Dioxin toxicity, aryl hydrocarbon receptor signaling, and apoptosis—Persistent pollutants affect programmed cell death

2011 ◽  
Vol 41 (4) ◽  
pp. 292-320 ◽  
Author(s):  
Martin Chopra ◽  
Dieter Schrenk
2005 ◽  
pp. 603-628 ◽  
Author(s):  
Robert L. Tanguay ◽  
Eric A. Andreasen ◽  
Mary K. Walker ◽  
Richard E. Peterson

2021 ◽  
Vol 70 ◽  
pp. 33-39
Author(s):  
Andreia Barroso ◽  
João V Mahler ◽  
Pedro H Fonseca-Castro ◽  
Francisco J Quintana

2017 ◽  
Vol 27 (2) ◽  
pp. 57-69 ◽  
Author(s):  
Alexey V. Polonikov ◽  
Olga Yu. Bushueva ◽  
Irina V. Bulgakova ◽  
Maxim B. Freidin ◽  
Mikhail I. Churnosov ◽  
...  

2005 ◽  
Vol 83 (5) ◽  
pp. 579-588 ◽  
Author(s):  
Claudio A Hetz ◽  
Vicente Torres ◽  
Andrew F.G Quest

Apoptosis is a morphologically defined form of programmed cell death (PCD) that is mediated by the activation of members of the caspase family. Analysis of death-receptor signaling in lymphocytes has revealed that caspase-dependent signaling pathways are also linked to cell death by nonapoptotic mechanisms, indicating that apoptosis is not the only form of PCD. Under physiological and pathological conditions, cells demonstrate a high degree of flexibility in cell-death responses, as is reflected in the existence of a variety of mechanisms, including necrosis-like PCD, autophagy (or type II PCD), and accidental necrosis. In this review, we discuss recent data suggesting that canonical apoptotic pathways, including death-receptor signaling, control caspase-dependent and -independent cell-death pathways.Key words: apoptosis, necrosis, nonapoptotic programmed cell death, death receptors, ceramides.


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