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Alpha cleavage mechanism

Fig. 3. The role of FKN/CX3R1 in inducing atherosclerosis may involve two mechanisms. The first is the release of soluble FKN through cleavage of membrane-expressed FKN by TNF-alpha converting enzyme (TACE). Soluble FKN is then able to attract circulating monocytes and effector T cells expressing CX3CR1. The second mechanism is that of firm adhesion of circulating cells to membrane-bound FKN. Fig. 3. The role of FKN/CX3R1 in inducing atherosclerosis may involve two mechanisms. The first is the release of soluble FKN through cleavage of membrane-expressed FKN by TNF-alpha converting enzyme (TACE). Soluble FKN is then able to attract circulating monocytes and effector T cells expressing CX3CR1. The second mechanism is that of firm adhesion of circulating cells to membrane-bound FKN.
A possible mechanism for the cleavage may involve the formation of an olefin-metal complex intermediate in which the silicon atom alpha to the vinyl group would be vulnerable to the attack of ethanol. [Pg.79]

Shyadehi, A.Z., D.C. Lamb, S.L. Kelly, D.E. Kelly, W.H. Schunck, and J.N. Wright et al. (1996). The mechanism of the acyl-carbon bond cleavage reaction catalyzed by recombinant sterol 14a-demethylase of Candida albicans (other names are Lanosterol 14 alpha-demethylase, P-45014DM, and CYP51). J. Biol. Chem. 271, 12445-12450. [Pg.615]

Akhtar M, Corina D, Miller S, Shyadehi AZ, Wright JN (1994) Mechanism of the acyl-carbon cleavage and related reactions catalyzed by multifunctional P-450s studies on cytochrome P-450(17)alpha. Biochemistry 33 4410-4418... [Pg.106]

B. W. Murray, V. Wittmann, M. D. Burkart, S. C. Hung, C. H. Wong, Mechanism of human alpha-l,3-fucosyItransferase V glycosidic cleavage occurs prior to nucleophilic attack. Biochemistry, (1997), 36, 823-31. [Pg.1329]

An elucidation of the mechanisms of brain iron homeostasis, as outlined in figure 1, will help our understanding of AD especially since iron binds to Ap-peptide and enhances beta-amyloid toxicity [35-38]. Excess iron accumulation is a consistent observation in the AD brain. As discussed above, patients with hemochromatosis are at risk developing AD at an earlier age [2]. Brain autopsy samples from AD patients have elevated levels of ferritin iron, particularly in the neurons of the basal ganglia [39] and most amyloid plaques contain iron and ferritin-rich cells [40]. Clinically there is a reported decrease in the rate of decline in AD patients who were treated with the intramuscular iron chelator, desferrioxamine [41]. Iron enhances cleavage of the Ap-peptide domain of APP by the metalloprotease alpha secretase [42, 43]. Part of the protective effect of the major cleavage product of APP, APP(s), may derive from its capacity to scavange metals to diminish metal-catalyzed oxidative stress to neuronal cells [44]. APP is, itself, a metalloprotein [4]. [Pg.218]

According to Wall and co-workers [2] the pyrolysis of polyethylene proceeds by a radical chain mechanism. The products formed result from the process of random-chain cleavage, followed by intermolecular or intramolecular hydrogen abstraction. Hydrogen abstraction occurs preferentially at tertiary carbon atoms, and product formation results from homolysis of the carbon-carbon bond at the beta position relative to the radical site. The major products formed are the -alkanes and alpha-omega-diolefins. The peaks between the triplets result from chain branching. [Pg.140]

Kalsheker NA, Beam S, Chambers L, Sreedharan S, Brocklehurst K, Lomas DA. The house dust mite allergen Der p 1 catalytically inactivates alpha 1-antitrypsin by specific reactive centre loop cleavage a mechanism that promotes airway inflammation and asthma. Biochem Biophys Res Commun 1996 221 59-61. [Pg.516]


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