Photodynamic therapy with hexyl aminolevulinate induces carbonylation, posttranslational modifications and changed expression of proteins in cell survival and cell death pathways

2011 ◽  
Vol 10 (7) ◽  
pp. 1137 ◽  
Author(s):  
Yan Baglo ◽  
Mirta M. L. Sousa ◽  
Geir Slupphaug ◽  
Lars Hagen ◽  
Sissel Håvåg ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Survival ◽  
Posttranslational Modifications ◽  
Cell Death Pathways

scholarly journals ZBP1/DAI ubiquitination and sensing of influenza vRNPs activate programmed cell death

2017 ◽  
Vol 214 (8) ◽  
pp. 2217-2229 ◽  
Author(s):  
Sannula Kesavardhana ◽  
Teneema Kuriakose ◽  
Clifford S. Guy ◽  
Parimal Samir ◽  
R.K. Subbarao Malireddi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Posttranslational Modifications ◽  
Influenza A ◽  
Influenza Virus Infection ◽  
Dna Binding Protein ◽  
Cell Death Pathways ◽  
Signaling Axis ◽  
Trigger Cell Death ◽  
Inducible Gene

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.

scholarly journals Cell Death Pathways in Photodynamic Therapy of Cancer

Cancers ◽  
2011 ◽  
Vol 3 (2) ◽  
pp. 2516-2539 ◽  
Author(s):  
Pawel Mroz ◽  
Anastasia Yaroslavsky ◽  
Gitika B Kharkwal ◽  
Michael R. Hamblin
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Death Pathways ◽  
Photodynamic Therapy Of Cancer

scholarly journals The actin nucleation factors JMY and WHAMM enable a rapid p53-dependent pathway of apoptosis

2020 ◽  
Author(s):  
Virginia L. King ◽  
Nathan K. Leclair ◽  
Kenneth G. Campellone
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Actin Cytoskeleton ◽  
Cell Survival ◽  
G Protein ◽  
Actin Nucleation ◽  
Caspase Cleavage ◽  
Cell Death Pathways ◽  
Small G Protein

AbstractThe actin cytoskeleton is a well-known player in most vital cellular processes, but comparably little is understood about how the actin assembly machinery impacts programmed cell death pathways. In the current study, we explored roles for the human Wiskott-Aldrich Syndrome Protein (WASP) family of actin nucleation factors in DNA damage-induced apoptosis. Inactivation of each WASP-family gene revealed that two, JMY and WHAMM, are required for rapid apoptotic responses. JMY and WHAMM enable p53-dependent cell death by enhancing mitochondrial permeabilization, initiator caspase cleavage, and executioner caspase activation. The loss of JMY additionally results in significant changes in gene expression, including upregulation of the small G-protein RhoD. Depletion or deletion of RHOD increases cell death, suggesting that RhoD normally plays a key role in cell survival. These results give rise to a model in which JMY and WHAMM promote intrinsic cell death responses that can be opposed by RhoD.Author SummaryThe actin cytoskeleton is a collection of protein polymers that assemble and disassemble within cells at specific times and locations. Cytoskeletal regulators called nucleation-promoting factors ensure that actin polymerizes when and where it is needed, and many of these factors are members of the Wiskott-Aldrich Syndrome Protein (WASP) family. Humans express 8 WASP-family proteins, but whether the different factors function in programmed cell death pathways is not well understood. In this study, we explored roles for each WASP-family member in apoptosis and found that a subfamily consisting of JMY and WHAMM are critical for a rapid pathway of cell death. Furthermore, the loss of JMY results in changes in gene expression, including a dramatic upregulation of the small G-protein RhoD, which appears to be crucial for cell survival. Collectively, our results point to the importance of JMY and WHAMM in driving intrinsic cell death responses plus a distinct function for RhoD in maintaining cell viability.

Autophagy in response to photodynamic therapy: cell survival vs. cell death

2009 ◽  
Author(s):  
Nancy L. Oleinick ◽  
Liang-yan Xue ◽  
Song-mao Chiu ◽  
Sheeba Joseph
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Survival

scholarly journals Cell Death Pathways Associated with Photodynamic Therapy: An Update

2018 ◽  
Vol 94 (2) ◽  
pp. 213-218 ◽  
Author(s):  
David Kessel ◽  
Nancy L. Oleinick
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Death Pathways

Anticancer Effects and Cell Death Pathways in Ultralow-Power 980 nm Laser-Triggered Photodynamic Therapy by Gd2O3:Yb, Tm Nanoparticles

2019 ◽  
Vol 15 (3) ◽  
pp. 462-476 ◽  
Author(s):  
Guoliang Li ◽  
Weihua Wang ◽  
Shaoxin Song ◽  
Yajun Sun ◽  
Jianfeng Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Death Pathways ◽  
Anticancer Effects ◽  
Ultralow Power
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