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SRP093274
Mus musculus
2 Downloadable Samples
Illumina HiSeq 2500
Description
BCAS2 (Breast cancer amplified sequence 2) is involved in multiple biological processes, including pre-mRNA splicing. However, the physiological roles of BCAS2 are still largely unclear. Here we report that BCAS2 is specifically enriched in spermatogonia of mouse testes. Conditional disruption of Bcas2 in male germ cells impairs spermatogenesis and leads to male mouse infertility. Although the spermatogonia appear grossly normal, spermatocytes in meiosis prophase I and meiosis events (recombination and synapsis) are rarely observed in the BCAS2-depleted testis. In BCAS2 null testis, 245 genes are altered in alternative splicing forms; at least three spermatogenesis-related genes (Dazl, Ehmt2 and Hmga1) can be verified. In addition, disruption of Bcas2 results in a significant decrease of the full-length form and an increase of the short form (lacking exon 8) of DAZL protein. Altogether, our results suggest that BCAS2 regulates alternative splicing in spermatogonia and the transition to meiosis initiation, and male fertility. Overall design: Transcriptional profiles of P9 testes from Control and Bcas2F/-;V-cre males
Publication Title
BCAS2 is involved in alternative mRNA splicing in spermatogonia and the transition to meiosis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 116 Downloadable Samples
- IlluminaHiSeq2000
Description
Differentiated cell can be reprogrammed into totipotent embryo through somatic cell nuclear transfer (SCNT). However, this process is highly inefficient and most cloned embryos arrest at certain developmental stages. Through single cell sequencing combined with embryo biopsy, here we generate a global map of DNA methylome and RNA transcriptome for SCNT embryos with distinct developmental fates. We subsequently demonstrate that the unfaithful reactivation of two histone demethylases, Kdm4b and Kdm5b, accounts for the arrest of cloned embryos at 2-cell and 4-cell stage, respectively. Ectopic expression of Kdm4b and Kdm5b in SCNT can remove H3K9me3 barrier, restore the transcription profile and facilitate the blastocyst developmental efficiency over 95%. Moreover, these cloned embryos can further support full-term development and the derivation of SCNT-embryonic stem cells with greater efficiency. Our study reveals that histone methylation reset is crucial for the development of SCNT embryos, which provides a clue to further improve therapeutic cloning. Overall design: For SCNT embryos or injected SCNT embryos 3-8 replicates were performed for each stage . As the control, 3-6 replicates were performed for each stage of wild type samples
Publication Title
Identification of key factors conquering developmental arrest of somatic cell cloned embryos by combining embryo biopsy and single-cell sequencing.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 12 Downloadable Samples
Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Acute lung injury (ALI) refers to a clinical syndrome characterized by bilateral lung injury, severe lung diffuse failure and hypoxemia caused by non-cardiogenic pulmonary edema.Sepsis is the leading etiology of ALI and a common admission to the intensive care unit, which induces pulmonary inflammation leading disruption of endothelial-epithelial barriers by surge release of pro-inflammatory cytokines that increases the permeability of the alveolar-capillary membrane, pulmonary infiltration, and edema.Ultimately, gas exchange across the alveolar-capillary membrane is severely impaired and acute respiratory failure and hypoxia occur. ALI patients may suffer from pulmonary inflammation and hypoxia simultaneously or sequentially, those two pathophysiological processes may interact mutually and contribute together to the development of ALI.
Publication Title
Hypoxia Exacerbates Inflammatory Acute Lung Injury <i>via</i> the Toll-Like Receptor 4 Signaling Pathway.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2500
Description
Human umbilical vein vascular endothelial cells (HUVECs) are crucial for angiogenesis that benefits functional recovery after cerebral infarction. This study aims to investigate the mechanisms underlying the effects of vascular endothelial growth factor (VEGF) on HUVECs. Overall design: HUVECs were treated with 16 ng/mL VEGF165 for 4 days
Publication Title
Transcriptome Sequencing to Identify Transcription Factor Regulatory Network and Alternative Splicing in Endothelial Cells Under VEGF Stimulation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 3 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
A GAPDH siRNA was overexpressed in HeLa cells and microarray expression profiling was performed to experimentally identify the off-targets of this siRNA at the transcriptome level. Among all predicted siRNA off-targets by MirTarget2, the majority were downregulated by at least 10% (i.e. less than 90% remaining gene expression). Moreover, more than one fifth were downregulated by at least 30%. The gene knockdown data is consistent with previous observations that siRNA off-targets are generally silenced at a more moderate level as compared to silencing of the single intended target
Publication Title
Rational design of microRNA-siRNA chimeras for multifunctional target suppression.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 53 Downloadable Samples
- Illumina HiSeq 2500
Description
Comprehensive knowledge of the dynamic changes in the cardiac transciptome can inform disease mechanism. Previous transcriptome profiling studies on heart failure rely on either microarray or RNA-Seq with low coverage, leaving a large portion of the transcriptome unexplored. Additionally, previous studies only examined two end stages of the disease, onset and late-stage heart failure. Profile of the transcriptome in the middle stage of disease progression can reveal critical molecular events underlying disease transition. Towards these goals, we conducted a multi-factorial RNA-Seq experiment, comparing the dynamic changes in the transcriptome of two murine models of heart failure, pressure overload and loss of mitochondrial complex I. Our data represents the deepest transcriptome coverage to date, covering onset, progression, and late stage of the disease. We found extensive differences in the expression magnitude and dynamics of the transciptomes in different heart failure models. In addition, such differences are associated with progressive worsening of cardiac physiology. Our analysis revealed that mitochondrial dysfunction combined with stress leads to increased number of differentially expressed long intergenic noncoding RNAs, including a recently identified lincRNA that is a master regulator of the cardiac lineage during development. Overall design: Cardiac tissues were cleaned with PBS and harvested at 1, 2, 4, and 8 weeks after surgeries by freezing in liquid nitrogen. Cardiac RNA profiles of wild type (WT) and ndufs4H-/- mice after surgeries were generated by deep sequencing at 4 time points, in quadruplicate, using Illumina HiSeq2000. The three factors of the data are genetic (WT vs. ndufs4H-/-), environmental stress (trans-aortic constriction vs. Sham controls), and time (Week 1, Week 2, Week 4 and Week 8). Thus, there are 16 samples in total and each sample has 4 replicates.
Publication Title
Revealing Pathway Dynamics in Heart Diseases by Analyzing Multiple Differential Networks.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 27 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
To identify the driver factors in liver metastasis of colorectal cancer, and seek for possible biomarkers, we applied array trascriptome detection using approaches tailored to FFPE derived RNA
Publication Title
Weighted gene co-expression network analysis of colorectal cancer liver metastasis genome sequencing data and screening of anti-metastasis drugs.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 20 Downloadable Samples
- IlluminaHiSeq2000
Description
Acute mountain sickness (AMS), which may progress to life-threatening high altitude cerebral edema, is a major threat to millions of people who live in or travel to high altitude. Although studies have revealed the risk factors and pathophysiology theories of AMS, the molecular mechanisms of it do not comprehensively illustrate. Here, we used a system-level methodology, RNA sequencing, to explore the molecular mechanisms of AMS at genome-wide level in 10 individuals. After exposure to high altitude, a total of 1,164 and 1,322 differentially expressed transcripts were identified in AMS and non-AMS groups, respectively. Among them, only 328 common transcripts presented between the two groups. Immune and inflammatory responses were overrepresented in participants with AMS, but not in non-AMS individuals. Anti-inflammatory cytokine IL10 and inflammation cytokines IF17F and CCL8 exhibited significantly different genetic connectivity in AMS compared to that of non-AMS individuals based on network analysis. IL10 was down-regulated and both IF17F and CCL8 were un-regulated in AMS individuals. Moreover, the serum concentration of IL10 significantly decreased in AMS patients after exposure to high altitude (p = 0.001) in another population (n=22). There was a large negative correlation between the changes of IL10 concentration, r(22) = -0.52, p = 0.013, and Lake Louise Score. Taken together, our analysis provides unprecedented characterization of AMS transcriptome and identifies that genes involved in immune and inflammatory responses were disturbed in AMS individuals by high altitude exposure. The reduction of IL10 after exposure to high altitude was associated with AMS. Overall design: Transcriptome from blood samples of AMS and non-AMS individuals were measured and analyzed before their departure and upon their arrival at high altitude (5300m).
Publication Title
Targeting JUN, CEBPB, and HDAC3: A Novel Strategy to Overcome Drug Resistance in Hypoxic Glioblastoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
It has been demonstrated previously that the reprogramming factors are sequestered in the pronuclei of zygote after fertilization, as the enucleated zygotes at interphase cannot support the development of cloned embryos whereas the enucleated zygotes at M-phase can reprogram somatic cells to full pluripotency. However, it remains unknown whether the parental pronucleus, derived either from the sperm or oocyte, possesses the similar reprogramming ability. Here, we provide evidence demonstrating that the parental pronuclei are asymmetric in reprogramming and the reprogramming factors reside mainly in the male pronucleus. As a result, only the female pronucleus-depleted mouse zygotes enucleated at M-phase of mitosis can support the somatic cell reprogramming, the derivation of chromosome transfer embryonic stem (ctES) cells with full pluripotency and the full term development of cloned embryos. In striking contrast, the male pronucleus-depleted zygotes enucleated at M-phase of mitosis fail to support the pre-implantation development of somatic cell cloned embryos. Furthermore, we demonstrated that the distinct epigenetic reprogramming ability of the parental pronucleus might contribute directly to the developmental difference of somatic cloned embryos. Our study highlights the developmental asymmetry of parental pronuclei in reprogramming.
Publication Title
Asymmetric reprogramming capacity of parental pronuclei in mouse zygotes.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
SMEI patient induced pluripotent stem cells (iPSCs) were derived from patient fibroblasts. In order to test the similarity between patient iPSCs and human embryonic stem (hES) cells, microarry analysis was carried out on SMEI patient iPSCs and human embryonic stem cells.
Publication Title
Modeling Dravet syndrome using induced pluripotent stem cells (iPSCs) and directly converted neurons.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples