scholarly journals Differentiating life and death: An inflammatory affair

2018 ◽  
Author(s):  
Dustin Lane
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Differentiation ◽  
Programmed Cell Death ◽  
Signaling Networks ◽  
Inhibitors Of Apoptosis ◽  
Life And Death ◽  
Cell Death Signaling ◽  
Cycle Dependent

Programmed cell death signaling networks are frequently activated to coordinate the process of cell differentiation, and a variety of apoptotic events can mediate the process. This can include the ligation of death receptors, the activation of downstream caspases, and the induction of chromatin fragmentation, and all of these events can occur without downstream induction of death. Importantly, regulators of programmed cell death also have established roles in mediating differentiation. This review will provide an overview of apoptosis and its regulation by Inhibitors of Apoptosis (IAPs) and Bcl-2 family members. It will then outline the cross-talk between NF-ĸB and apoptotic signaling in the regulation of apoptosis before discussing the function of these regulators in the control of cell differentiation. It will end on a discussion of how a DNA damage-directed, cell cycle-dependent differentiation program may be controlled across multiple passages through cell cycle, and will assert that the failure to properly differentiate is the underlying cause of cancer.

scholarly journals Differentiating life and death: An inflammatory affair

2018 ◽  
Author(s):  
Dustin Lane
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Differentiation ◽  
Programmed Cell Death ◽  
Signaling Networks ◽  
Inhibitors Of Apoptosis ◽  
Life And Death ◽  
Cell Death Signaling ◽  
Cycle Dependent

Programmed cell death signaling networks are frequently activated to coordinate the process of cell differentiation, and a variety of apoptotic events can mediate the process. This can include the ligation of death receptors, the activation of downstream caspases, and the induction of chromatin fragmentation, and all of these events can occur without downstream induction of death. Importantly, regulators of programmed cell death also have established roles in mediating differentiation. This review will provide an overview of apoptosis and its regulation by Inhibitors of Apoptosis (IAPs) and Bcl-2 family members. It will then outline the cross-talk between NF-ĸB and apoptotic signaling in the regulation of apoptosis before discussing the function of these regulators in the control of cell differentiation. It will end on a discussion of how a DNA damage-directed, cell cycle-dependent differentiation program may be controlled across multiple passages through cell cycle, and will assert that the failure to properly differentiate is the underlying cause of cancer.

scholarly journals SOG1 transcription factor promotes the onset of endoreduplication under salinity stress in Arabidopsis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kalyan Mahapatra ◽  
Sujit Roy
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Transcription Factor ◽  
Programmed Cell Death ◽  
Salinity Stress ◽  
Crucial Role ◽  
Genome Stability ◽  
Cell Cycle Checkpoint ◽  
Cell Cycle Regulators

AbstractAs like in mammalian system, the DNA damage responsive cell cycle checkpoint functions play crucial role for maintenance of genome stability in plants through repairing of damages in DNA and induction of programmed cell death or endoreduplication by extensive regulation of progression of cell cycle. ATM and ATR (ATAXIA-TELANGIECTASIA-MUTATED and -RAD3-RELATED) function as sensor kinases and play key role in the transmission of DNA damage signals to the downstream components of cell cycle regulatory network. The plant-specific NAC domain family transcription factor SOG1 (SUPPRESSOR OF GAMMA RESPONSE 1) plays crucial role in transducing signals from both ATM and ATR in presence of double strand breaks (DSBs) in the genome and found to play crucial role in the regulation of key genes involved in cell cycle progression, DNA damage repair, endoreduplication and programmed cell death. Here we report that Arabidopsis exposed to high salinity shows generation of oxidative stress induced DSBs along with the concomitant induction of endoreduplication, displaying increased cell size and DNA ploidy level without any change in chromosome number. These responses were significantly prominent in SOG1 overexpression line than wild-type Arabidopsis, while sog1 mutant lines showed much compromised induction of endoreduplication under salinity stress. We have found that both ATM-SOG1 and ATR-SOG1 pathways are involved in the salinity mediated induction of endoreduplication. SOG1was found to promote G2-M phase arrest in Arabidopsis under salinity stress by downregulating the expression of the key cell cycle regulators, including CDKB1;1, CDKB2;1, and CYCB1;1, while upregulating the expression of WEE1 kinase, CCS52A and E2Fa, which act as important regulators for induction of endoreduplication. Our results suggest that Arabidopsis undergoes endoreduplicative cycle in response to salinity induced DSBs, showcasing an adaptive response in plants under salinity stress.

G2/M Arrest Sensitizes Chronic Myelogenous Leukemia Cells to TRAIL-Induced Apoptosis

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4465-4465
Author(s):  
David Devlin ◽  
Eva Szegezdi ◽  
Paavilainen Tanja ◽  
Orsolya Orosz ◽  
Michael O'Dwyer ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Cycle Progression ◽  
Cell Cycle Checkpoint ◽  
Myelogenous Leukemia ◽  
Leukemia Cells ◽  
Induced Apoptosis ◽  
Cycle Dependent ◽  
Low Sensitivity

Abstract Abstract 4465 The death ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receives great interest as it targets and kills cancerous cells, but not non-transformed cells. While it is in phase I/II clinical trials for a range of solid tumours, the generally low sensitivity of leukemia cells to TRAIL makes it a less attractive therapeutic for these cancers. We found that doxorubicin and cytarabine, agents that induce DNA damage and impair cell cycle progression, can sensitize CML cells to TRAIL with CI<1 at Fa of ED25 and ED50 (based on median-effect method using the isobologram equation). Inhibition of the cell cycle checkpoint kinases Chk1/2 with UCN-01 did not influence TRAIL-induced apoptosis nor could it abolish the sensitizing effect of doxorubicin. Interestingly, inhibition of Ataxia Telangiectasia Mutated (ATM), a key DNA damage response kinase, with KU-55933 induced a G2/M arrest and enhanced TRAIL-induced apoptosis. Inhibition of ATM alone induced 22±3.1% apoptosis and increased TRAIL-induced apoptosis from 27.2±4.7% to 68±7.2%. Cell cycle analysis revealed that while the proportion of cells in the G0/G1 and S phases slightly increased, the proportion of the cells in the G2/M phase dropped by 31.6±3.2% (p<0.05) indicating that G2/M arrested cells were more sensitive to TRAIL than cells in G0/G1 and S phases. TRAIL-induced CML cell death was also synergistically enhanced by arresting the cells in G2/M using the microtubule disrupting drugs, nocodazole or colcemide. Cells were treated with a concentration of nocodazole or colcemide that induced above 90% G2/M arrest for 16 h (0.3 mM and 0.1 mg/ml, respectively) followed by treatment with 250 ng/ml of TRAIL for 24 h. Nocodazole, colcemide and TRAIL individually induced 19±3.7% 26.3±4.4% and 27.2±4.7% cell death, while combination of nocodazole or colcemide with TRAIL resulted 89±6.8% and 93±5.9% cell death, respectively. In summary, we found that induction of DNA damage sensitizes CML cells to TRAIL and that TRAIL-sensitivity of CML cells is cell cycle-dependent. Disclosures: O'Dwyer: Novartis: Honoraria.

Cell cycle-dependent reactivity with the monoclonal antibody Ki-67 during myeloid cell differentiation

1988 ◽  
Vol 179 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Robert P. Wersto ◽  
Fritz Herz ◽  
Robert E. Gallagher ◽  
Leopold G. Koss
Keyword(s):  
Cell Cycle ◽  
Monoclonal Antibody ◽  
Cell Differentiation ◽  
Myeloid Cell ◽  
Ki 67 ◽  
Cycle Dependent

scholarly journals Control of a programmed cell death pathway in Pseudomonas aeruginosa by an antiterminator

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jennifer M. Peña ◽  
Samantha M. Prezioso ◽  
Kirsty A. McFarland ◽  
Tracy K. Kambara ◽  
Kathryn M. Ramsey ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Dna Damage ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Rna Polymerase ◽  
Virulence Genes ◽  
Opportunistic Pathogen ◽  
Transcription Activator ◽  
Present Evidence ◽  
Cell Death Pathway

AbstractIn Pseudomonas aeruginosa the alp system encodes a programmed cell death pathway that is switched on in a subset of cells in response to DNA damage and is linked to the virulence of the organism. Here we show that the central regulator of this pathway, AlpA, exerts its effects by acting as an antiterminator rather than a transcription activator. In particular, we present evidence that AlpA positively regulates the alpBCDE cell lysis genes, as well as genes in a second newly identified target locus, by recognizing specific DNA sites within the promoter, then binding RNA polymerase directly and allowing it to bypass intrinsic terminators positioned downstream. AlpA thus functions in a mechanistically unusual manner to control the expression of virulence genes in this opportunistic pathogen.

Cell cycle kinetics, tissue transglutaminase and programmed cell death (apoptosis)

FEBS Letters ◽  
1992 ◽  
Vol 311 (2) ◽  
pp. 174-178 ◽  
Author(s):  
S. El Alaoui ◽  
S. Mian ◽  
J. Lawry ◽  
G. Quash ◽  
M. Griffin
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Tissue Transglutaminase ◽  
Cell Cycle Kinetics
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