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

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.

ORGANISM(S): Homo sapiens

SUBMITTER: Philip Larson Lorenzi

PROVIDER: E-GEOD-1862 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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N-methylpurine DNA glycosylase and 8-oxoguanine dna glycosylase metabolize the antiviral nucleoside 2-bromo-5,6-dichloro-1-(beta-D-ribofuranosyl)benzimidazole.

Lorenzi Philip L PL Landowski Christopher P CP Brancale Andrea A Song Xueqin X Townsend Leroy B LB Drach John C JC Amidon Gordon L GL

Drug metabolism and disposition: the biological fate of chemicals 20060324 6

The rapid in vivo degradation of the potent human cytomegalovirus inhibitor 2-bromo-5,6-dichloro-1-(beta-D-ribofuranosyl)benzimidazole (BDCRB) compared with a structural L-analog, maribavir (5,6-dichloro-2-(isopropylamino)-1-beta-L-ribofuranosyl-1H-benzimidazole), has been attributed to selective glycosidic bond cleavage. An enzyme responsible for this selective BDCRB degradation, however, has not been identified. Here, we report the identification of two enzymes, 8-oxoguanine DNA glycosylase (O ...[more]

PMID: 16565170

Similar Datasets

The search for enzymes responsible for metabolism of nucleoside analogs

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. Keywords = glycosylase Keywords = phosphorylase Keywords = nucleoside Keywords: parallel sample

2005-10-30 | GSE1862 | GEO

Transcription profiling of mouse models with liver-specific deletion or global hypomorphic expression of the NADPH-cytochrome P450 reductase gene to study molecular mechanisms for the regulation of microsomal cytochrome P450 and the fatty liver phenotype.

Project description:NADPH-cytochrome P450 reductase (CPR) is important for the functions of many enzymes, such as microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. Two mouse models with deficient CPR expression in adults were recently generated in this laboratory: liver-Cpr-null (with liver-specific Cpr deletion) (Gu et al., J. Biol. Chem., 278, 25895-25901, 2003) and Cpr-low (with reduced CPR expression in all organs examined) (Wu et al. J. Pharmacol. Expt. Ther. 312, 35-43, 2005). The phenotypes included a reduced serum cholesterol level and an induction of hepatic P450 in both models, and hepatomegaly and fatty liver in the liver-Cpr-null mouse alone. Our aim was to identify hepatic gene-expression changes related to these phenotypes. Cpr-lox mice, which have normal CPR expression (Wu et al., Genesis, 36, 177-181, 2003.), were used as the control in microarray analysis. A detailed analysis of the gene-expression changes in lipid metabolism and transport pathways revealed potential mechanisms, such as an increased activation of constitutive androstane receptor (CAR) and a decreased activation of peroxisomal proliferators activated receptor alpha (PPARï?¡) by precursors of cholesterol biosynthesis, that underlie common changes (e.g., induction of multiple P450s and inhibition of genes for fatty acids metabolism) in response to CPR-loss in the two mouse models. Moreover, we also uncovered model-specific gene-expression changes, such as the induction of a lipid translocase (CD36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (CPT1a) and acyl-CoA synthetase long-chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis observed in liver-Cpr-null, but not Cpr-low mice.

2007-08-31 | E-GEOD-2362 | biostudies-arrayexpress

Homo sapiens

Project description:The search for enzymes responsible for metabolism of nucleoside analogs

| PRJNA90485 | ENA

Intestinal Microbiota Composition is Predictive of Radiotherapy-induced Acute Gastrointestinal Toxicity in Prostate Cancer Patients

Project description:The search for factors beyond the radiotherapy dose that could identify patients more at risk of developing radio-induced toxicity is essential to establish personalised treatment protocols for improving the quality-of-life of survivors. To investigate the role of the intestinal microbiota in the development of radiotherapy-induced gastrointestinal toxicity, the MicroLearner observational cohort study characterised the intestinal microbiota of 136 (discovery) and 79 (validation) consecutive prostate cancer patients at baseline radiotherapy. Gastrointestinal toxicity was assessed weekly during RT using CTCAE. An average grade >1.3 over time points was used to identify patients suffering from persistent acute toxicity (endpoint). The intestinal microbiota of patients was quantified from the baseline faecal samples using 16S rRNA gene sequencing technology.

2024-07-25 | GSE268869 | GEO

Transcription profiling of mouse C3H10T1/2 cells stimulated to differentiate using IDMB to investigate adipogenesis

Project description:Confluent C3H10T1/2 cells stimulated to differentiate using IDMB (1uM BRL49653, 1uM Dexamethasone, 0.5uM IBMX, 10ug/mL Insulin). Expression was examined 24 hours after IDMB treatment. Additionally, the effects of addition of TCDD 48 hours prior to IDMB treatment, and EGF addition concurrent with IDMB treatment were examined.

2007-12-14 | E-GEOD-1123 | biostudies-arrayexpress

Transcription profiling of cancer progression to study the intrinsic regulation of transforming growth factor-beta signaling in ErbB2/Neu-induced tumors

Project description:To identify early events of erbB2-induced mammary tumorigenesis, we compared datasets from 14 genechip experiments including MMTV-neu tumors, preneoplastic neu mammary gland (adjacent neu), and age-matched, wild-type control mammary glands

2007-09-04 | E-GEOD-2528 | biostudies-arrayexpress

Transcription profiling of murine olfactory epithelium during neuronal death and replacement to study adult neurogenesis in the olfactory epithelium

Project description:Expression profiling of mRNA abundance in the adult mouse olfactory epithelium during replacement of OSNs forced by the bilateral ablation of the olfactory bulbs. The experiment was done on 6 week old male C57Bl/6 mice. Olfactory epithelium tissue samples were collected on days 1, 5, and 7 after bulbectomy. The cellular processes activated by bulbectomy include apoptosis of mature olfactory sensory neurons, infiltration of macrophages and dendritic cells, stimulation of proliferation of basal cell progenitors, and differentation of new sensory neurons.

2007-09-04 | E-GEOD-2437 | biostudies-arrayexpress

Mouse Intestinal HMGCR complex

Project description:Mice lacking 3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr) in intestinal villus and crypt epithelial cells were generated using a Villin-Cre transgene. Label free proteome profiling was measure for Wild type and KO mouse.

2021-06-08 | MSV000087589 | MassIVE

The protein disulfide isomerase AGR2 is essential for the production of intestinal mucus

Project description:Protein disulfide isomerases (PDIs) aid protein folding and assembly by catalyzing formation and shuffling of cysteine disulfide bonds in the endoplasmic reticulum (ER). Many members of the PDI family are expressed in mammals but the roles of specific PDIs in vivo are poorly understood. A recent homology-based search for additional PDI family members identified anterior gradient homolog 2 (AGR2), a protein originally presumed to be secreted by intestinal epithelial cells, but the function of AGR2 has been obscure. Here we show that AGR2 is expressed in the ER of secretory cells and is essential for in vivo production of intestinal mucin, a large cysteine-rich glycoprotein that forms the protective mucus gel lining the intestine. A cysteine residue within the AGR2 thioredoxin-like domain forms mixed disulfide bonds with MUC2, consistent with a direct role for AGR2 in mucin processing. Despite a complete absence of intestinal mucin, mice lacking AGR2 appeared healthy but were highly susceptible to dextran sodium sulfate-induced experimental colitis, indicating a critical role for AGR2 in protection from environmental insults. We conclude that AGR2 is a unique member of the PDI family that has a specialized and non-redundant role in intestinal mucus production. Keywords: small intestine and colon gene expression profiles for Agr2-/- and littermate control mice

2009-05-15 | GSE12503 | GEO

EFHD2 Suppresses Intestinal Inflammation by Blocking Intestinal Epithelial Cell TNFR1 Internalization and Cell Death

Project description:Death of intestinal epithelial cells (IECs) is important in the pathological process of intestinal inflammatory diseases. TNF acts as one pathogenic driver for inducing IEC death and substantial intestinal inflammation. However, the physiological protective mechanisms for suppressing TNF-induced IEC death remain poorly understood. Here, we report that EF-hand domain-containing protein D2 (EFHD2), highly expressed in normal intestine tissues but decreased in intestinal biopsy samples of ulcerative colitis patients, protects the intestinal epithelium from TNF-induced IEC apoptosis. EFHD2 inhibits TNF-induced apoptosis in primary IECs and intestinal organoids (enteroids). Mice deficient of Efhd2 in IECs exhibit excessive IEC death and exacerbated experimental colitis. Mechanistically, EFHD2 interacts with Cofilin to suppress the phosphorylation of Cofilin, leading to the inhibition of TNF receptor Ⅰ (TNFR1) internalization and TNF-induced apoptosis. Our findings define EFHD2 as an endogenous suppressor of IEC death to protect intestine inflammation, providing new insight to the regulation of death receptor signaling and control of intestinal inflammatory diseases.

2024-01-14 | PXD048587 |

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