This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16.
Cigarette smoke modulates expression of human rhinovirus-induced airway epithelial host defense genes.
Specimen part, Subject
View SamplesAnalysis of MCF-7 cells treated for 4h with Ethanol, Estradiol (E2), Dexamethasone (Dex), or Estradiol + Dexamethasone (E2 + Dex)
GR and ER Coactivation Alters the Expression of Differentiation Genes and Associates with Improved ER+ Breast Cancer Outcome.
Cell line
View SamplesTo identify candidate genes involved in enhanced tumorigenicity and metastasis of CD90+ esophageal tumor-initiating cells.
A CD90(+) tumor-initiating cell population with an aggressive signature and metastatic capacity in esophageal cancer.
Specimen part, Cell line
View SamplesThe tumor suppressor p53 is a transcription factor that coordinates the cellular response to DNA damage. Here we provide an integrated analysis of p53 genomic occupancy and p53-dependent gene regulation in the splenic B and non-B cell compartments of mice exposed to whole-body ionizing radiation, providing insight into general principles of p53 activity in vivo. In unstressed conditions, p53 bound few genomic targets; induction of p53 by ionizing radiation increased the number of p53 bound sites, leading to highly overlapping profiles in the different cell types. Comparison of these profiles with chromatin features in unstressed B cells revealed that, upon activation, p53 localized at active promoters, distal enhancers, and a smaller set of unmarked distal regions. At promoters, recognition of the canonical p53 motif as well as binding strength were associated with p53-dependent transcriptional activation, but not repression, indicating that the latter was most likely indirect. p53-activated targets constituted the core of a cell type-independent response, superimposed onto a cell type-specific program. Core response genes included most of the known p53-regulated genes, as well as many new ones. Our data represent a unique characterization of the p53-regulated response to ionizing radiation in vivo. Overall design: Total RNA profiling of gene expression in the splenic B and non-B cell compartments of wild-type and Trp53-/-mice exposed to whole-body ionizing radiation by Illumina sequencing
p53 transcriptional programs in B cells upon exposure to genotoxic stress in vivo: Computational analysis of next-generation sequencing data.
No sample metadata fields
View SamplesTranscriptomic studies revealed that hundreds of mRNAs show differential expression in the brains of sleeping versus awake rats, mice, flies, and sparrows. Although these results have offered clues regarding the molecular consequences of sleep and sleep loss, their functional significance thus far has been limited. This is because the previous studies pooled transcripts from all brain cells, including neurons and glia.
Transcriptome profiling of sleeping, waking, and sleep deprived adult heterozygous Aldh1L1 - eGFP-L10a mice.
Disease
View SamplesActivity-dependent transcriptional profiling was performed in the basolateral amygdala in order to identify unique genetic markers for functionally distinct neuronal populations
Antagonistic negative and positive neurons of the basolateral amygdala.
No sample metadata fields
View SamplesUsing a CML mouse model, we identified differences in gene expression between leukemic compared with non-leukemic LTHSC, including increased expression of the thrombopoietin (THPO) receptor MPL. LTHSC expressing high levels of MPL showed enhanced JAK/STAT signaling and proliferation in response to THPO in vitro, and increased leukemogenic capacity in vivo compared to LTHSC with low MPL expression. Although both G0 and S-phase subpopulations were increased in MPL expressing LTHSC, LSC capacity was restricted to quiescent cells. Inhibition of MPL expression in CML LTHSC resulted in reduced THPO-induced JAK/STAT signaling and leukemogenic potential. Similar observations were made with LTHSC from CML patients. MPL expressing LTHSC demonstrated reduced sensitivity to BCR-ABL TKI treatment but demonstrated increased sensitivity to JAK inhibitors. Our studies identify MPL expression levels as a key determinant of heterogeneous leukemia-initiating capacity and drug sensitivity of CML LTHSC, and suggest that MPL-expressing CML stem cells are critical targets for therapy. Overall design: To evaluate heterogeneity in LSC potential, donor LTHSC from SCL-tTA/BCR-ABL mice (200 cells/mouse) were transplanted into a cohort of congenic FVBN mice. Recipient mice were followed for engraftment of donor CML cells and development of CML. LTHSCs were isolated from leukemic and non-leukemic recipient mice and global gene expression was analyzed using RNA-Seq.
Heterogeneity of leukemia-initiating capacity of chronic myelogenous leukemia stem cells.
Specimen part, Subject
View SamplesThe adaptor protein Lnk is an important negative regulator of HSC homeostasis and self-renewal. This study aims to investigate the role of Lnk in HSC aging. Here we performed expression profiling of bone marrow CD150+CD48-LSK LT-HSCs from young and old WT and Lnk-/- mice. Results identify select Lnk-mediated pathways with potential involvement in HSC self-renewal and aging.
Lnk deficiency partially mitigates hematopoietic stem cell aging.
Specimen part
View SamplesThe human ribosomal protein S3 (RPS3), a component of the small 40S ribosomal subunit, is mainly involved in ribosomal maturation and initiation of translation through association with initiation factors. In this study, we firstly identified that RPS3 played an important role in HCC progression. We performed RNA sequencing to profile gene expression patterns before and after RPS3 knockdown. Overall design: SMMC-7721 cells were transfected with RPS3 siRNA or negative control, and overall transcriptomic changes were then examined by RNA sequencing, in duplicate, using Illumina Hiseq 2500 platform.
RNA-binding protein RPS3 contributes to hepatocarcinogenesis by post-transcriptionally up-regulating SIRT1.
Specimen part, Cell line, Treatment, Subject
View SamplesPurpose: The goal of this sequencing is to investigate alterations in gene expression that result from impaired retinoid signaling compared with control, and how the RA signaling controls spermatogonia differentiation Methods: THY1+ spermatogonia mRNA profiles of 4-day-old control and germ cell specific impaired retinoid signaling mice were generated by High-throughput sequencing Results: Gene ontology (GO) analysis of the genes at the top of the ranked genes indicated enrichment in genes associated with roles in reproduction, transcription and spermatogenesis. In total, we identified 1633 and 742 transcripts (Reads Per Kilobase of transcript per Million mapped reads (RPKM) > 1) that were significantly (p-value < 0.05, > 1.5-fold difference) down- and up-regulated, respectively, in the germ cell mutants compared with the controls. Most importantly, we found that the majority of transcripts of replication-dependent core histone genes, histone cluster 1 (Hist1) were downregulated in germ cell mutants. Overall design: THY1+ spermatogonia mRNA profiles of 4-day old germ cell specific impaired retinoid signaling and control mice were generated by deep sequencing, twice, using Illumina HiSeq 2000
Retinoid signaling controls spermatogonial differentiation by regulating expression of replication-dependent core histone genes.
Specimen part, Cell line, Subject
View Samples