gray arrow). In the model illustrated here, in addition to upregulation of chaperones to directly assist the folding of proteins, the UPR enhances the rate of secretion to the distal secretory pathway and the degradation of misfoided species. (Reproduced from Travers et aL, 2000.)...

A FIGURE 23-24 Schematic model of the proofreading function of DNA polymerases. All DNA polymerases have a similar three-dimensional structure, which resembles a half-opened right hand. The "fingers" bind the single-stranded segment of the template strand, and the polymerase catalytic activity (Pol) lies in the junction between the fingers and palm. 

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... 

Hirschfelder, in discussing a simpler and more schematic model of stepwise activation in unimolecular reactions assumed the absorption coefficient a kplk = 1 in Hirschfelder notation) to be 0.5 and obtained the equation... 

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