The gene encoding a protein (AmGSTF1) associated with multiple herbicide resistance (MHR) in black-grass was transgenically expressed in Arabidopsis thaliana.The goal of this study was to determine if AmGSTF1 could elicit an MHR phenotype in the transgenic host.
Key role for a glutathione transferase in multiple-herbicide resistance in grass weeds.
Specimen part
View SamplesIntrauterine growth restriction is a common complication of pregnancy. We induce IUGR in rats by bilateral uterine artery ligation at e18 of a 23 day gestation.
Neutralizing Th2 inflammation in neonatal islets prevents β-cell failure in adult IUGR rats.
Specimen part, Treatment
View SamplesNormal human colorectal mucosa was sampled at points along the colon.
Map of differential transcript expression in the normal human large intestine.
Specimen part
View SamplesWe investigated the specificity profiles of a variety of RNA guided adenosine deaminases while exploring roles of NLS/NES and hyperactive mutants via analysis of the transcriptome-wide off-target A->G editing effected by these tools. To this end, HEK 293T cells were transfected with each construct and analyzed by RNA-seq. Untransfected cells were included as controls. From each sample, we collected ~40 million uniquely aligned sequencing reads. We then used Fisher's exact test to quantify significant changes in A->G editing yields, relative to untransfected cells, at each reference adenosine site having sufficient read coverage. The number of sites with at least one A->G editing event detected in any of the samples was computed. Overall design: Study of transcriptome wide A->G off-targets arising due to the overexpression of a variety of RNA guided adenosine deaminases.
In vivo RNA editing of point mutations via RNA-guided adenosine deaminases.
No sample metadata fields
View SamplesThere are significant differences in the expression of genes that regulate metabolic pathways in HCC as compared to Cirrhosis or non-tumor liver tissues. These charcteristic pathways can be exploited for metabolic imaging biomarkers of HCC.
The aspartate metabolism pathway is differentiable in human hepatocellular carcinoma: transcriptomics and (13) C-isotope based metabolomics.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesTo identify transcripts altered upon LIN-41 knockdown, we transfected either a control siRNA or one of two different LIN-41 siRNAs into human embryonic stem cells and collected total RNA 72 hours after transfection. Overall design: We compared transcript levels between control siRNA or LIN-41 siRNA treated cells.
The let-7/LIN-41 pathway regulates reprogramming to human induced pluripotent stem cells by controlling expression of prodifferentiation genes.
No sample metadata fields
View SamplesInflammation has pleiotropic effects on carcinogenesis and tumor progression. Signaling through the adaptor protein MyD88 promotes carcinogenesis in several chemically induced cancer models. Interestingly, we observed a protective role for MyD88 in the development of AOM/DSS colitis-associated cancer. The inability of Myd88-/- mice to heal ulcers generated upon injury creates an inflammatory environment that increases the frequency of mutations and results in a dramatic increase in adenoma formation and cancer progression. Susceptibility to colitis development and enhanced polyp formation were also observed in Il18-/- mice upon AOM/DSS treatment, suggesting that the phenotype of MyD88 knockouts is in part due to their inability to signal through the IL-18 receptor. This study revealed a previously unknown level of complexity surrounding MyD88 activities downstream of different receptors that differentially impact tissue homeostasis and carcinogenesis.
MyD88-mediated signaling prevents development of adenocarcinomas of the colon: role of interleukin 18.
Specimen part, Disease, Disease stage
View SamplesThe role of myeloid cells in supporting cancer growth is well established. Most work has focused on myeloid-derived suppressor cells (MDSC) that accumulate in tumor-bearing animals, but tumor-associated neutrophils (TAN) are also known to be capable of augmenting tumor growth. However, little is known about their evolution, phenotype, and relationship to naive neutrophils (NN) and to the granulocytic fraction of MDSC (G-MDSC). In the current study, a transcriptomics approach was used in mice to compare these cell types. Our data show that the three populations of neutrophils are significantly different in their mRNA profiles with NN and G-MDSC being more closely related to each other than to TAN. Structural genes and genes related to cell-cytotoxicity (i.e. respiratory burst) were significantly down-regulated in TAN. In contrast, many immune-related genes and pathways, including genes related to the antigen presenting complex (e.g. all six MHC-II complex genes), and cytokines (e.g. TNF-a, IL-1-a/b), were up-regulated in G-MDSC, and further up-regulated in TAN. Thirteen of the 25 chemokines tested were markedly up-regulated in TAN compared to NN, including striking up-regulation of chemoattractants for T/B-cells, neutrophils and macrophages. This study characterizes different populations of neutrophils related to cancer, pointing out the major differences between TAN and the other neutrophil populations.
Transcriptomic analysis comparing tumor-associated neutrophils with granulocytic myeloid-derived suppressor cells and normal neutrophils.
No sample metadata fields
View SamplesOverexpression of human progastrin (hGAS) in mice has been observed to increase colonic mucosa proliferation significantly,
Progastrin stimulates colonic cell proliferation via CCK2R- and β-arrestin-dependent suppression of BMP2.
Sex, Age, Specimen part
View SamplesCells adapt to environmental changes, including fluctuations in oxygen levels, through the induction of specific gene expression programs. To identify genes regulated by hypoxia at the transcriptional level, we pulse-labeled HUVEC cells with 4-thiouridine and sequenced nascent transcripts. Then, we searched genome-wide binding profiles from the ENCODE project for factors that correlated with changes in transcription and identified binding of several components of the Sin3A co-repressor complex, including SIN3A, SAP30 and HDAC1/2, proximal to genes repressed by hypoxia. SIN3A interference revealed that it participates in the downregulation of 75% of the hypoxia-repressed genes in endothelial cells. Unexpectedly, it also blunted the induction of 47% of the upregulated genes, suggesting a role for this corepressor in gene induction. In agreement, ChIP-seq experiments showed that SIN3A preferentially localizes to the promoter region of actively transcribed genes and that SIN3A signal was enriched in hypoxia-repressed genes, prior exposure to the stimulus. Importantly, SINA3 occupancy was not altered by hypoxia in spite of changes in H3K27ac signal. In summary, our results reveal a prominent role for SIN3A in the transcriptional response to hypoxia and suggest a model where modulation of the associated histone deacetylase activity, rather than its recruitment, determines the transcriptional output. Overall design: Exponentially growing non-synchronized HUVEC were exposed to normoxia or hypoxia (21% or 1% oxygen respectively) for 8 hours and pulse-labelled with 4-thiouridine during the last two hours of treatment. RNA was extracted from samples in each condition (total RNA) and an aliquot was subjected to affinity chromatography to purify the 4-thiouridine-labelled (newly transcribed RNA, Newly Tr) and non-labelled (Pre-existent) RNA fractions. All three RNA fractions (total, newly transcribed and pre-existent) from each sample were analyzed by high-throughput sequencing. Submission includes 12 samples corresponding to 3 independent biological replicates.
The SIN3A histone deacetylase complex is required for a complete transcriptional response to hypoxia.
Cell line, Treatment, Subject
View Samples