Endoplasmic reticulum ER stress

ERSE Endoplasmic reticulum (ER) stress-response element... 

Qian, Y.. and Tilfany-Casiiglioni, E. (2003). Lead-induced endoplasmic reticulum (ER) stress respon.ses in the nervous system. Aewrocficui. Res. 28, 153-162. 

TD alters protein processing and induces endoplasmic reticulum (ER) stress which is a response to unfolded proteins. The microsomal fractions contain 20-24% of the thiamine in the cells (Balaghi and Pearson, 1966). TD up-regulates several markers... 

There are some studies where the ability of berberine to inhibit the HIV-I has been evaluated [107,119].Zhaet al. identified a key cellular mechanism underlying the protective effect of berberine on HIV Pl-induced inflammatoiy response in macrophages. Modulation of the endoplasmic reticulum (ER) stress response represents a potential therapeutic target for various inflammatory diseases and metabolic syndromes, including HIV Pl-associated atherosclerosis. However, in vivo and clinical studies are needed to further clarify the putative application of berberine in anti-HIV therapy. 

Ramos-Castaneda, J., Park, Y.N., Liu, M., Hauser, K., Rudolph, H., Shull, G.E., Jonkman, M.F., Mori, K., Ikeda, S., Ogawa, H., and Arvan, P., 2005, Deficiency of ATP2C1, a Golgi ion pump, induces secretory pathway defects in endoplasmic reticulum (ER)-associated degradation and sensitivity to ER stress. J. Biol. Chem. 280, 9467—9473... 

Yoneda T, Imaizumi K, Oono K, Yui D, Gomi F, Katayama T, Tohyama M (2001), Activation of caspase-12, an endoplasmic reticulum (ER) resident caspase, through tumor necrosis factor receptor-associated factor 2-dependent mechanism in response to the ER stress, J. Biol. Chem. 276 13935-13940. 

In addition to cytochrome c, other factors such as apoptosis inducing factor (AIF), endonuclease G, and second mitochondria-derived activator of caspases (Smac/DIABLO) may also be released from the inter-mitochondrial membrane space to exert their pro-apoptotic effects (see later). Recently, the endoplasmic reticulum (ER) has been identified as another organelle that can initiate the intrinsic apoptotic cascade in response to cellular stress. The ER is essential for proper... 

Interactions between Ap and x-protein are also related to mitochondrial dysfunction [20]. Ap and x-protein can mutually reinforce their neurotoxic effects by inhibiting the function of mitochondria and their axonal transport. Ap-induced stress affects endoplasmic reticulum (ER) [21]. Experimental findings support the hypothesis that just oligomers are the toxic forms of the x-protein showing during the AD [22]. 

The mutations prevent the formation of disulphide bonds preventing normal folding of proinsuUn in the endoplasmic reticulum (ER) leading to ER stress, 3-cell apoptosis and neonatal diabetes mellitus (INS-NDM) Inactivating mutations cause decreased transcriptional activity influencing both pancreatic development and the transcription of key genes for insulin secretion (HNFIA-MODY)... 

MHC to exit the endoplasmic reticulum (ER). As a result, there is an endoplasmic reticulum stress response, which leads to activation of the transcription factor nuclear factor kB (NFkB) and further cytokine release with subsequent accumulation of misfoided MHC glycoproteins, including phosphorylated tau and amyloid-related proteins. (Reproduced fromDalakas [72].)... 

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