scholarly journals The brace helices of MLKL mediate interdomain communication and oligomerisation to regulate cell death by necroptosis

2018 ◽  
Vol 25 (9) ◽  
pp. 1567-1580 ◽  
Author(s):  
Katherine A. Davies ◽  
Maria C. Tanzer ◽  
Michael D. W. Griffin ◽  
Yee Foong Mok ◽  
Samuel N. Young ◽  
...  
Keyword(s):  
Cell Death ◽  
Regulate Cell Death ◽  
Interdomain Communication

scholarly journals Conserved Actin Cysteine Residues Are Oxidative Stress Sensors That Can Regulate Cell Death in Yeast

2007 ◽  
Vol 18 (4) ◽  
pp. 1359-1365 ◽  
Author(s):  
Michelle E. Farah ◽  
David C. Amberg
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cellular Response ◽  
Yeast Cells ◽  
Nuclear Fragmentation ◽  
Actin Isoforms ◽  
Chronological Aging ◽  
Stress Sensors ◽  
Universal Mechanism ◽  
Regulate Cell Death

Actin's functional complexity makes it a likely target of oxidative stress but also places it in a prime position to coordinate the response to oxidative stress. We have previously shown that the NADPH oxidoreductase Oye2p protects the actin cytoskeleton from oxidative stress. Here we demonstrate that the physiological consequence of actin oxidation is to accelerate cell death in yeast. Loss of Oye2p leads to reactive oxygen species accumulation, activation of the oxidative stress response, nuclear fragmentation and DNA degradation, and premature chronological aging of yeast cells. The oye2Δ phenotype can be completely suppressed by removing the potential for formation of the actin C285-C374 disulfide bond, the likely substrate of the Oye2p enzyme or by treating the cells with the clinically important reductant N-acetylcysteine. Because these two cysteines are coconserved in all actin isoforms, we theorize that we have uncovered a universal mechanism whereby actin helps to coordinate the cellular response to oxidative stress by both sensing and responding to oxidative load.

RanBPM Has Proapoptotic Activities That Regulate Cell Death Pathways in Response to DNA Damage

2009 ◽  
Vol 7 (12) ◽  
pp. 1962-1972 ◽  
Author(s):  
Elnaz Atabakhsh ◽  
Dawn M. Bryce ◽  
Karen J. Lefebvre ◽  
Caroline Schild-Poulter
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cell Death Pathways ◽  
Regulate Cell Death

scholarly journals Polarity proteins PAR6 and aPKC regulate cell death through GSK-3beta in 3D epithelial morphogenesis

2007 ◽  
Vol 120 (14) ◽  
pp. 2309-2317 ◽  
Author(s):  
M. Kim ◽  
A. Datta ◽  
P. Brakeman ◽  
W. Yu ◽  
K. E. Mostov
Keyword(s):  
Cell Death ◽  
Epithelial Morphogenesis ◽  
Polarity Proteins ◽  
Regulate Cell Death

scholarly journals The Role of Mitochondria in Pyroptosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Qian Li ◽  
Nengxian Shi ◽  
Chen Cai ◽  
Mingming Zhang ◽  
Jing He ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Pathological Process ◽  
Mitochondrial Outer Membrane ◽  
Therapeutic Effects ◽  
Mitochondrial Outer Membrane Permeabilization ◽  
Regulated Cell Death ◽  
Clinical Benefits ◽  
Regulate Cell Death

Pyroptosis is a recently discovered aspartic aspart-specific cysteine protease (Caspase-1/4/5/11) dependent mode of gene-regulated cell death cell death, which is represented by the rupture of cell membrane perforations and the production of proinflammatory mediaters like interleukin-18(IL-18) and interleukin-1β (IL-1β). Mitochondria also play an important role in apoptotic cell death. When it comes to apoptosis of mitochondrion, mitochondrial outer membrane permeabilization (MOMP) is commonly known to cause cell death. As a downstream pathological process of apoptotic signaling, MOMP participates in the leakage of cytochrome-c from mitochondrion to the cytosol and subsequently activate caspase proteases. Hence, targeting MOMP for the sake of manipulating cell death presents potential therapeutic effects among various types of diseases, such as autoimmune disorders, neurodegenerative diseases, and cancer. In this review, we highlights the roles and significance of mitochondria in pyroptosis to provide unexplored strategies that target the mitochondria to regulate cell death for clinical benefits.

Regulation of apoptosis by vasoactive peptides

2001 ◽  
Vol 281 (4) ◽  
pp. L749-L761 ◽  
Author(s):  
Gerasimos S. Filippatos ◽  
Nupur Gangopadhyay ◽  
Omosalewa Lalude ◽  
Narayanan Parameswaran ◽  
Sami I. Said ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Target Cell ◽  
Potential Role ◽  
Regulatory Activity ◽  
Vasoactive Peptides ◽  
Pulmonary Physiology ◽  
Cell Specificity ◽  
Growing Body ◽  
Regulate Cell Death

Although originally discovered because of their ability to affect hemodynamics, vasoactive peptides have been found to function in a variety of capacities including neurotransmission, endocrine functions, and the regulation of cell proliferation. A growing body of evidence describes the ability of vasoactive peptides to regulate cell death by apoptosis in either a positive or negative fashion depending on the peptide and the type of target cell. The available evidence to date is strongest for the peptides endothelin, angiotensin II, vasoactive intestinal peptide, atrial natriuretic peptide, and adrenomedullin. Each of these peptides is discussed, with specific regard to apoptosis, in terms of regulatory activity, target cell specificity, and potential role in pulmonary physiology.

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