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ABSTRACT:
PROVIDER: PRJNA1120370 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:High-resolution quantitative profiling of tRNA abundance and modification status in hematopoietic cells upon Trmt6 deletion by mim-tRNAseq
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Project description:tRNA m1A modification regulate hematopoietic stem cell maintenance via mTORC1 signaling [mim-tRNAseq]
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Project description:High-resolution quantitative profiling of tRNA abundance and modification status in eukaryotes by mim-tRNAseq
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Project description:au07-10_mpk - mpk - Gain insight into the function of mpk genes by characterizing the transcriptional profile of the mpk5, mpk10 and mpk11 KO mutants in comparison with that of the Arabidopsis wt plants. - 1) mpk5 (WS genetic background) versus wt-WS 2) mpk11 (Col0 genetic background) versus wt-Col0 3) mpk10 (Col0 genetic background) versus wt-Col0 Seeds were surface sterilized and grown in MS agar medium (3% sucrose) for 11 days in long day conditions. Entire seedling were harvested and deep frozen in liquid nitrogen. Keywords: gene knock out
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Project description:Breakdown products of some glucosinolates M-bM-^@M-^S defense chemicals of Brassicales M-bM-^@M-^S induce detoxifying enzymes and demonstrate preventive activities against chemically induced tumorigenesis in animal models. However, other breakdown products are genotoxic. 1-Methoxy-3-indolylmethyl alcohol (1-MIM-OH) is mutagenic in bacterial and mammalian cells upon activation by sulphotransferases and forms DNA adducts in mouse tissues. This effect was enhanced in mice transgenic for human sulphotransferases 1A1/2 (FVB/N-hSULT1A1/2). In this study we explored gene expression changes induced by 1-MIM-OH in mouse liver. FVB/N-hSULT1A1/2 mice were orally treated with 1-MIM-OH for 21 or 90 days, leading to high levels of hepatic 1-MIM-DNA adducts. Genome-wide expression analyzes in this tissue demonstrated no influence on detoxifying enzymes, but up-regulation of many mediators of the tumour suppressor p53 and down-regulation of Fhit and other long genes. In conclusion, 1-MIM-OH did not induce protective enzymes, but formed high levels of DNA adducts, which were recognized by affected cells as reflected by p53 activation. While this p53 response might aim to protection, it was unable to prevent the accumulation of DNA adducts. However, various epdemiological studies reported inverse associations between the intake of cruciferous vegetables and cancer. This association might be due to the presence of other glucosinolates with tumour-preventing influences possibly outweighing adverse effects of some metabolites. Nevertheless, 1-MIM-OH is a genotoxic substance inducing a gene expression profile similar to the expression signature caused by known genotoxic hepatocarcinogens. Male FVB/N-SULT1A1/2 mice were orally treated with 1-MIM-OH, trice per week, 26 mg/kg body mass per treatment. Control animals only received the vehicle (glyceryl trioctanoate) over the same period. Animals were killed after 10 and 40 treatments (over a period of 21 and 90 d, respectively), always 24 h after the last treatment (6 treated and 6 control mice, respectively). Organs were weighed, shock-frozen in liquid nitrogen and stored for a few days at -80M-BM-0C until further processing. Liver organs were ground in a Tissuelyser ball mill (Qiagen, Hilden, Germany) under cooling with liquid nitrogen. The frozen liver tissue was crushed and total RNA was isolated using the RNeasy Mini Kit (Qiagen, Hilden, Germany) according to the manufacturerM-bM-^@M-^Ys instructions. For genome-wide microarray analysis quality of RNA was controlled using the BioAnalyzer (Agilent, Santa Clara, CA, USA). Affymetrix GeneChip hybridization (GeneChip MouseGenome 430 2.0) was performed with 1 M-BM-5g total RNA according to the manufacturerM-bM-^@M-^Ys recommendations. RNA from six individual animals per group (21-day and 90-day treatments with 1-MIM-OH or the vehicle only) was analyzed. For the analysis one hybridized GeneChip (mouse 6 [treated for 21 days with 1-MIM-OH]) was excluded due to hybridization artefacts.
2015-02-18 | E-GEOD-61494 | biostudies-arrayexpress
Project description:Breakdown products of some glucosinolates – defense chemicals of Brassicales – induce detoxifying enzymes and demonstrate preventive activities against chemically induced tumorigenesis in animal models. However, other breakdown products are genotoxic. 1-Methoxy-3-indolylmethyl alcohol (1-MIM-OH) is mutagenic in bacterial and mammalian cells upon activation by sulphotransferases and forms DNA adducts in mouse tissues. This effect was enhanced in mice transgenic for human sulphotransferases 1A1/2 (FVB/N-hSULT1A1/2). In this study we explored gene expression changes induced by 1-MIM-OH in mouse liver. FVB/N-hSULT1A1/2 mice were orally treated with 1-MIM-OH for 21 or 90 days, leading to high levels of hepatic 1-MIM-DNA adducts. Genome-wide expression analyzes in this tissue demonstrated no influence on detoxifying enzymes, but up-regulation of many mediators of the tumour suppressor p53 and down-regulation of Fhit and other long genes. In conclusion, 1-MIM-OH did not induce protective enzymes, but formed high levels of DNA adducts, which were recognized by affected cells as reflected by p53 activation. While this p53 response might aim to protection, it was unable to prevent the accumulation of DNA adducts. However, various epdemiological studies reported inverse associations between the intake of cruciferous vegetables and cancer. This association might be due to the presence of other glucosinolates with tumour-preventing influences possibly outweighing adverse effects of some metabolites. Nevertheless, 1-MIM-OH is a genotoxic substance inducing a gene expression profile similar to the expression signature caused by known genotoxic hepatocarcinogens.
2015-02-18 | GSE61494 | GEO
Project description:To determine the role of the hepatic microenvironment in HCC metastasis, we compared the gene expression profiles of 20 noncancerous surrounding hepatic tissues from two HCC patient groups, those with primary HCC together with venous metastasis which we termed a metastasis-inclined microenvironment (MIM) and those with HCC without detectable metastasis, which we termed a metastasis-averse microenvironment (MAM). There were a total of 20 cDNA microarrays performed, comparing 9 MIM or 11 MAM HCC patient samples to a common reference pool of 8 normal liver tissues.
2010-07-01 | E-GEOD-5093 | biostudies-arrayexpress