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GSE64028
Homo sapiens
20 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Human PB B cell subsets are functionally distinct and may derive from different developmental pathways, reflected by their differential gene expression profiles.
Publication Title
Functional capacities of human IgM memory B cells in early inflammatory responses and secondary germinal center reactions.
Sample Metadata Fields
Specimen part
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
Illumina HiSeq 2500
Description
Developmentally synchronized animals were obtained by hypochlorite treatment of gravid adults to release embryos. Synchronized embryos were hatched on NGM plates and grown at 20°C until 48 h after the L4 stage of development. Fluorodeoxyuridine was used to prevent the development of second-generation embryos once animals reached fertile adulthood. For each RNA-seq experiment, populations for odIs77[Pcol-19::UbG76V-GFP] and dop-1(vs100); [Pcol- 19::UbG76V-GFP] were grown simultaneously under the same conditions. Total RNA was isolated from animals using trizol (Invitrogen) combined with Bead Beater lysis in 3 biological replicates, and an mRNA library (single-end, 50-bp reads) was prepared for each sample/replicate using Illumina Truseq with PolyA selection. Overall design: Examination of mRNA levels in adults dop-1 mutants and wild-type animals.
Publication Title
Dopamine signaling promotes the xenobiotic stress response and protein homeostasis.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Embryonic fibroblast from C57BL/6 (B6) mice were reprogrammed to EiPS without exogenous DNA integration using an single episomal vector. The EiPS cells and B6 ES cells were then transplanted into B6 mice to form teratomas.
Publication Title
Immunogenicity of induced pluripotent stem cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina Genome Analyzer II
Description
Hematopoietic stem cell (HSC) is under dynamic controlled in the bone marrow to differentiate into cells of all lineages that constitute the blood. The bone marrow niches form a specific microenvironment to maintain and regulate HSC. However, the mechanisms that the effect of cytokines from blood on HSC function still remain largely unknown. Leukocyte chemotactic factor 2 (LECT2), a liver-derived cytokine, is involved in many immune dysfunctions, such as sepsis, cancer and diabetes. Here we showed that LECT2 affected the gene expression of bone marrow cells in mice. Especially, we found that LECT2 treatment for 3 and 5 days led to the down-regulation of cytokines such as, TNF, IL-6, IL-1ß, CXCL10, CCL4, CCL3 et al. Moreover, the functions and mechanisms for LECT2 regulated HSC in bone marrow is still needed further investigation. Overall design: Recombinant LECT2 was subcutaneously injected at a dose of 300 µg/kg body weight (once a day for 0, 3, or 5 days) in mice. The bone marrow cells were flushed out from femur, tibia, pelvis, and humerous in PBS.
Publication Title
LECT2 drives haematopoietic stem cell expansion and mobilization via regulating the macrophages and osteolineage cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The total abundance of phosphatidylcholine (PC) is known to influence lipoprotein production. However, the role of specific phospholipid species in lipid transport has been difficult to assess due to an inability to selectively manipulate membrane composition in vivo. Here we show that the LXR-regulated phospholipid remodeling enzyme lysophosphatidylcholine acyltransferase 3 (Lpcat3) is a critical determinant of membrane phospholipid composition and lipoprotein production. Mice lacking Lpcat3 in the liver show defects in lipoprotein production.
Publication Title
Lpcat3-dependent production of arachidonoyl phospholipids is a key determinant of triglyceride secretion.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The total abundance of phosphatidylcholine (PC) is known to influence lipoprotein production. However, the role of specific phospholipid species in lipid transport has been difficult to assess due to an inability to selectively manipulate membrane composition in vivo. Here we show that the LXR-regulated phospholipid remodeling enzyme lysophosphatidylcholine acyltransferase 3 (Lpcat3) is a critical determinant of membrane phospholipid composition and lipoprotein production. Mice lacking Lpcat3 in the liver show defects in lipoprotein production.
Publication Title
Lpcat3-dependent production of arachidonoyl phospholipids is a key determinant of triglyceride secretion.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2500
Description
Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer “brake” to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. Overall design: nascent RNA-seq of parental and RACK7-KO cells
Publication Title
Suppression of Enhancer Overactivation by a RACK7-Histone Demethylase Complex.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Mouse Gene 1.1 ST Array (mogene11st)
Description
Caspases, proteolytic enzymes involved in cell death could play a role independent of cell death in the developing heart
Publication Title
Executioner Caspase-3 and 7 Deficiency Reduces Myocyte Number in the Developing Mouse Heart.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
DNA methylation, at CpG islands and promoters, is often inversely correlated with gene expression.
Publication Title
The human colon cancer methylome shows similar hypo- and hypermethylation at conserved tissue-specific CpG island shores.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2500
Description
RNA sequencing of wild-type or Interferon Alpha receptor 1 Knockout MEF cells treated with DMSO or the Caspase Inhibitor Q-VD-OPh. The mechanism by which cells undergo death determines whether dying cells trigger inflammatory responses or remain immunologically silent. Mitochondria play a central role in the induction of cell death, as well as in immune signaling pathways. Here, we identify of a mechanism by which mitochondria and downstream pro-apoptotic caspases regulate the activation of antiviral immunity. In the absence of active caspases, mitochondrial outer membrane permeabilization by Bax and Bak results in the expression of type I interferons (IFNs). This induction is mediated by mitochondrial DNA-dependent activation of the cGAS/STING pathway and results in the establishment of a potent state of viral resistance. Our results show that mitochondria have the capacity to simultaneously expose a cell-intrinsic inducer of the IFN response, and to inactivate this response in a caspase-dependent manner. This mechanism provides a dual control, which determines whether mitochondria initiate an immunologically silent or a pro-inflammatory type of cell death. In order to determine whether the pharmacological inhibition of caspases could activate the type I interferon response, we treated WT MEFs with the caspase inhibitor Q-VD-OPH. The inhibitor induced an increased expression of ISGs, which was dependent on type I IFN receptor (IFNAR1) signaling. Overall design: RNA was extracted from duplicate samples and libraries generated for sequencing using the directional RNA-Seq library prep at the Yale Center for Genome Analysis. Libraries were sequenced using a Hiseq2500 sequencer to generate 76bp single-end reads. Duplicate samples were analyzed for each condition.
Publication Title
Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA.
Sample Metadata Fields
No sample metadata fields
View Samples