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Hypothetical model for the membrane binding of microsomal P450s. The cartoon depicts the experimentally determined fold of the modified CYP2C5 catalytic domain, PDB 1N6B, attached to a hypothetical model for the N-terminal transmembrane helix. The latter is flanked by a modeled array of phospholipid molecules depicted as CPK atoms. The heme and bound substrate, DMZ, of CYP2C5 are also rendered as CPK atoms.

Hypothetical model for the metallobiology of AP in Alzheimer s disease. The proposed sequence of events

Hypothetical model for the mobilization of 16-methoxytabersonine into the chloroplast in order to accommodate the 4th to last steps in vindoline biosynthesis.

Hypothetical model for the oxidative burst in plant cells, in response to mechanical stress. Based on and

Hypothetical model for the regulation of prostanoid biosynthesis in normal and inflammatory states. Based on results published in ref 40.

Hypothetical model for the vacuole compartmentation of the reactions leading to secologanin secologanin synthase,

Hypothetical model of a muscarinic receptor showing the location of the transmembrane helical protein domains and the extracellular and Intracellular domains connecting the seven n helical proteins in the membrane. Reprinted from Goyal. R K.

Hypothetical model of a PSII-phycobilisome complex of Porphyridium cruentum. One hemi-ellipsoidal phycobilisome is bound to four PSII-complexes.

Hypothetical model of a synkinetic system producing hydrogen and oxygen from water and light.

Hypothetical model of cadmium metabolism in a marine diatom showing the buffering of Cd by PC binding and its use in periplasmic and cytoplasmic carbonic anhy-drases as part of C4 metabolism.

Hypothetical model of cause of damage from intracellular freezing. See text for details.

Hypothetical model of CIA PLA binding to a DMPC membrane surface

Hypothetical model of deacetamidocolchinyl methyl ether interacting with two sites on tubulin.

Hypothetical model of decaorganocyclohexasiloxane polymer Chain .

Hypothetical model of esterification reaction between the hydroxyl groups of sisal fibers and anhydride rings of MAPP .

Hypothetical model of filled rubber

Hypothetical model of how initiators and modulators that affect insulin release may reach A-, B- and D-cells. The first target of arterial blood containing nutrients, hormones, peptides and drugs is the B-cell. From there, via an intraislet portal vein system, blood which now also contains released insulin flows to the mantle where A- and D-cells are localized and from there enters the circulation. Nerves derived from the autonomous nervous system which contain neurotransmitters reach other endocrine cells in the islet in a paracrine manner. The B-cell may also be the target of previously released insulin via a short loop.

Hypothetical model of how insulin secretion is regulated. The most important event is the depolarization of the B-cell which causes Ca influx along L-type Ca2 channels and subsequent increase in cytosolic Ca . Depolarization is produced by nutrient . Insulin release in response to depolarization is also modulated by factors affecting PLC and adenylate cyclase. Here, production of IP3 leads to release of stored Ca2 from the endoplasmic reticiulum. DAG activates PKC whereas cAMP activates PKA. CaMK, PKC and PKA cause protein phosphorylations which finally cause granule movement and exocytosis. But there will also be other effects of phosphorylations related to stimulus-secretion coupling, e.g. a possible interaction with voltage-dependent Ca2 channels.

Hypothetical model of inhibitor binding to the active site of iNOS. This inhibitor binds f 700-fold more tightly to iNOS than eNOS. One obvious and significant difference between the two isoforms is that the residue corresponding to Asp382 iu iNOS is Asn in eNOS. Asn would not be able to donate an H-bond to the inhibitor OH group as shown, which could contribute to the difference in binding affinity.

Hypothetical model of lipoprotein particle.

Hypothetical model of pathogenesis of pain in DSP.

Hypothetical model of POCS-4.

Hypothetical model of protein kinase C activation by non-esterified arachidonate. Shown schematically are a presynaptic terminal juxtaposed to a postsynaptic spine. Glutamate, released by presynaptic electrical activity, binds to and stimulates postsynaptic NMDA receptors as well as presynaptic metabotropic receptors. NMDA receptors are linked to the release of free arachidonate, which in turn is thought to diffuse to the presynaptic terminal and to enhance 1,2-diacylglycerol -stimulatedprotein kinase C activity. Alternatively, non esterified arachidonate may be produced presynaptically, by stimulation of phospholipase-linked neurotransmitter receptors. Based on results published in ref 22.

Hypothetical model of pyrocatechase.

Hypothetical model of regulations in cytokinin metabolism.



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