Faculty Opinions recommendation of p53 isoform delta113p53 is a p53 target gene that antagonizes p53 apoptotic activity via BclxL activation in zebrafish.

Author(s):  
Andreas Villunger
2009 ◽  
Vol 23 (3) ◽  
pp. 278-290 ◽  
Author(s):  
J. Chen ◽  
S. M. Ng ◽  
C. Chang ◽  
Z. Zhang ◽  
J.-C. Bourdon ◽  
...  

1999 ◽  
Vol 878 (1 INHIBITION OF) ◽  
pp. 638-641 ◽  
Author(s):  
YUBO SUN ◽  
YI SUN ◽  
LEONOR WENGER ◽  
JONI L. RUTTER ◽  
CONSTANCE E. BRINCKERHOFF ◽  
...  

Blood ◽  
2004 ◽  
Vol 103 (7) ◽  
pp. 2691-2698 ◽  
Author(s):  
Michael D. Rosenblum ◽  
Edit Olasz ◽  
Jeffery E. Woodliff ◽  
Bryon D. Johnson ◽  
Marja C. Konkol ◽  
...  

Abstract During apoptotic cell death, biochemical processes modify self-proteins and create potential autoantigens. To maintain self-tolerance in the face of natural cell turnover, the immune system must prevent or control responses to apoptosis-associated autoantigens or risk autoimmunity. The molecular mechanisms governing this process remain largely unknown. Here, we show that expression of the immunoregulatory protein CD200 increases as murine dendritic cells (DCs) undergo apoptosis. We define CD200 as a p53-target gene and identify both p53- and caspase-dependent pathways that control CD200 expression during apoptosis. CD200 expression on apoptotic DCs diminishes proinflammatory cytokine production in response to self-antigens in vitro and is required for UVB-mediated tolerance to haptenated self-proteins in vivo. Up-regulation of CD200 may represent a novel mechanism, whereby immune reactivity to apoptosis-associated self-antigens is suppressed under steady state conditions. (Blood. 2004;103: 2691-2698)


2015 ◽  
Vol 1849 (8) ◽  
pp. 1003-1016 ◽  
Author(s):  
Bianca Gilbert ◽  
Khalil Ahmad ◽  
Jessica Roos ◽  
Christoph Lehmann ◽  
Tomohiro Chiba ◽  
...  
Keyword(s):  

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 508 ◽  
Author(s):  
Alba Rodríguez-García ◽  
María Luz Morales ◽  
Vanesa Garrido-García ◽  
Irene García-Baquero ◽  
Alejandra Leivas ◽  
...  

Control of oxidative stress in the bone marrow (BM) is key for maintaining the interplay between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an indicator of oxidative stress in the BM of patients with MDS and control subjects, and also patients with MDS under treatment with the iron chelator deferasirox (DFX). As expected, differences in the pattern of protein carbonylation were observed in BM samples between MDS patients and controls, with an increase in protein carbonylation in the former. Strikingly, patients under DFX treatment had lower levels of protein carbonylation in BM with respect to untreated patients. Proteomic analysis identified four proteins with high carbonylation levels in MDS BM cells. Finally, as oxidative stress-related signaling pathways can modulate the cell cycle through p53, we analyzed the expression of the p53 target gene p21 in BM cells, finding that it was significantly upregulated in patients with MDS and was significantly downregulated after DFX treatment. Overall, our results suggest that the fine-tuning of oxidative stress levels in the BM of patients with MDS might control malignant progression.


PLoS ONE ◽  
2020 ◽  
Vol 15 (8) ◽  
pp. e0236881
Author(s):  
Hye Jeong Kim ◽  
Seung Eon Lee ◽  
Heeju Na ◽  
Jae-Seok Roe ◽  
Jae-il Roh ◽  
...  
Keyword(s):  

2008 ◽  
Vol 28 (15) ◽  
pp. 4745-4758 ◽  
Author(s):  
Pingxin Li ◽  
Hongjie Yao ◽  
Zhiqiang Zhang ◽  
Ming Li ◽  
Yuan Luo ◽  
...  

ABSTRACT Histone Arg methylation has been correlated with transcriptional activation of p53 target genes. However, whether this modification is reversed to repress the expression of p53 target genes is unclear. Here, we report that peptidylarginine deiminase 4, a histone citrullination enzyme, is involved in the repression of p53 target genes. Inhibition or depletion of PAD4 elevated the expression of a subset of p53 target genes, including p21/CIP1/WAF1, leading to cell cycle arrest and apoptosis. Moreover, the induction of p21, cell cycle arrest, and apoptosis by PAD4 depletion is p53 dependent. Protein-protein interaction studies showed an interaction between p53 and PAD4. Chromatin immunoprecipitation assays showed that PAD4 is recruited to the p21 promoter in a p53-dependent manner. RNA polymerase II (Pol II) activities and the association of PAD4 are dynamically regulated at the p21 promoter during UV irradiation. Paused RNA Pol II and high levels of PAD4 were detected before UV treatment. At early time points after UV treatment, an increase of histone Arg methylation and a decrease of citrullination were correlated with a transient activation of p21. At later times after UV irradiation, a loss of RNA Pol II and an increase of PAD4 were detected at the p21 promoter. The dynamics of RNA Pol II activities after UV treatment were further corroborated by permanganate footprinting. Together, these results suggest a role of PAD4 in the regulation of p53 target gene expression.


2015 ◽  
Vol 141 (10) ◽  
pp. 1791-1798 ◽  
Author(s):  
Jiehui Di ◽  
Hui Huang ◽  
Yan Wang ◽  
Debao Qu ◽  
Juanjuan Tang ◽  
...  

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