scholarly journals Two Phytophthora parasitica cysteine protease genes, PpCys44 and PpCys45 , trigger cell death in various Nicotiana spp. and act as virulence factors

2020 ◽  
Vol 21 (4) ◽  
pp. 541-554 ◽  
Author(s):  
Qiang Zhang ◽  
Weiwei Li ◽  
Jiapeng Yang ◽  
Junjie Xu ◽  
Yuling Meng ◽  
...  
2019 ◽  
Vol 16 (1) ◽  
pp. 3-11
Author(s):  
Luisa Halbe ◽  
Abdelhaq Rami

Introduction: Endoplasmic reticulum (ER) stress induced the mobilization of two protein breakdown routes, the proteasomal- and autophagy-associated degradation. During ERassociated degradation, unfolded ER proteins are translocated to the cytosol where they are cleaved by the proteasome. When the accumulation of misfolded or unfolded proteins excels the ER capacity, autophagy can be activated in order to undertake the degradative machinery and to attenuate the ER stress. Autophagy is a mechanism by which macromolecules and defective organelles are included in autophagosomes and delivered to lysosomes for degradation and recycling of bioenergetics substrate. Materials and Methods: Autophagy upon ER stress serves initially as a protective mechanism, however when the stress is more pronounced the autophagic response will trigger cell death. Because autophagy could function as a double edged sword in cell viability, we examined the effects autophagy modulation on ER stress-induced cell death in HT22 murine hippocampal neuronal cells. We investigated the effects of both autophagy-inhibition by 3-methyladenine (3-MA) and autophagy-activation by trehalose on ER-stress induced damage in hippocampal HT22 neurons. We evaluated the expression of ER stress- and autophagy-sensors as well as the neuronal viability. Results and Conclusion: Based on our findings, we conclude that under ER-stress conditions, inhibition of autophagy exacerbates cell damage and induction of autophagy by trehalose failed to be neuroprotective.


2014 ◽  
Vol 26 (7) ◽  
pp. 2939-2961 ◽  
Author(s):  
Dandan Zhang ◽  
Di Liu ◽  
Xiaomeng Lv ◽  
Ying Wang ◽  
Zhili Xun ◽  
...  

Leukemia ◽  
2009 ◽  
Vol 23 (6) ◽  
pp. 1205-1206 ◽  
Author(s):  
D K Hiwase ◽  
D L White ◽  
V A Saunders ◽  
S Kumar ◽  
J V Melo ◽  
...  

2011 ◽  
Vol 55 (1) ◽  
pp. 297-311 ◽  
Author(s):  
Naina Sharma ◽  
Dinesh Mohanakrishnan ◽  
Amit Shard ◽  
Abhishek Sharma ◽  
Saima ◽  
...  

2019 ◽  
Vol 126 ◽  
pp. 45-55 ◽  
Author(s):  
Xuan Peng ◽  
Tao Luo ◽  
Xiaoqian Zhai ◽  
Chunxi Zhang ◽  
Jing Suo ◽  
...  

2017 ◽  
Vol 214 (8) ◽  
pp. 2217-2229 ◽  
Author(s):  
Sannula Kesavardhana ◽  
Teneema Kuriakose ◽  
Clifford S. Guy ◽  
Parimal Samir ◽  
R.K. Subbarao Malireddi ◽  
...  

Innate sensing of influenza virus infection induces activation of programmed cell death pathways. We have recently identified Z-DNA–binding protein 1 (ZBP1) as an innate sensor of influenza A virus (IAV). ZBP1-mediated IAV sensing is critical for triggering programmed cell death in the infected lungs. Surprisingly, little is known about the mechanisms regulating ZBP1 activation to induce programmed cell death. Here, we report that the sensing of IAV RNA by retinoic acid inducible gene I (RIG-I) initiates ZBP1-mediated cell death via the RIG-I–MAVS–IFN-β signaling axis. IAV infection induces ubiquitination of ZBP1, suggesting potential regulation of ZBP1 function through posttranslational modifications. We further demonstrate that ZBP1 senses viral ribonucleoprotein (vRNP) complexes of IAV to trigger cell death. These findings collectively indicate that ZBP1 activation requires RIG-I signaling, ubiquitination, and vRNP sensing to trigger activation of programmed cell death pathways during IAV infection. The mechanism of ZBP1 activation described here may have broader implications in the context of virus-induced cell death.


2005 ◽  
Vol 7 (9) ◽  
pp. 1365-1378 ◽  
Author(s):  
Eric Galiana ◽  
Marie-Pierre Rivière ◽  
Sophie Pagnotta ◽  
Emmanuel Baudouin ◽  
Franck Panabières ◽  
...  

2014 ◽  
Vol 106 (2) ◽  
pp. 529a
Author(s):  
Plamena R. Stroh ◽  
Marthe H.R. Ludtmann ◽  
Nicholas W. Wood ◽  
David Klenerman ◽  
Sonia Gandhi ◽  
...  

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