Regulation of NFAT by poly(ADP-ribose) polymerase activity in T cells

Valdor, Rut; Schreiber, Valérie; Sáenz, Luis; Martínez, Teresa; Muñoz-Suano, Alba; Dominguez‐Villar, Margarita; Ramı́rez, Pablo; Parrilla, Pascual; Aguado, Enrique; García-Cózar, Francisco

doi:10.1016/j.molimm.2007.10.044

Cited by 69 publications

(62 citation statements)

References 32 publications

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“…Studies have shown that PARP-1, as a ADP-ribose transferase, poly(ADP-ribosyl)ates not only histones but also several transcription factors, including Smad2/3 and NFAT (10,23). Therefore, we first set out to examine whether FOXP3 could be a substrate of PARP-1 in Treg cells.…”

Section: Parp-1 Interacts With and Poly(adp-ribosyl)ates Foxp3-mentioning

confidence: 99%

Poly(ADP-ribosyl)ation of FOXP3 Protein Mediated by PARP-1 Protein Regulates the Function of Regulatory T Cells

Luo

Nie

Wang

et al. 2015

Journal of Biological Chemistry

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Section: Parp-1 Interacts With and Poly(adp-ribosyl)ates Foxp3-mentioning

confidence: 99%

Poly(ADP-ribosyl)ation of FOXP3 Protein Mediated by PARP-1 Protein Regulates the Function of Regulatory T Cells

Luo

Nie

Wang

et al. 2015

Journal of Biological Chemistry

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“…It should be noted, however, that PARP inhibitors show only moderate specificity toward PARP1 and also inhibit other ADP-ribosylating enzymes, a fact which poses an important drawback to this approach. Besides NF-B, other transcription factors also require PARP1 as a cofactor (20,28,31,38). PARP1-dependent genes typically are not completely silenced in cells lacking PARP1, but instead show a 30 to 70% reduced expression (our unpublished observation).…”

Section: Discussionmentioning

confidence: 74%

Absence of Poly(ADP-Ribose) Polymerase 1 Delays the Onset of Salmonella enterica Serovar Typhimurium-Induced Gut Inflammation

et al. 2010

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The immune system comprises an innate and an adaptive immune response to combat pathogenic agents. The human enteropathogen Salmonella enterica serovar Typhimurium invades the intestinal mucosa and triggers an early innate proinflammatory host gene response, which results in diarrheal disease. Several host factors, including transcription factors and transcription coregulators, are involved in the acute early response to Salmonella infection. We found in a mouse model of enterocolitis induced by S. Typhimurium that the absence of the nuclear protein poly(ADP-ribose) polymerase 1 (PARP1), a previously described cofactor for NF-B-mediated proinflammatory gene expression, is associated with a delayed proinflammatory immune response after Salmonella infection. Our data reveal that PARP1 is expressed in the proliferative zone of cecum crypts, where it is required for the efficient expression of proinflammatory genes, many of which are related to interferon signaling. Consequently, animals lacking PARP1 show impaired infiltration of immune cells into the gut, with severely delayed inflammation.

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“…Human PBMCs have been extensively employed for investigating the activation of resting T lymphocytes, a physiologically relevant system of quiescence. Interestingly, it has been recently reported that PARP activity is rapidly induced upon T-cell activation, in the absence of DNA damage (Valdor et al, 2008), and that poly(ADP-ribosyl)ation regulates NFAT-dependent cytokine expression (Olabisi et al, 2008). In light of our above results, we asked whether, in this cell system, PARP activity is also involved in the upregulation of IEGs, an even earlier event than the induction of interleukin-2 (Reed et al, 1986).…”

Section: Resultsmentioning

confidence: 79%

Poly(ADP-ribosyl)ation is implicated in the G0–G1 transition of resting cells

et al. 2008

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Poly(ADP-ribosyl)ation, catalysed by a family of poly (ADP-ribose) polymerases (PARPs), plays an important role in a large variety of physiological processes, including cell proliferation, but its role in cell cycle progression is not yet completely defined. As reported here, the examination of early times following serum stimulation of quiescent fibroblasts suggests that poly(ADP-ribosyl) ation is necessary for the transition from the G0 phase to the G1 phase. We show that PARP activity is involved in this step through the regulation of immediate-early response genes, such as c-Fos and c-Myc. This is supported by the finding that exogenous Myc expression substantially restores cell cycle reactivation in the absence of polymer synthesis. Furthermore, using RNA interference, we show that PARP-1 is the PARP family member playing the most prominent role in the upregulation of c-Fos and c-Myc during G0-G1 transition. We report that even in lectin-stimulated peripheral blood mononucleated cells, the inhibition of PARP activity interferes with the upregulation of immediate-early genes and delays the induction of proliferation, suggesting a general role for PARP-1 in linking growth factor signaling with cell cycle entry.

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Regulation of NFAT by poly(ADP-ribose) polymerase activity in T cells

Cited by 69 publications

References 32 publications

Poly(ADP-ribosyl)ation of FOXP3 Protein Mediated by PARP-1 Protein Regulates the Function of Regulatory T Cells

Poly(ADP-ribosyl)ation of FOXP3 Protein Mediated by PARP-1 Protein Regulates the Function of Regulatory T Cells

Absence of Poly(ADP-Ribose) Polymerase 1 Delays the Onset of Salmonella enterica Serovar Typhimurium-Induced Gut Inflammation

Poly(ADP-ribosyl)ation is implicated in the G0–G1 transition of resting cells

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