ArticleMolecular and cellular biochemistry2008
Mono ADP-ribosylation inhibitors prevent inflammatory cytokine release in alveolar epithelial cells.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- ART1 knockdown decreases the IL-6-induced proliferation of colorectal cancer cells.BMC cancer · 2024Article
- Article
- Mono-ADP-ribosylation sites of human CD73 inhibit its adenosine-generating enzymatic activity.Purinergic signalling · 2022Article
- TiPARP forms nuclear condensates to degrade HIF-1α and suppress tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Arginine ADP-ribosyltransferase 1 promotes angiogenesis in colorectal cancer via the PI3K/Akt pathway.International journal of molecular medicine · 2016Article
- Tubb3 regulation by the Erk and Akt signaling pathways: a mechanism involved in the effect of arginine ADP-ribosyltransferase 1 (Art1) on apoptosis of colon carcinoma CT26 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Side chain specificity of ADP-ribosylation by a sirtuin.The FEBS journal · 2009Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A549, a type II alveolar epithelial cell line stimulated with LPS (10 mug/ml), released high levels of the inflammatory cytokines IL-6 and IL-8. Here, we have investigated whether ADP-ribosylation inhibitors block the LPS-triggered cytokine release in epithelial cells. When coincubating A549 with LPS and meta-iodobenzylguanidine or novobiocin, selective arginine-dependent ART-inhibitors, the release of IL-6 and IL-8 was inhibited in a concentration-dependent manner. This effect has been linked with the presence of a functionally active arginine ADP-ribosylating enzyme on the cell surface. To this aim, we amplified by RT-PCR the ART1 transcript and identified four ADP-ribosylated proteins likely substrate for ART1. The mechanism behind the cytokine inhibition in epithelial cells seems to be correlated with the presence of ART1, which behaves as an essential positive regulator of inflammatory cytokines. This novel observation indicates this enzyme as well as other novobiocin/MIBG sensitive ARTs as potential targets for the development of new therapeutic strategies.
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