Search Results

You are looking at 21 - 30 of 70 items for :

  • "ER stress" x
Clear All
Free access

Gábor Bánhegyi, Miklós Csala and Angelo Benedetti

-cells, etc.) can adapt their ER capabilities to cope with the alterations of metabolic demand. Extreme metabolic conditions (either over- or undernutrition) result in ER stress sensed fundamentally by the luminal machinery of protein folding. ER stress causes

Free access

Stacey N Walters, Jude Luzuriaga, Jeng Yie Chan, Shane T Grey and D Ross Laybutt

-cell glucotoxicity ( Poitout & Robertson 2008 , Weir et al . 2009 , Bensellam et al . 2012 ), but they remain poorly understood. Endoplasmic reticulum (ER) stress has emerged over the last few years as an important mechanism of β-cell failure ( Laybutt et al

Free access

Emily Tubbs and Jennifer Rieusset

the regulation of whole-body metabolism. In agreement, mitochondrial dysfunction and ER stress have been largely and independently associated with metabolic diseases, such as obesity, type 2 diabetes mellitus (T2DM) ( Chang et al . 2015 , Rieusset

Free access

Hanna K Nyblom, Ernest Sargsyan and Peter Bergsten

. Figure 5 Apoptosis in INS-1E cells cultured for 5 days at 5.5, 11 or 27 mM glucose in the presence or absence of AICAR. Results show means± s.e.m. ( n =4). * P <0.05 compared with 5.5 mM glucose. # P <0.05 compared with the absence of AICAR. ER stress

Free access

Jinghua Peng and Ling He

leads to the activation of three canonical pathways: inositol-requiring enzyme 1 (IRE1)-XBP1s, PKR-like ER-regulating kinase and activating transcription factor 6 ( Ron & Walter 2007 ). The activation of these pathways can alleviate ER stress by placing

Free access

Bo Zhou, Huixia Li, Jiali Liu, Lin Xu, Qinyue Guo, Hongzhi Sun and Shufang Wu

-mediated activation of Erk1/2 and Akt signaling and protection against apoptosis in response to ER-stress ( Li et al . 2014 ). Autophagy induction is an indirect message that protein synthesis is in suspended state, and it is possible that it could benefit in

Free access

Tarlliza R Nardelli, Emerielle C Vanzela, Keli C Benedicto, Flora Brozzi, André Fujita, Alessandra K Cardozo, Décio L Eizirik, Antonio C Boschero and Fernanda Ortis

reticulum (ER) stress (via NO production in the case of rat beta cells) and cell death ( Cardozo et al . 2001 a , Darville et al . 2004 ). The canonical process of NFκB activation is initiated by the phosphorylation of the inhibitor of kappa B ( IkB

Free access

Srividya Vasu, R Charlotte Moffett, Neville H McClenaghan and Peter R Flatt

58 R – TGGTGGACCCTCTTCCGGCC Nos2 Nitric oxide synthase 2, inducible F – GCTCGCTTTGCCACGGACGA 146 58 R – AAGGCAGCGGGCACATGCAA ER stress Hspa4 Hsp70, Heat shock 70 kDa protein 4 F – GCACTGTGCACTGTACCAGGGGA 135 58 R – TCTCCAGGGAACTGGGCAGCTA Hspa5 BiP

Free access

Matthew L Rise, Susan E Douglas, Dionne Sakhrani, Jason Williams, K Vanya Ewart, Marlies Rise, William S Davidson, Ben F Koop and Robert H Devlin

stress response. In the absence of ER stress, transducers of ER stress signaling (e.g. activating tanscription factor 6 (ATF6), proteinkinase-like ER kinase (PERK)) are kept inactive through interaction with GRP78 ( Lee 2005 ). Conditions causing ER

Free access

Luis Varela, María J Vázquez, Fernando Cordido, Rubén Nogueiras, Antonio Vidal-Puig, Carlos Diéguez and Miguel López

context, increased levels of pFOXO1 after ghrelin treatment elicit a protective effect against lipotoxicity, as shown by inhibition of endoplasmic reticulum (ER) stress and reduced levels of C/EBP homologous protein (CHOP-10; Wang et al . 2010 a ), a pro