The influence of ADAR1’s regulation on lymphocyte cell function during rejection

Li, Yan; Liu, Feng; Zhang, Wei; Huo, Binliang; Wei, Zheng; Ding, Rui; Guo, Jiyuan; Zhao, Qingchuan; Dou, Kefeng

doi:10.1007/s11033-009-9804-z

Cited by 5 publications

(2 citation statements)

References 36 publications

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“…However, because editing levels were not assessed in these animals, it remains unknown what distinct function, if any, p150 serves in the editing of specific RNA targets. As p150 has been implicated in numerous cellular activities which are either editing-independent or involve unknown substrates (Cai et al, 2010; Herbert et al, 2002; Nie et al, 2005; Wang et al, 2006; Wang and Samuel, 2009; Zhang and Rabinovici, 2007), the precise functional role(s) for this ADAR1 isoform remain to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Reovirus-mediated induction of ADAR1 (p150) minimally alters RNA editing patterns in discrete brain regions

Hood

Morabito

Martínez

et al. 2014

Molecular and Cellular Neuroscience

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Transcripts encoding ADAR1, a double-stranded, RNA-specific adenosine deaminase involved in the adenosine-to-inosine (A-to-I) editing of mammalian RNAs, can be alternatively spliced to produce an interferon-inducible protein isoform (p150) that is up-regulated in both cell culture and in vivo model systems in response to pathogen or interferon stimulation. In contrast to other tissues, p150 is expressed at extremely low levels in the brain and it is unclear what role, if any, this isoform may play in the innate immune response of the central nervous system (CNS) or whether the extent of editing for RNA substrates critical for CNS function is affected by its induction. To investigate the expression of ADAR1 isoforms in response to viral infection and subsequent alterations in A-to-I editing profiles for endogenous ADAR targets, we used a neuro-tropic strain of reovirus to infect neonatal mice and quantify A-to-I editing in discrete brain regions using a multiplexed, high-throughput sequencing strategy. While intracranial injection of reovirus resulted in a widespread increase in the expression of ADAR1 (p150) in multiple brain regions and peripheral organs, significant changes in site-specific A-to-I conversion were quite limited, suggesting that steady-state levels of p150 expression are not a primary determinant for modulating the extent of editing for numerous ADAR targets in vivo.

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Section: Discussionmentioning

confidence: 99%

Reovirus-mediated induction of ADAR1 (p150) minimally alters RNA editing patterns in discrete brain regions

Hood

Morabito

Martínez

et al. 2014

Molecular and Cellular Neuroscience

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“…Little is known about the role of RNA editing and ADARs in immune function. Recent studies have identified ADAR1 as an essential regulator of hematopoietic stem cell maintenance and suppressor of interferon signaling [ 22 ] and as a dominant player in the regulation of primary T lymphocytes function during acute transplant rejection [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

A novel immune resistance mechanism of melanoma cells controlled by the ADAR1 enzyme

et al. 2015

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The blossom of immunotherapy in melanoma highlights the need to delineate mechanisms of immune resistance. Recently, we have demonstrated that the RNA editing protein, adenosine deaminase acting on RNA-1 (ADAR1) is down-regulated during metastatic transition of melanoma, which enhances melanoma cell proliferation and tumorigenicity. Here we investigate the role of ADAR1 in melanoma immune resistance.Importantly, knockdown of ADAR1 in human melanoma cells induces resistance to tumor infiltrating lymphocytes in a cell contact-dependent mechanism. We show that ADAR1, in an editing-independent manner, regulates the biogenesis of miR-222 at the transcription level and thereby Intercellular Adhesion Molecule 1 (ICAM1) expression, which consequently affects melanoma immune resistance. ADAR1 thus has a novel, pivotal, role in cancer immune resistance. Corroborating with these results, the expression of miR-222 in melanoma tissue specimens was significantly higher in patients who had no clinical benefit from treatment with ipilimumab as compared to patients that responded clinically, suggesting that miR-222 could function as a biomarker for the prediction of response to ipilimumab.These results provide not only novel insights on melanoma immune resistance, but also pave the way to the development of innovative personalized tools to enable optimal drug selection and treatment.

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Glutamate receptors and signal transduction in learning and memory

Peng

Zhang

et al. 2010

Mol Biol Rep

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The plasticity of the central nervous system helps form the basis for the neurobiology of learning and memory. Long-term potentiation (LTP) is the main form of synaptic plasticity, reflecting the activity level of the synaptic information storage process, and provides a good model to study the underlying mechanisms of learning and memory. The glutamate receptor-mediated signal pathway plays a key role in the induction and maintenance of LTP, and hence the regulation of learning and memory. The progress in the understanding of the glutamate receptors and related signal transduction systems in learning and memory research are reviewed in this article.

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The influence of ADAR1’s regulation on lymphocyte cell function during rejection

Cited by 5 publications

References 36 publications

Reovirus-mediated induction of ADAR1 (p150) minimally alters RNA editing patterns in discrete brain regions

Reovirus-mediated induction of ADAR1 (p150) minimally alters RNA editing patterns in discrete brain regions

A novel immune resistance mechanism of melanoma cells controlled by the ADAR1 enzyme

Glutamate receptors and signal transduction in learning and memory

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