scholarly journals Identification of Primary Transcriptional Regulation of Cell Cycle-Regulated Genes upon DNA Damage

Cell Cycle ◽  
2007 ◽  
Vol 6 (8) ◽  
pp. 972-981 ◽  
Author(s):  
Tong Zhou ◽  
Jeff Chou ◽  
Thomas E. Mullen ◽  
Rani Elkon ◽  
Yingchun Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Transcriptional Regulation ◽  
Regulation Of Cell Cycle

scholarly journals The transcription factors TFE3 and TFEB amplify p53 dependent transcriptional programs in response to DNA damage

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Eutteum Jeong ◽  
Owen A Brady ◽  
José A Martina ◽  
Mehdi Pirooznia ◽  
Ilker Tunc ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Transcription Factors ◽  
P53 Protein ◽  
Cell Cycle Control ◽  
Cell Cycle Checkpoints ◽  
Dependent Manner ◽  
Double Knockout ◽  
Protein Levels ◽  
Regulation Of Cell Cycle

The transcription factors TFE3 and TFEB cooperate to regulate autophagy induction and lysosome biogenesis in response to starvation. Here we demonstrate that DNA damage activates TFE3 and TFEB in a p53 and mTORC1 dependent manner. RNA-Seq analysis of TFEB/TFE3 double-knockout cells exposed to etoposide reveals a profound dysregulation of the DNA damage response, including upstream regulators and downstream p53 targets. TFE3 and TFEB contribute to sustain p53-dependent response by stabilizing p53 protein levels. In TFEB/TFE3 DKOs, p53 half-life is significantly decreased due to elevated Mdm2 levels. Transcriptional profiles of genes involved in lysosome membrane permeabilization and cell death pathways are dysregulated in TFEB/TFE3-depleted cells. Consequently, prolonged DNA damage results in impaired LMP and apoptosis induction. Finally, expression of multiple genes implicated in cell cycle control is altered in TFEB/TFE3 DKOs, revealing a previously unrecognized role of TFEB and TFE3 in the regulation of cell cycle checkpoints in response to stress.

scholarly journals ADAR1 Transcriptome editing promotes breast cancer progression through the regulation of cell cycle and DNA damage response

2020 ◽  
Vol 1867 (8) ◽  
pp. 118716 ◽  
Author(s):  
Eduardo A. Sagredo ◽  
Alfredo I. Sagredo ◽  
Alejandro Blanco ◽  
Pamela Rojas De Santiago ◽  
Solange Rivas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Damage Response ◽  
Regulation Of Cell Cycle

Isoxazole derivatives of 6-fluoro-N-(6-methoxybenzo[d]thiazol-2-yl)benzo[d]thiazol-2-amine and N-(pyrimidin-2-yl)benzo[d]thiazol-2-amine: regulation of cell cycle and apoptosis by p53 activation via mitochondrial-dependent pathways

MedChemComm ◽  
2014 ◽  
Vol 5 (11) ◽  
pp. 1744-1750 ◽  
Author(s):  
Ravindra M. Kumbhare ◽  
Tulshiram L. Dadmal ◽  
T. Anjana Devi ◽  
Dinesh Kumar ◽  
Umesh B. Kosurkar ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
P53 Activation ◽  
Regulation Of Cell Cycle ◽  
Derivatives Of ◽  
Isoxazole Derivatives

The compounds depicted were shown to induce DNA damage and activate p53, which in turn activates Bax and decreases Bcl2 levels. This resulted in apoptosis in Colo205 cells.

scholarly journals Rescue of DNA damage in cells after constricted migration reveals bimodal mechano-regulation of cell cycle

2018 ◽  
Author(s):  
Yuntao Xia ◽  
Charlotte R Pfeifer ◽  
Kuangzheng Zhu ◽  
Jerome Irianto ◽  
Dazhen Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Genomic Variation ◽  
Chromatin Binding ◽  
Cell Cycle Delay ◽  
Repair Factor ◽  
Regulation Of Cell Cycle ◽  
Break Formation ◽  
Damage Marker ◽  
Partial Effects

Migration through constrictions can clearly rupture nuclei and mis-localize nuclear proteins but damage to DNA remains uncertain as does any effect on cell cycle. Here, myosin-II inhibition rescues rupture and partially rescues the DNA damage marker γH2AX, but an apparent delay in cell cycle is unaffected. Co-overexpression of multiple DNA repair factors and antioxidant inhibition of break formation also have partial effects, independent of rupture. Complete rescue of both DNA damage and cell cycle delay by myosin inhibition plus antioxidant reveals a bimodal dependence of cell cycle on DNA damage. Migration through custom-etched pores yields the same bimodal, with ~4-um pores causing intermediate levels of damage and cell cycle delay. Micronuclei (generated in faulty division) of the smallest diameter appear similar to ruptured nuclei, with high DNA damage and entry of chromatin-binding cGAS (cyclic-GMP-AMP-synthase) from cytoplasm but low repair factor levels. Increased genomic variation after constricted migration is quantified in expanding clones and is consistent with (mis)repair of excess DNA damage and subsequent proliferation.

scholarly journals Transcriptional Regulation of Cell Cycle Promoting Genes by Ikaros in Leukemia

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Elanora Dovat ◽  
Jonathon Payne ◽  
Chandrika Gowda ◽  
Chunhua Song
Keyword(s):  
Cell Cycle ◽  
Transcriptional Regulation ◽  
Regulation Of Cell Cycle

scholarly journals Pin1 inhibits PP2A-mediated Rb dephosphorylation in regulation of cell cycle and S-phase DNA damage

2015 ◽  
Vol 6 (2) ◽  
pp. e1640-e1640 ◽  
Author(s):  
Y Tong ◽  
H Ying ◽  
R Liu ◽  
L Li ◽  
J Bergholz ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
S Phase ◽  
Regulation Of Cell Cycle

scholarly journals Transcriptional Regulation of thep53Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
David Reisman ◽  
Paula Takahashi ◽  
Amanda Polson ◽  
Kristy Boggs
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Transcriptional Regulation ◽  
Cellular Response ◽  
Genome Stability ◽  
Suppressor Gene ◽  
S Phase ◽  
Dna Binding Factors ◽  
Combined Action ◽  
Cellular Stressors

Thep53tumor suppressor induces the transcription of genes that negatively regulate progression of the cell cycle in response to DNA damage or other cellular stressors and thus participates in maintaining genome stability. Numerous studies have demonstrated thatp53transcription is activated before or during early S-phase in cells progressing from G0/G1into S-phase through the combined action of two DNA-binding factors RBP-Jκand C/EBPβ-2. Here, we review evidence that this induction occurs to provide availablep53mRNA in order to prepare the cell for DNA damage in S-phase, this ensuring a rapid response to DNA damage before exiting this stage of the cell cycle.

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