Stress cells

Welch W, Brown CR (1996) Influence of molecular and chemical chaperones on protein folding. Cell Stress Chaperones 1 109-115... 

Proteasomal inhibition represents a novel strategy in cancer treatment and the small molecule Bortezomid (PS-341, Velcade ) has been approved for the treatment of refractory and relapsed multiple myeloma, a proliferative disease of plasma cells. Bortezomid inhibits an active site in a proteasome subunit and remarkably shows selective cytotoxicity to cancer cells. Although the underlying mechanisms are not completely understood bortezomid apparently induces a cell stress response in these tumor cells followed by caspase-dependent apoptosis. Whether bortezomid is beneficial for the treatment of other proliferative disease is currently being tested in clinical trials. 

Growth characteristics of cells exposed to water stress mimic some of the structural responses of organised plant tissues. A frequently observed response of plants exposed to water stress is a reduction in cell size (Cutler, Rains Loomis, 1977). This cellular phenomenon was observed in tomato cells stressed with PEG (Handa et al., 1983). Concomitantly with a decrease in cell size with increasing osmotic stress was a reduction in fresh weight. In contrast the dry weight was not affected. 

Chow, A. M. Brown, I. R. Induction of heat shock proteins in differentiated human and rodent neurons by celastrol. Cell Stress Chaperones 2007, 12, 237-244. 

Pinot, F., el Yaagoubi, A., Christie, R, Dinh-Xuan, A.T., and Polla, B.S. 1997. Induction of stress proteins by tobacco smoke in human monocytes Modulation by antioxidants. Cell Stress Chaperones 2 156-161. 

Wang, X., Flynn, A., Waskiewicz, A. J., Webb, B. L. J., Vries, R. G., Baines, I. A., Cooper, J., and Proud, C. G. (1998). The phosphorylation of eukaryotic initiation factor eIF4E in response to phorbol esters, cell stresses, and cytokines is mediated by distinct MAP kinase pathways. J. Biol. Chem. 273, 9373-9377. 

B. L. Bennett, JNK - A Central Effector of Cell Stress Response, 6th World Congress on Inflammation, August 2-6, 2003, Vancouver, Canada. 

Radad, K., Gille, G., Moldzio, R., Saito, H., and Rausch, W.-D. (2004b). Ginsenosides Rbl and Rgl effects on mesencephalic dopaminergic cells stressed with glutamate. Brain Res. 1021, 41-53. 

NAD Metabolism Chromatin structure Cell stress responses Apoptosis Aging... 

The inflammasome first line of the immune response to cell stress. Cell 2006 126 659-662. 

At the top of this list of false positives are the heat shock proteins. These could be termed real positives as they may reflect the fact that the bait protein does not fold appropriately and thus binds as in a normal cell stress response to the heat shock proteins. 

Sakagami, M., P. Morrison, and W. J. Welch. Benzoquinoid ansamycins (herbimycin A and geldanamycin) interfere with the maturation of growth factor receptor tyrosine kinases. Cell Stress Chaperones. 4 19-28.1999. 

Table 14.2 Progressive response to sub-lethal cell stress.

Based on the kno vledge of the processes of T cell sensitization by chemicals and the importance of T cells in induction of autoimmune diseases a number of key indicators of autoimmunogenic compounds can be defined. These include the possibility to be subject of metabolic conversion (either intra- or extra-hepatically), the capacity to activate dendritic cells, to induce cytokine production (in any cell type), or the potency to cause cell stress or cell death. Most of these processes can be studied in vitro, but none of the available methods have been tested for this purpose and often chemicals may behave completely different in vitro than in vivo. However, much can be learned from initiatives to design alternative methods for contact allergens, as many of these basic processes that lead to T cell sensitization are similar for allergenic and autoimmunogenic chemicals. 

An unusual feature of the herpes viruses is their preference for nerve cells. Stress to the nervous system, such as emotional stress or sunburn, can cause the virus to replicate, which leads to an outbreak through the skin. When they are not replicating, these viruses remain in nerve cells where they are not detected by the body s immune system, which has little activity in nerve cells. While remaining dormant in the nervous system, the viruses evade not only the immune system but antiviral drugs as well. 

Calabrese V, Mancuso C, Sapienza M, Puleo E, Calafato S, Cornelius C, Finocchiaro M, Mangiameli A, Di Mauro M, Stella AM, Castellino P. 2007c. Oxidative stress and cellular stress response in diabetic nephropathy. Cell Stress Chaperones 12 299-306. 

Stern, D., et al. 2002. Receptor for advanced glycation endproducts A multiligand receptor magnifying cell stress in diverse pathologic settings. Adv Drug Del Rev 54 1615. 

Cheetham ME. 1995. Cell stress genes and chronic neurodegenerative disorders. Neuropathol Appl Neurobiol 21 486-488. 

McLeod, K.J., Rubin, C.T., et.al.(1998) Skeletal cell stresses and bone adaptation. American Journal of Medical Science 316 176-183... 

Malago, J.J., Koninkx, J.F.J.G., and van Dijk, J.E. 2002. The heat shock response and cytoprotection of the intestinal epithelium. Cell Stress Chaperon 7 191-199. 

Fig. 3.5 Metabolism of 2 furnishes 118 metabolites via 25 different pathways ofwhich those are depicted in this scheme that are gluthatione (GSH) dependent. From the exemplary biotransformation of 2 can be inferred that besides stereoselective reduction there exist competing pathways in S. cerevisiae as a result of xenobiotic cell stress (/) stereoselective reduction,...

Jorg, G., Hemery, T., Bertau, M. Effects of cell-stress protectant glutathione on the whole-cell biotransformation of ethyl 2-chloro-acetoacetate with Saccharomyces cerevisiae. Biocatal. Biotransform. 2005, 23 9-17. 

Mechanosensing is postulated to involve many different cellular and extracellular components. Mechanical forces cause direct stretching of protein-cell surface integrin binding sites that occur on all eukaryotic cells. Stress-induced conformational changes in the extracellular matrix may alter integrin structure and lead to activation of several secondary messenger pathways within the cell. Activation of these pathways leads to altered reg-... 

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