PARP-14 combines with tristetraprolin in the selective posttranscriptional control of macrophage tissue factor expression

Iqbal, M. Bilal; Johns, Michael; Cao, Jun; Liu, Yü; Yu, Sheng; Hyde, Gareth; Laffan, Michael; Marchese, Francesco P.; Cho, Sung Hoon; Clark, Andrew R.; Gavins, Felicity N. E.; Woollard, Kevin J.; Blackshear, Perry J.; Mackman, Nigel; Dean, Jonathan L. E.; Boothby, Mark; Haskard, Dorian O.

doi:10.1182/blood-2014-07-588046

Cited by 59 publications

(61 citation statements)

References 54 publications

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“…The anti-inflammatory role of PARP14 reported by us are consistent with other reports. Iqbal et al (2014) demonstrated in macrophages that PARP14 reduces mRNA stability and thus expression levels of tissue factor, a surface glycoprotein that plays a major thrombogenic role in macrophage-rich atherosclerotic lesions. PARP14's association with anti-flammatory STAT6 was first described using a yeast two-hybrid screen (Goenka and Boothby 2006).…”

Section: Parp9 and Parp14 Regulate Macrophage Activationmentioning

confidence: 99%

The impact of PARPs and ADP-ribosylation on inflammation and host–pathogen interactions

et al. 2020

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Poly-adenosine diphosphate-ribose polymerases (PARPs) promote ADP-ribosylation, a highly conserved, fundamental posttranslational modification (PTM). PARP catalytic domains transfer the ADP-ribose moiety from NAD+ to amino acid residues of target proteins, leading to mono- or poly-ADP-ribosylation (MARylation or PARylation). This PTM regulates various key biological and pathological processes. In this review, we focus on the roles of the PARP family members in inflammation and host–pathogen interactions. Here we give an overview the current understanding of the mechanisms by which PARPs promote or suppress proinflammatory activation of macrophages, and various roles PARPs play in virus infections. We also demonstrate how innovative technologies, such as proteomics and systems biology, help to advance this research field and describe unanswered questions.

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Section: Parp9 and Parp14 Regulate Macrophage Activationmentioning

confidence: 99%

The impact of PARPs and ADP-ribosylation on inflammation and host–pathogen interactions

et al. 2020

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“…Recent study also shows that ARTD8 is involved in mRNA stability. ARTD8 is found to form a complex with tristetraprolin (TTP) and 3’ untranslated region of mRNA, which suppresses the degradation of mRNA [88]. …”

Section: Adp-ribosyltransferasementioning

confidence: 99%

ADP-Ribosyltransferases and Poly ADP-Ribosylation

Liu

2015

CPPS

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Protein ADP-ribosylation is an important posttranslational modification that plays versatile roles in multiple biological processes. ADP-ribosylation is catalyzed by a group of enzymes known as ADP-ribosyltransferases (ARTs). Using nicotinamide adenine dinucleotide (NAD+) as the donor, ARTs covalently link single or multiple ADP-ribose moieties from NAD+ to the substrates, forming mono ADP-ribosylation or poly ADP-ribosylation (PARylation). Novel functions of ARTs and ADP-ribosylation have been revealed over the past few years. Here we summarize the current knowledge on ARTs and PARylation.

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“…Previous reports indicated that PARP14 enhances IL-4-induced gene expression by interacting with the cytokine-induced signal transducer and activator of transcription 6 (STAT6) in B and T cells, thereby functioning as a transcriptional co-activator2526 that may mediate this effect. A recent study reported that PARP14 regulates the stability of tissue factor mRNA in M(LPS) in mouse27. Less information exists regarding the molecular function of PARP9/ARTD9.…”

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confidence: 99%

PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation

et al. 2016

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Despite the global impact of macrophage activation in vascular disease, the underlying mechanisms remain obscure. Here we show, with global proteomic analysis of macrophage cell lines treated with either IFNγ or IL-4, that PARP9 and PARP14 regulate macrophage activation. In primary macrophages, PARP9 and PARP14 have opposing roles in macrophage activation. PARP14 silencing induces pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells, whereas it suppresses anti-inflammatory gene expression and STAT6 phosphorylation in M(IL-4) cells. PARP9 silencing suppresses pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells. PARP14 induces ADP-ribosylation of STAT1, which is suppressed by PARP9. Mutations at these ADP-ribosylation sites lead to increased phosphorylation. Network analysis links PARP9–PARP14 with human coronary artery disease. PARP14 deficiency in haematopoietic cells accelerates the development and inflammatory burden of acute and chronic arterial lesions in mice. These findings suggest that PARP9 and PARP14 cross-regulate macrophage activation.

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PARP-14 combines with tristetraprolin in the selective posttranscriptional control of macrophage tissue factor expression

Abstract: Key Points This study has identified a novel mechanism by which TF expression is posttranscriptionally regulated in macrophages. The mechanism involves the control of mRNA stability by a cooperation between PARP-14 and TTP.

Cited by 59 publications

References 54 publications

The impact of PARPs and ADP-ribosylation on inflammation and host–pathogen interactions

The impact of PARPs and ADP-ribosylation on inflammation and host–pathogen interactions

ADP-Ribosyltransferases and Poly ADP-Ribosylation

PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation

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