Differential gene expression profile of CD4+ T cells from 10 months old Wt, miR-155-/-, miR-146a-/- and DKO mice spleens. Overall design: Wt, miR-155-/-, miR-146a-/- and DKO mice were aged 10 months, CD4+ T cells were sorted from mice spleens for analyses.
miR-155 promotes T follicular helper cell accumulation during chronic, low-grade inflammation.
No sample metadata fields
View SamplesDifferential gene expression profile of Tfh and non-Tfh cells from both Wt and miR-155-/- mice spleens. Overall design: Wt and miR-155-/- mice were immunized with OVA. 8 days post immunization, CD4+CXCR+PD1+ Tfh cells and CD4+CXCR5-PD1- non Tfh cells were sorted from mice spleens for analyses.
miR-155 promotes T follicular helper cell accumulation during chronic, low-grade inflammation.
No sample metadata fields
View SamplesTumor associated CD4+ and CD8+ T cells were sorted from B16f10 OVA expressing tumors in miR-155 flox, miR-155 flox CD4Cre+, and miR-155 flox CD4Cre+ mice treated with immune checkpoint blocking (ICB) antibodies by flow sorting on CD45+CD3+CD4+ cells and CD45+ CD3+CD8+ cells. RNA was collected from these cells to perform RNA sequencing of total RNA. Overall design: Each sample represents cells from 2 to 3 individual tumors grown on individual mice that were pooled together before sorting via flow cytometry
Antitumor immunity is defective in T cell-specific microRNA-155-deficient mice and is rescued by immune checkpoint blockade.
Cell line, Subject
View SamplesThe miR-155-dependent differences in gene expression in the HSPC compartment of FLT3-ITD mice is unknown. In this experiment, we performed RNA sequencing on FLT3-ITD and FLT3-ITD miR-155-/- mouse LKS cells. Overall design: RNA sequencing was performed on RNA extracted from Lin-, cKit+, Sca1+ cells isolated via flow cytometry from FLT3-ITD and FLT3-ITD miR-155-/- mice. 3 samples were submitted for sequencing for each experimental group. Each sample contains RNA from 3 mice, in order to get enough RNA from this rare stem cell population.
miR-155 promotes FLT3-ITD-induced myeloproliferative disease through inhibition of the interferon response.
Specimen part, Subject
View SamplesWe identify regulatory mechanisms that influence inflammation and metabolism during metabolic disease development. In addition to the other data represented in our paper, we performed RNA-seq to demonstrate a role for miR-146a, an anti-inflammatory miRNA, in regulating both inflammation and cellular metabolism during obesity. Overall design: Each sample represents pooled cells from three mice of the same genotype and treatment group. Samples were pooled before FACS to ensure sufficient cell numbers for sorting and RNA collection. WT or miR-146a-/- mice were treated with either high fat diet or normal chow diet for 14 weeks starting from 6 weeks of age. Mice were sacrificed and live, singlet CD45+ CD11b+ F4/80+ cells were sorted from the stromal vascular fraction of adipose tissue using FACS Aria. RNA was collected from the sorted cells via Qiazol/RNeasy Kit (Qiagen) and library preparation used Illumina TruSeq Stranded RNA Kit with Ribo-Zero Gold. RNA-seq was performed using Illumina HiSeq 50 cycle single-read sequencing version 4. Sequence alignment was performed through the University of Utah Bioinformatics Core Facility.
Anti-inflammatory microRNA-146a protects mice from diet-induced metabolic disease.
Specimen part, Subject
View SamplesWe stratified colorectal tumor samples using a new unsupervised, iterative method based on non-negative matrix factorization (NMF). The resulting five subtypes exhibited activation of specific signaling pathways, and significant differences in microsatellite status and tumor location. We could also align three CRC cell lines panels to these subtypes.
Subtypes of primary colorectal tumors correlate with response to targeted treatment in colorectal cell lines.
Sex, Race
View SamplesAnopheles gambiae,the primary African malarial mosquito, exhibits numerous behaviors that are under diel and circadian control, including locomotor activity, swarming, mating, host seeking, eclosion, egg laying and sugar feeding. However, little has been performed to elucidate the molecular basis for these daily rhythms. To study how gene expression is globally regulated by diel and circadian mechanisms, we have undertaken a DNA microarray analysis ofA. gambiaehead and bodies under 12:12 light:dark cycle (LD) and constant dark (DD, free-running) conditions. Zeitgeber Time (ZT) with ZT12 defined as time of lights OFF under the light:dark cycle, and ZT0 defined as end of the dawn transition. Circadian Time (CT) with CT0 defined as subjective dawn, inferred from ZT0 of the previous light:dark cycle.
Genome-wide profiling of diel and circadian gene expression in the malaria vector Anopheles gambiae.
Sex, Specimen part
View SamplesNitrogen and light are two major regulators of plant metabolism and development. While genes involved in the control of each of these signals have begun to be identified, regulators that integrate gene responses to nitrogen and light signals have yet to be determined.
Modeling the global effect of the basic-leucine zipper transcription factor 1 (bZIP1) on nitrogen and light regulation in Arabidopsis.
Specimen part
View SamplesAndrogen receptor (AR) is a hormone-activated transcription factor that plays important roles in prostate development, function, as well as malignant transformation. The downstream pathways of AR, however, are incompletely understood. AR has been primarily known as a transcriptional activator inducing prostate-specific gene expression. Through integrative analysis of genome-wide AR occupancy and androgen-regulated gene expression, here we report AR as a globally acting transcriptional repressor. This repression is mediated by androgen responsive elements (ARE) and dictated by Polycomb group protein EZH2 and repressive chromatin remodeling. In embryonic stem cells, AR-repressed genes are occupied by EZH2 and harbor bivalent H3K4me3 and H3K27me3 modifications that are characteristic of differentiation regulators, the silencing of which maintains the undifferentiated state. Concordantly, these genes are silenced in castration-resistant prostate cancer rendering a stem cell-like lack of differentiation and tumor progression. Collectively, our data reveal an unexpected role of AR as a transcriptional repressor inhibiting non-prostatic differentiation and, upon excessive signaling, resulting in cancerous de-differentiation. It provides an innovative mechanism for castration resistance and highlights novel therapeutic strategies to treat advanced prostate cancer.
Cooperation between Polycomb and androgen receptor during oncogenic transformation.
Cell line, Treatment
View SamplesHsa-mir-365-2 is one of the two precursors that give rise to miR-365. We discovered that miR-365 directly regulates a lung cancer and developmental gene termed thyroid transcription factor 1 (TTF-1 or NKX2-1).
MiR-365 regulates lung cancer and developmental gene thyroid transcription factor 1.
Cell line
View Samples