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The search for enzymes responsible for metabolism of nucleoside analogs

ABSTRACT: Affymetrix U95Av2 expression data from human intestinal cells (Caco-2) and tissues from all intestinal segments (duodenum, jejunum, ileum, colon). Entries contain the search terms "glycosylase, phosphorylase, cytochrome or nucleoside," which were relevant to our search for enzymes capable of cleaving the N-glycosidic bond of nucleoside analog drugs. Keywords = glycosylase Keywords = phosphorylase Keywords = nucleoside Keywords: parallel sample

ORGANISM(S): Homo sapiens

PROVIDER: GSE1862 | GEO | 2005/10/30

SECONDARY ACCESSION(S): PRJNA90485

REPOSITORIES: GEO

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Transcription profiling of human intestinal cells (Caco-2) and tissues from all intestinal segments (duodenum, jejunum, ileum, colon)

Project description:Affymetrix U95Av2 expression data from human intestinal cells (Caco-2) and tissues from all intestinal segments (duodenum, jejunum, ileum, colon). Entries contain the search terms glycosylase, phosphorylase, cytochrome or nucleoside, which were relevant to our search for enzymes capable of cleaving the N-glycosidic bond of nucleoside analog drugs.

2007-06-21 | E-GEOD-1862 | biostudies-arrayexpress

Purine nucleoside phosphorylase enables dual metabolic checkpoints that prevent T cell immunodeficiency and TLR7-associated autoimmunity

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2022-06-02 | GSE203003 | GEO

Purine nucleoside phosphorylase enables dual metabolic checkpoints that prevent T cell immunodeficiency and TLR7-associated autoimmunity

Project description:Purine nucleoside phosphorylase enables dual metabolic checkpoints that prevent T cell immunodeficiency and TLR7-associated autoimmunity

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Dual protein kinase/ nucleoside kinase modulat ors for rationally designed polypharmacology

Project description:Masitinib, a highly selective protein kinase inhibitor, can sensitise gemcitabine-refractory cancer cell lines when used in combination with gemcitabine. A reverse proteomic approach has identified the target responsible for this sensitisation: the deoxycytidine kinase (dCK). Masitinib, as well as other protein kinase inhibitors such as imatinib, interact with dCK and provoke an unforeseen conformational-dependent activation of this nucleoside kinase, modulating phosphorylation of nucleoside analogue drugs. This phenomenon leads to an increase of prodrug phosphorylation of most of the chemotherapeutic drugs activated by this nucleoside kinase. The unforeseen dual activity of protein kinase inhibition/nucleoside kinase activation could be of great therapeutic benefit, through either reducing toxicity of therapeutic agents by maintaining effectiveness at lower doses or by counteracting drug resistance initiated via down modulation of dCK target.

2017-11-13 | PXD007765 | Pride

Chemosensitization of DLBCL cells in vitro and in vivo by demethylating nucleoside analogues

Project description:This SuperSeries is composed of the following subset Series: GSE28744: Chemosensitization of DLBCL cells in vitro and in vivo by demethylating nucleoside analogues [gene expression] GSE31101: Chemosensitization of DLBCL cells in vitro and in vivo by demethylating nucleoside analogues [methylation] Refer to individual Series. Supplementary file [gene expression]: To better approach the delta analysis and find differences between sensitive cell lines and resistant cell lines to doxorubicin, we filtered the gene expression matrix for probes with a greater standard deviation among all samples greater than 0.5. We therefore kept 11842 probesets that we used for the analysis.

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Nucleoside Analogues are Potent Inducers of Bacterial Mutagenesis

Project description:Drugs targeting DNA and RNA in mammalian cells or viruses can also affect bacteria present in the host and thereby induce the bacterial SOS system. This has the potential to increase mutagenesis and the development of antimicrobial resistance (AMR). Here we have examined nucleoside analogues (NAs) commonly used in anti-viral and anti-cancer therapies for potential effects on mutagenesis in Escherichia coli using the Rifampicin mutagenicity assay. To further explore the mode of action of the NAs, we appliedanalyzed metabolome and proteome of E.coli deletion mutants., and metabolome and proteome analyses. Five out of the thirteen NAs examined, including three nucleoside reverse transcriptase inhibitors (NRTIs) and two anti-cancer drugs, increased the mutation frequency in E. coli more than 25-fold at doses that were within reported plasma concentration range (Pl.CR), but that did not affect bacterial growth. We show that the SOS response is induced and that the increase in mutation frequency is mediated by the TLS polymerase Pol V. Quantitative mass spectrometry based metabolite profiling did not reveal large changes in nucleoside phosphate or other central carbon metabolite pools, which suggests that the SOS induction is an effect of increased replicative stress. Our results suggest that NAs/NRTIs can contribute to the development of AMR.

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Bacterial nucleoside catabolism controls quorum sensing and commensal-to-pathogen transition in the Drosophila gut

Project description:Although gut microbiomes are generally symbiotic or commensal, some of microbiomes become pathogenic under certain circumstances, which is one of key processes of pathogenesis. However, the factors involved in these complex gut-microbe interactions are largely unknown. Here we show that bacterial nucleoside catabolism using gut luminal uridine is required to boost inter-bacterial communications and gut pathogenesis in Drosophila. We found that uridine-derived uracil is required for DUOX-dependent ROS generation on the host side, whereas uridine-derived ribose induces quorum sensing and virulence gene expression on the bacterial side. Importantly, genetic ablation of bacterial nucleoside catabolism is sufficient to block the commensal-to-pathogen transition in vivo. Furthermore, we found that major commensal bacteria lack functional nucleoside catabolism, which is required to achieve gut-microbe symbiosis. The discovery of a novel role of bacterial nucleoside catabolism will greatly help to better understand the molecular mechanism of the commensal-to-pathogen transition in different contexts of host-microbe interactions.

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Repurposing Nucleoside Analogs for Human Coronaviruses.

Project description: Not available

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Acyclic nucleoside phosphonates: a study on cytochrome P450 gene expression

Project description:Focused on the cytochromes P450 (CYPs), we studied gene expression changes in mice treated with acyclic nucleoside antivirals adefovir and tenofovir. Positive control group was treated by prototypic CYP inducers phenobarbital and beta-naphthoflavone. Expression profiling with Steroltalk cDNA arrays revealed major changes in CYP mRNA expression in the inducers-treated group but only minor changes in CYP expression in the adefovir and tenofovir groups. 3 groups representing treatments with adefovir, tenofovir and phenobarbital + beta-naphthoflavone. 4-5 animals in each group + a dye swap. Pooled samples from 10 animals treated with saline was used as a reference. Daily application of antivirals for three days, samples were collected after 24 hours from the last treatment.

2014-06-03 | E-GEOD-47698 | biostudies-arrayexpress

Acyclic nucleoside phosphonates: a study on cytochrome P450 gene expression

2014-06-03 | GSE47698 | GEO

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