Protein induction

Vass, K., Welch, W.J., Nowak, T.S.J. (1988). Localization of 70 kD stress protein induction in gerbil brain after ischemia. Acta Neuropath. (Berl.) 77, 128-135. 

Goering PL, Fisher BR, Chaudhary PP, Dick CA. 1992. Relationship between stress protein induction in rat kidney by mercuric chloride and nephrotoxicity. Toxicol Appl Pharmacol 113 184-191. 

Helqvist, S., Polla, B. S., Johannesen, J., and Nerup, J. (1991). Heat shock protein induction in rat pancreatic islets by human recombinant interleukin lj8. Diabetologia 34, 150-156. 

Yoo, C.G., Lee, S., Lee, C.T., Kim, Y.W., Han, S.K. and Shim, Y.S. (2000) Anti-inflammatory effect of heat shock protein induction is related to stabilization of IkappaB alpha through preventing IkappaB kinase activation in respiratory epithelial cells. J. Immunol., 164, 5416-5423. 

Berchtold, N.C. et al., Exercise primes a molecular memory for brain-derived neurotrophic factor protein induction in the rat hippocampus, Neuroscience, 133, 853, 2005. 

Until recently, intestinal metabolism via CYP3A4-mediated metabolic pathways was thought to be insignificant because of the lower levels of expression compared with that seen in the liver and slower metabolic rates measured for intestinal microsomes (224). However, similar Km values have been reported for midazolam 1 -hydroxylation by microsomes obtained in the upper intestine and the liver (254,255). This correlation indicates that the upper intestine and hepatic CYP3 A4 are functionally equivalent. Such findings further establish the importance of the intestine in the elimination of orally administered substrates for CYP3 A4-mediated metabolic pathways. Additionally, coadministration of substrates/inhibitors that may alter the function of these proteins (induction, inhibition) could further be responsible for the variability in intestinal absorption (dmg interactions) seen for some dmgs. 

Matsuda, H., Kagerura, T., Toguchida, I., Ueda, H., Morikawa, T. and Yoshikawa, M. (2000) Inhibitory effects of sesquiterpenes from bay leaf on nitric oxide production in lipopolysaccharide activated macrophages structure requirement and role of heat shock protein induction. Life Sciences 66(22), 2151-21 57. 

Balia, J. Jacob H.S. Balia, G. Nath, K. Eaton, J. W. Vercellotti, G.M. Endothelial-cell heme uptake from heme proteins induction of sensitization and desensitization to oxidant damage. Proc. Natl. Acad. Sci. USA. 90 9285-9289 1993. 

Liu X, Squibb KS, Akkerman M, Nordberg GF, Lipsky M, Fowler BA. Cytotoxicity, zinc protection and stress protein induction in rat proximal tubule cells exposed to cadmium chloride in primary cell culture. Renal Failure 1996 8 867-882. 

Heat shock proteins is a family of proteins which were identified in relation to heat stress response and they are categorized on the basis of their approximate molecular weights. Heat shock protein induction is a rapid response to altered redox state and closely corresponds to the activity of antioxidant enzymes such as catalase. Heat shock proteins are induced in response to a number of stresses, including sublethal heal, hypoxia, reoxygenation and ischemia and reperfusion. 

K. A. Nieforth, R. Nadeau, I. H. Patel, and D. Mould, Use of an indirect pharmacodynamic stimulation model of MX protein induction to compare in vivo activity of interferon alfa-2a and a polyethylene glycol-modified derivative in healthy subjects. Clin Pharmacol Ther 59(6) 636-646 (1996). 

These results again indicate that TNF specifically induces Mn-SOD protein but not Cu,Zn-SOD protein. Induction of Mn-SOD was also seen in A549 cells, a human adenocarcinoma cell line. 

Although l,25(OH)2D3 is a potent inhibitor of Thl-dominated EAE and IFN-y secretion is clearly inhibited in vitro, l,25-(OH)2 D3 failed to suppress Thl cells in vivo using a myelin basic protein induction model of EAE [106]. At the same time, whatsoever, no upregulation of IL-4 transcription was observed in animals protected from EAE through l,25(OH)2D3 [106]. This study speaks against both putative immunoregulatory mechanisms in l,25(OH)2D3 action, inhibition ofThl responses as well as induction of Th2 responses. The immunomodulatory effects of 1,25 (OH)2D3 can therefore not entirely be attributed to and explained by effects on the Thl /Th2 cytokine balance. However, the majority of reports consistently demonstrate that Thl Tcells are relatively more susceptible to l,25(OH)2D3 treatment. This may also explain the clinical efficacy of l,25(OH)2D3 predominantly in the treatment of Thl-mediated diseases as outlined below. 

Ren M et al (2004) Valproic acid reduces brain damage induced by transient focal cerebral ischemia in rats potential roles of histone deacetylase inhibition and heat shock protein induction. J Neurochem 89(6) 1358-1367... 

Hollnagel, A., Oehlmann, V., Heymer, J., Ruther, U., Nordheim, A. 1999. Id genes are direct targets of bone morphogenetic protein induction in embryonic stem cells. J. Biol. Chem. 274, 19838-19845. 

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