Twenty eight genes in PAO1 persister cells were consistently induced by treatment with 1 ug/mL BF8 for 1 h.
Reverting antibiotic tolerance of Pseudomonas aeruginosa PAO1 persister cells by (Z)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one.
Specimen part, Treatment
View SamplesIn response to viral pathogens, the host upregulates antiviral genes that suppress translation of viral mRNAs. However, induction of such antiviral responses may not be exclusive to viruses as the pathways lie at the intersection of broad inflammatory networks that can also be induced by bacterial pathogens. Using a model of Gram-negative sepsis, we show that propagation of kidney damage initiated by a bacterial origin ultimately involves antiviral responses that result in host translation shutdown. We determined that activation of the Eif2ak2-Eif2a axis is the key mediator of translation initiation block in late phase sepsis. Reversal of this axis mitigated kidney injury. Furthermore, temporal profiling of the kidney translatome revealed that multiple genes involved in formation of the initiation complex were translationally altered during bacterial sepsis. Collectively, our findings implicate that translation shutdown is indifferent to the specific initiating pathogen and is an important determinant of tissue injury in sepsis. Overall design: Bulk 20 um thickness specimens from cross-sectional human kidney biopsies embedded in OCT underwent RNA sequencing. All subjects had ATN, AIN, or a mix of both conditions.
Bacterial sepsis triggers an antiviral response that causes translation shutdown.
Sex, Age, Specimen part, Disease, Subject
View SamplesWe expressed either only the E7 oncoprotein or the complete early genome region (CER) of the human papillomavirus type 8 in primary human adult skin keratinocytes.
Novel Insights Into Cellular Changes in HPV8-E7 Positive Keratinocytes: A Transcriptomic and Proteomic Analysis.
Specimen part
View SamplesPyrrole-imidazole polyamides (PIPs) have been shown to inhibit gene expression by interrupting the DNA-protein interface. Human Ectopic viral integration site 1 (EVI1) is an oncogenic transcription factor which plays a key role in many aggressive forms of cancer. We have developed a novel pyrroleimidazole polyamide, PIP1 targeting the REL/ELK1 binding site in the EVI1 minimal promoter that can significantly repress the expression of EVI1 in MDA-MB-231 cells. Whole-transcriptome analysis revealed that a fraction of EVI1-driven genes were modulated by PIP1.
Targeted suppression of EVI1 oncogene expression by sequence-specific pyrrole-imidazole polyamide.
Specimen part, Cell line
View SamplesAn antagonistic interplay between YAP and RUNX where RUNX proteins abrogate YAP-mediated transcription of EMT and Stemness associated genes in mammary epithelial cells in an interaction dependent manner.
RUNX1 and RUNX3 protect against YAP-mediated EMT, stem-ness and shorter survival outcomes in breast cancer.
Cell line
View SamplesMicroarray is widely used to monitor gene expression changes in breast cancer. The transcriptomic changes in breast cancer is commonly occured during the transition of normal cells to cancerous cells. This is the first study on gene expression profiling of multi ethnic of Malaysian breast cancer patients (Malays, Chinese and Indian). We aim to identify differentially expressed genes between tumors and normal tissues. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001.
Gene expression patterns distinguish breast carcinomas from normal breast tissues: the Malaysian context.
Specimen part, Disease stage, Race
View SamplesPurpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of abiotic stress molecular pathways. The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of contrasting slow wilting lines to quantify transcript abumdance under drought stress condition Overall design: Methods: The three biological replicates of DS line, Pana (control and drought samples) and DT line, PI 567690 (control and drought samples) leaf sample RNA were multiplexed and sequenced on an Illumina Hi-Seq 2000 platform. The RNA concentration of each sample was approximately 200ng/µl with a quantity of 50 µl.isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays
Comparative analysis of the drought-responsive transcriptome in soybean lines contrasting for canopy wilting.
Specimen part, Treatment, Subject
View SamplesChanges in the transcript profile due to ABCA1 expression in murine liver samples was evaluated in LDL receptor -/- genetic backgrounds.
ABCA1 overexpression in the liver of LDLr-KO mice leads to accumulation of pro-atherogenic lipoproteins and enhanced atherosclerosis.
Sex, Specimen part
View SamplesInterstitial cells of Cajal (ICC) are electrical pacemakers and mediators of neuromuscular neurotransmission in the gastrointestinal tract. Gastrointestinal stromal tumors (GIST) arise within the ICC lineage due to activating KIT/PDGFRA mutations. In this study we developed a method for isolation of human ICC by immunolabeling and fluorescence-activated cell sorting (FACS). Briefly, human gastric musculature was dissociated and incubated with antibodies against CD45, FCER1A, CD11B, KIT, and CD34. ICC (defined as HP-KIT+CD34- cells), NOT ICC (defined as HP-KIT-CD34- cells), and hematopoietic (HP) cells (defined as HP+ cells) were isolated using FACS. Microarray was performed on ICC, NOT ICC, HP+ cells, and unfractionated gastric tunica muscularis. This study utilized micorarray for the phenotypic characterization of FACS-sorted human ICC, allowing comparison of ICC to other cells of the gastric musculature, including GIST.
Hedgehog pathway dysregulation contributes to the pathogenesis of human gastrointestinal stromal tumors via GLI-mediated activation of KIT expression.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Age, Specimen part, Cell line, Treatment
View Samples