We present key transcription factors (TFs) and transcriptional regulatory networks (TRNs) delineating how they control cellular processes related to the SSC reprogramming.
Transcriptional regulatory networks underlying the reprogramming of spermatogonial stem cells to multipotent stem cells.
Specimen part
View SamplesTo analyze transcription in plants induced by total bacterial RNAs, we examined the transcriptomes of RNAs-treated plants at 0 and 6 h compared to those of control plants at the same time points.
Bacterial RNAs activate innate immunity in Arabidopsis.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transition into inflammatory cancer-associated adipocytes in breast cancer microenvironment requires microRNA regulatory mechanism.
Specimen part, Cell line
View SamplesTranscriptional profiling of mouse fibroblast-like synoviocytes (FLS) comparing FLS infected with empty adenovirus and Epas1 adenovirus. RNA was extracted from each FLS. We used microarrays to determine the effect of Epas1 overexpression on FLS and identifying the noble regulatory molecules during rheumatoid arthritic pathogenesis
Crosstalk between FLS and chondrocytes is regulated by HIF-2α-mediated cytokines in arthritis.
Specimen part
View SamplesWe performed an mRNA-sequencing experiment using Drosophila midgut to find uracil-induced signaling pathways and biological processes in response to uracil. The sequenced reads from Illumina Hiseq2000 that passed quality filters were mapped to Drosophila genome (NCBI build 5.3) using Tophat and then quantitatively analyzed by HTseq at the gene level. By comparing uracil-treated and non-treated samplesl, we profiled uracil-dependent gene expression changes. Overall design: mRNA expression profiles of uracil-treated Drosophila midgut and control Drosophila midgut were examined by Illumina Hiseq2000.
Bacterial uracil modulates Drosophila DUOX-dependent gut immunity via Hedgehog-induced signaling endosomes.
Specimen part, Treatment, Subject, Time
View SamplesIn this study, similarities between EECs and -cells were evaluated in detail. To obtain specific subtypes of EECs, cell sorting by flow cytometry was conducted from STC-1 cells (a heterogenous EEC line), and each single cell was cultured and passaged. Five EEC subtypes were established according to hormone expression, measured by quantitative RT-PCR and immunostaining: L, K, I, G and S cells expressing glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, cholecystokinin, gastrin and secretin, respectively.
Comparison of enteroendocrine cells and pancreatic β-cells using gene expression profiling and insulin gene methylation.
Specimen part
View SamplesChemotherapy resistance and disease recurrence remains major causes of gastric cancer patient mortality. We describe possible relationship between Wnt/b-catenin and RAS/ERK pathways in GC patients and acquired-resistant GC PDX tumors against FOLFOX, 5-fluorouracil-based chemotherapy. RNA sequencing analysis also demonstrates that Wnt/b-catenin pathway is an actionable target pathway for overcoming the chemotherapy resistance. These provide that an approach targeting both Wnt/b-catenin and RAS/ERK pathways could be novel therapeutic strategy in GC resistant to standard chemotherapy. Overall design: Examination of vehicle- and FOLFOX-treated gastric cancer PDX tumors
A Therapeutic Strategy for Chemotherapy-Resistant Gastric Cancer via Destabilization of Both β-Catenin and RAS.
Specimen part, Treatment, Subject
View SamplesTo investigate the relationship between genetic and transcriptional heterogeneity in a context of cancer progression, we devised a computational approach called HoneyBADGER to identify copy number variation and loss-of-heterozygosity in individual cells from single-cell RNA-sequencing data. By combining allele frequency and expression magnitude deviations, HoneyBADGER is able to infer the presence of subclone-specific alterations in individual cells and reconstruct subclonal architecture. Also HoneyBADGER to analyze single cells from a progressive multiple myeloma (MM) patient to identify major genetic subclones that exhibit distinct transcriptional signatures relevant to cancer progression. Overall design: We performed single cell RNA sequencing (RNA-seq) for multiple myeloma from the bone marrow and/or extramedullary sites from 3 patients. Data contain 173 and 1,339 single-cell RNA-seq from Fluidigm C1 and 10x Genomics respectively.
Alterations in the Transcriptional Programs of Myeloma Cells and the Microenvironment during Extramedullary Progression Affect Proliferation and Immune Evasion.
Specimen part, Subject
View SamplesDrug-induced alterations in transcriptional regulation play a central role in establishing the persistent neuroplasticities that occur during drug addiction. Additionally, changes in gene expression associated with drug administration provide valuable insight into the molecular basis of drug abuse. The molecular mechanisms that underlie susceptibility to psychostimulant addiction remain unknown. Identifying the common gene transcriptional responses to psychostimulants can provide a mechanistic insight to elucidate the molecular nature of drug dependence.
Neuronal development genes are key elements mediating the reinforcing effects of methamphetamine, amphetamine, and methylphenidate.
Specimen part
View SamplesAutism spectrum disorders (ASDs) are a group of developmental disorders that cause variable and heterogeneous phenotypes across three behavioral domains such as atypical social behavior, disrupted communications, and highly restricted and repetitive behaviors. In addition to these core symptoms, other neurological abnormalities are associated with ASD, including intellectual disability (ID). However, the molecular etiology underlying these behavioral heterogeneities in ASD is unclear. Mutations in SHANK2 genes are associated with ASD and ID. Interestingly, two lines of Shank2 knockout mice (e6-7 KO and e7 KO) showed shared and distinct phenotypes. Here, we found that the expression levels of Gabra2, as well as of GABA receptor-mediated inhibitory neurotransmission, are reduced in Shank2 e6-7, but not in e7 KO mice compared with their own wild type littermates. Furthermore, treatment of Shank2 e6-7 KO mice with an allosteric modulator for the GABAA receptor reverses spatial memory deficits, indicating that reduced inhibitory neurotransmission may cause memory deficits in Shank2 e6-7 KO mice. This article is part of the Special Issue entitled ''Ionotropic glutamate receptors''. Overall design: Compare gene expression profiles between wild-type and knock-out mutants mice using RNA-Seq (Illumina platform: Hi-Seq 2500)
Enhancing inhibitory synaptic function reverses spatial memory deficits in Shank2 mutant mice.
Specimen part, Cell line, Subject
View Samples