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Mus musculus
20 Downloadable Samples
Illumina Genome Analyzer IIx
Description
Leber congenital amaurosis (LCA) includes congenital or early-onset blinding diseases, characterized by vision loss together with nystagmus and nonrecordable electroretinogram (ERG). At least 19 genes are associated with LCA. While most LCA is recessive, mutations in the homeodomain transcription factor gene CRX lead to autosomal dominant LCA. The mechanism of CRX-LCA is not understood. Here, we report a new spontaneous mouse mutant carrying a frameshift mutation in Crx (CrxRip). We show that, unlike Crx-/- mouse retina, the dominant Crx c.763del1 mutation in CrxRip results in congenital blindness with complete loss of ERG, yet the photoreceptors do not degenerate. Dominant CRX frameshift mutations associated with LCA mimic the CrxRip phenotype that can be rescued by Crx. RNA-Seq profiling reveals progressive and complete loss of rod differentiation factor Nrl in CrxRip, while residual Nrl remains in Crx-/- retina. Moreover, Nrl partially restores the rod phenotype in CrxRip/+ mice. We show that the binding of Otx2 to Nrl promoter is obliterated in CrxRip mutant, and ectopic Otx2 can rescue the rod phenotype. Therefore, Otx2 is required to maintain Nrl expression in developing rods to consolidate rod fate. Our studies provide the mechanism of congenital blindness caused by dominant CRX mutations and should assist in therapeutic design. Overall design: Retinal samples were harvested from WT, CrxRip/+, CrxRip/Rip, Crx-/- and Nrl-/- retina at postnatal days 2 and 21 for whole transcriptome sequencing (RNAseq). Each sample included 2 independent frozen retina and experiments were performed in duplicates. RNA-seq transcriptome libraries were constructed from 1 µg of total RNA.
Publication Title
OTX2 loss causes rod differentiation defect in CRX-associated congenital blindness.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 11 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor 1 apoprotein.
Publication Title
During hormone depletion or tamoxifen treatment of breast cancer cells the estrogen receptor apoprotein supports cell cycling through the retinoic acid receptor α1 apoprotein.
Sample Metadata Fields
Cell line
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Mapping the transcriptomes governed by TCER-1 and DAF-16 upon germline loss
Publication Title
DAF-16 and TCER-1 Facilitate Adaptation to Germline Loss by Restoring Lipid Homeostasis and Repressing Reproductive Physiology in C. elegans.
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line
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GSE59545- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
p65-/-Ras cells show delayed tumor formation in SCID mice. However, after prolonged latency, tumor formation was observed from these mice. To understand the changes of NF-kB regulated genes before and after tumor formation, RNA from p65+/+Ras, p65+/+RasTumor, p65-/-Ras, p65-/-RasTumor cells were isolated and microarray were performed.
Publication Title
NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Elk1 directs selective gene induction that is a substantial and critical component of growth signaling by AR in PC cells.
Publication Title
The ETS domain transcription factor ELK1 directs a critical component of growth signaling by the androgen receptor in prostate cancer cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Treatment of late passage (LP50) LNCaP cells with R1881 (androgen) and AR shRNA identified a gene program controlled by androgen receptor in the absence of androgen.
Publication Title
Hormone depletion-insensitivity of prostate cancer cells is supported by the AR without binding to classical response elements.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 16 Downloadable Samples
- Affymetrix Yeast Genome S98 Array (ygs98)
Description
Response of Saccharomyces cerevisiae strain BY4741 to desiccation
Publication Title
Phenomic and transcriptomic analyses reveal that autophagy plays a major role in desiccation tolerance in Saccharomyces cerevisiae.
Sample Metadata Fields
Time
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2500
Description
Plexiform neurofibroma is a major contributor to morbidity in Neurofibromatosis type I (NF1) patients. Macrophages and mast cells infiltrate neurofibroma, and data from mouse models implicate these leukocytes in neurofibroma development. Anti-inflammatory therapy targeting these cell populations has been suggested as a means to prevent neurofibroma development. Here, we compare gene expression in inflamed nerves from NF1 models which invariably form neurofibroma to those with inflammation driven by EGFR overexpression which rarely progresses to neurofibroma. We find that the chemokine Cxcl10 is uniquely up-regulated in NF1 mice that invariably develop neurofibroma. Global deletion of the CXCL10 receptor, Cxcr3, prevented neurofibroma development in these neurofibroma-prone mice. Cxcr3 expression localized to T cells and dendritic cells (DCs) in both inflamed nerves and neurofibromas. These data support a heretofore unappreciated role for T cells/DCs in neurofibroma initiation. Overall design: To identify cell populations associated with Cxcl10 expression, we utilized a single-cell RNA-Seq (scRNA-Seq) data set collected from 2-month Dhh-Cre;Nf1 fl/fl nerve/DRG using the 10x Genomics Chromium platform.
Publication Title
Cxcr3-expressing leukocytes are necessary for neurofibroma formation in mice.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
To elucidate the mode of action of apratyramide, we performed microarray profiling using the Affymetrix GeneChip Human Transcriptome Array 2.0 to determine global changes in transcript levels in HaCaT cells treated with apratyramide. Comparativel analysis identified 371 differentially expressed genes after 12 h treatment with 30 M apratyramide (p < 0.05, FDR corrected, fold change >1.5 or <0.67). Consistent with our previous data, VEGF-A appeared to be one of the most up-regulated genes. To examine the molecular functions and genetic networks, the microarray data was analyzed using Ingenuity Pathways Aanalysis (IPA).The global changes of transcript levels are associated with increased downstream phenotypic effects including angiogenesis, mitogenesis, differentiation of epithelial tissue and formation of skin, and decreased effects such as apoptosis of liver cells and hypoplasia of organs. IPA analysis of 371 microarray hits indicated the unfolded protein response (UPR) as the top canonical pathway with a p-value of 1.45 10-16. The IPA also elucidated that the 371 hits were most related to a molecular network associated with the function of cellular compromise and cellular maintenance. The network contains molecular components from UPR pathway, NRF2-mediated oxidative stress response signaling as well as glucocorticoid receptor signaling.
Publication Title
Apratyramide, a Marine-Derived Peptidic Stimulator of VEGF-A and Other Growth Factors with Potential Application in Wound Healing.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
- NextSeq 550
Description
RNA seqeuncing was performed to identifiy changes in genes expression and alternative splicing following SRSF3 depletion in pluripotent stem cells. Overall design: Induced pluripotent stem cells (iPSCs) generated from reprogrammable conditional SRSF3 knockout (SRSF3-KO/OKSM) mouse embryonic fibroblasts (MEFs) were induced for 24h to deplete SRSF3 and RNA seqeuncing was performed.
Publication Title
SRSF3 promotes pluripotency through <i>Nanog</i> mRNA export and coordination of the pluripotency gene expression program.
Sample Metadata Fields
Specimen part, Subject
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