Dependent Pathways

Histone acetyltransferases (HATs) and histone deacetylases (HDACs) represent two enzyme classes that, respectively, catalyze forward and backward reaction kinetics of lysine residne acetylation of nucleosomal histones and varions transcription 

HDACs attain facilitated gain-of-function, thereby unsettling the acetylation homeostasis. At this stage, transcription of pro-survival genes is profoundly repressed due to collapsed histone gates at their promoter regions. Furthermore, several transcription factors like CREB, NF-kB, Spl, and HIF fail to perform their pro-survival transcription duties as all these TFs require to be acetylated for activation. 

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Both prokaryotes and eukaryotes are capable of introducing a single cis double bond in a newly synthesized fatty acid. Bacteria such as E. coli carry out this process in an Og-independent pathway, whereas eukaryotes have adopted an Og-dependent pathway. There is a fundamental chemical difference between the two. The Og-dependent reaction can occur anywhere in the fatty acid chain. 

The tethering of PKA through AKAPs by itself is not sufficient to compartmentalize and control a cAMP/ PKA-dependent pathway. Cyclic AMP readily diffuses throughout the cell. Therefore, discrete cAMP/PKA signalling compartments are only conceivable if this diffusion is limited. Phosphodiesterases (PDE) establish gradients of cAMP by local hydrolysis of the... 

The key end result of TLR signalling is the induction of cytokines. Cytokines are proteins produced during an immune response that allow the maturation, activation and differentiation of effector cells in the immune system. The activation of NFkB and AP-1 by the MyD88 and the TREF dependent pathways leads to the production of proinflammatory cytokines such as IL-6, TNF-a and various chemokines. This pathway can also activate IRF-7 via TLR-7and TLR-9 allowing Type-I interferons to be produced. 

The activation of DRF-3 through the TREF dependent pathway allows for chemokines such as RANTES to be produced. It also leads to the production of DFN-a and EFN-(3, which are involved in anti-viral immunity. The TREF pathway, activated by either TLR-3 or TLR-4, can also induce MHC class-II expression and costimulatory molecules, thus leading to T-cell activation. This provides an important link between innate and adaptive immunity. 

Besides the well-established Wnt/(3-catenin-dependent pathway components mentioned above, several additional cytoplasmic inhibitors of Wnt/ 3-catenin-dependent signaling have been identified that share... 

Wnt/non-P-catenin signaling is not as well characterized biochemically as the Wnt/p-catenin-dependent pathway this may reflect that it is molecularly more diverse, at least in vertebrates. In Drosophila the best characterized Wnt/non-P-catenin pathway is planar cell polarity (PCP) signaling. Ironically, although it certainly depends on a Fz receptor, it remains... 

The cytochrome P-450-dependent metabolism of trichloroethylene was studied in hepatic microsomal fractions from 23 different humans (Lipscomb et al. 1997). CYP2E1 was the predominant form of P-450 responsible for the metabolism of trichloroethylene in humans. Incubations of trichloroethylene with the microsomal preparations resulted in hyperbolic plots consistent with Michaelis-Menton kinetics. The values ranged from 12 to 55.7 pM, and were not normally distributed, and the values range from 490 to 3,455 pmol/min/mg protein and were normally distributed. The study authors concluded that the human variability in metabolism of trichloroethylene via P-450-dependent pathways was within a 10-fold range. 

These data show that disruption of chrysobactin biosynthesis enhances the expression of pelD uidA. In addition, the lack of repression of the fusion by iron in chrysobactin-deficient cells indicates that the iron supplied cannot be internalized via the achromobactin dependent pathway. Hence, IF must contain strong iron-free ligands scavenging the Fe(III) supplied. 

The degradation of trichloroethene by Alcaligenes eutrophus JMP134 is carried out by either a chromosomal phenol-dependent pathway, or by the plasmid-borne 2,4-dichloro-phenoxyacetate pathway (Harker and Kim 1990). 

Boyd JM, A Ellsworth, SA Ensign (2006) Characterization of 2-bromoethanesulfonate as a selective inhibitor of the coenzyme M-dependent pathway and enzymes of bacterial aliphatic epoxide metabolism. J Bacteriol 188 8062-8069. 

Sluis MK, El Small, JR Allen, SA Ensign (1996) Involvement of an ATP-dependent carboxylase in a COj-dependent pathway of acetone metabolism by Xanthobacter strain Py2. J Bacteriol 178 4020-4026. 

McNally, A.K., Chisholm, G.M., Morel, D.W. and Cathcart, M. (1990). Activated human monocytes oxidise low density lipoprotein by a lipoxygenase dependent pathway. J. Immunol. 145, 254-259. 

Smit MJ, Verdijk P, van der Raaij-Helmer EM, et al. CXCR3-mediated chemotaxis of human T cells is regulated by a Gi- and phospholipase C-dependent pathway and not via activation of MEK/p44/p42 MAPK nor Akt/PI-3 kinase. Blood 2003 102(6) 1959-1965. 

Iwabu A, Smith K, Allen FD, Lauffenburger DA, Wells A. Epidermal growth factor induces fibroblast contractility and motility via a protein kinase C delta-dependent pathway. J Biol Chem 2004 279(15) 14551-14560. 

Becker, C. G., Van Hamont, N., Wagner, M., Tobacco, cocoa, coffee and ragweed Crossreacting allergens that activate factor-XII-dependent pathways, Blood, 58, 861, 1981. (CA96 33194b)... 

Kl. Kalter, E. S., Daha, M. R Ten Cate, J. W Verhoef, J., and Bouma, B. N., Activation and inhibition of Hageman factor-dependent pathways and the complement system in uncomplicated bacteremia or bacterial shock. J. Infect. Dis. 151,1019-1027 (1985). 

Machovich R Owen W. G. An elastase-dependent pathway of plasminogen activation. Biochemistry 1989 28,4517-22. 

A Rich, JL Rae. (1995). Calcium entry in rabbit corneal epithelial cells Evidence for a non-voltage dependent pathway. J Membr Biol 144 177-184. 

Kessey, K. 8r Mogul, D. J. (1998). Adenosine A2 receptors modulate hippocampal synaptic transmission via a cyclic-AMP-dependent pathway. Neuroscience 84 (1), 59-69. 

A potentially powerful probe for sorting out the contribution of hydroperoxide-dependent and mixed-function oxidase-dependent polycyclic hydrocarbon oxidation is stereochemistry. Figure 9 summarizes the stereochemical differences in epoxidation of ( )-BP-7,8-dihydrodiol by hydroperoxide-dependent and mixed-function oxidase-dependent pathways (31,55,56). The (-)-enantiomer of BP-7,8-dihydrodiol is converted primarily to the (+)-anti-diol epoxide by both pathways whereas the (+)-enantiomer of BP-7,8-dihydrodiol is converted primarily to the (-)-anti-diol epoxide by hydroperoxide-dependent oxidation and to the (+)-syn-diol epoxide by mixed-function oxidases. The stereochemical course of oxidation by cytochrome P-450 isoenzymes was first elucidated for the methycholanthrene-inducible form but we have detected the same stereochemical profile using rat liver microsomes from control, phenobarbital-, or methyl-cholanthrene-induced animals (32). The only difference between the microsomal preparations is the rate of oxidation. 

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