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Maciej Pietrzak and Monika Puzianowska-Kuznicka

figure represents the mean results of nine experiments, ± s.d . Discussion In this work, we showed that MCL-1, an anti-apoptotic member of the BCL-2 family, is activated by T 3 using a non-genomic mechanism that involves the PI3-K signal transduction

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J Liu, X-D Li, A Ora, P Heikkilä, A Vaheri and R Voutilainen

inhibition of the death signal. For the latter, evidence for an important role of nuclear factor-κB-mediated anti-apoptotic gene expression has already been obtained. When both pathways are activated by TNFα, the final decision to survive or die is mostly

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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

following three categories: pro-survival (BCL2, BCLxl, MCL1, BCLw and A1), pro-apoptotic (BAX, BAK and BOK) and BH3-only proteins, which are also pro-apoptotic and divided in sensitizers (DP5, BIK, NOXA and BAD) and activators (BIM, PUMA and BID) ( Kim et

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Ian L P Beales and Olorunseun O Ogunwobi

system to describe in detail the cell signalling pathway activated by G-Gly leading to anti-apoptotic effects. This further strengthens the implications that endocrine, paracrine or autocrine secretion of G-Gly is a growth factor or anti-apoptotic factor

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Lykke Blaabjerg, Gitte L Christensen, Masahito Matsumoto, Talitha van der Meulen, Mark O Huising, Nils Billestrup and Wylie W Vale

types of diabetes as they converge on common effectors. This is true for interleukin 1 beta (IL1β) and tumour necrosis factor alpha (TNFα) signaling, as both these pathways lead to the activation of two key pro-apoptotic signaling pathways in the β

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Kira Meyerovich, Fernanda Ortis, Florent Allagnat and Alessandra K Cardozo

. 2011 ). However, PERK/ATF4 can initiate pro-apoptotic responses via upregulation of the C/EBP homologous protein (CHOP) ( McCullough et al. 2001 , Oyadomari et al. 2002a , b , Oyadomari & Mori 2004 ). Activation of the third UPR branch, the

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Özlem Erdogdu, Linnéa Eriksson, Hua Xu, Åke Sjöholm, Qimin Zhang and Thomas Nyström

endothelial cells (HCAECs) express the GLP1 receptor and that exendin-4 is able to activate the receptor, leading to increased cell proliferation, involving the eNOS pathway ( Erdogdu et al . 2010 ). GLP1 has also been described as an anti-apoptotic factor in

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Ying Ying, Huazhang Zhu, Zhen Liang, Xiaosong Ma and Shiwei Li

. Our results further validated that application of exendin-(9–39) markedly abrogated the anti-apoptotic effect of GLP1 on cardiomyocytes under palmitate stimulus, leading to increased activation of caspase-3 and PARP ( Fig. 6C ). Moreover, inhibition of

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Hanna K Nyblom, Ernest Sargsyan and Peter Bergsten

( Berne 1975 , Nyblom et al . 2008 ). Such lipid accumulation has been implicated in the deterioration of β-cell function ( Unger et al . 1999 ). Under conditions of nutrient abundance, AMP-activated protein kinase (AMPK), a key regulator of cellular

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A Pestka, B Toth, C Kuhn, S Hofmann, I Wiest, G Wypior, K Friese and U Jeschke

al . 2007 ). Trophoblasts react to maternal immunological dysregulation by activation of the intrauterine pro-apoptotic Fas/Fas ligand (FasL) system ( Minas et al . 2007 ). We further observed that an increased expression of FasL is associated with