Filters
Technology
Platform
SRP061361
Drosophila melanogaster
377 Downloadable Samples
Illumina HiSeq 2000
Description
We sequenced mRNA from transverse slices of embryos from a variety of D. melanogaster mutants (bicoid over-expression, bicoid knockdown, hunchback knocdown, and zelda mutant) at the blastoderm stage to determine genome-wide patterns of gene expression. Overall design: mRNA from transverse sections of single D. melanogaster embryos mutant for patterning TFs was sequenced.
Publication Title
Genome-wide measurement of spatial expression in patterning mutants of <i>Drosophila melanogaster</i>.
Sample Metadata Fields
Specimen part, Subject
View Samples- Drosophila melanogaster
- 117 Downloadable Samples
- Illumina HiSeq 2000
Description
We sequenced mRNA from transverse slices of embryos at the blastoderm stage to determine genome-wide patterns of gene expression. Overall design: mRNA from transverse sections of single D. melanogaster embryos was sequenced
Publication Title
Sequencing mRNA from cryo-sliced Drosophila embryos to determine genome-wide spatial patterns of gene expression.
Sample Metadata Fields
Specimen part, Disease, Cell line, Subject
View Samples- Drosophila melanogaster
- 26 Downloadable Samples
- Illumina HiSeq 2000
Description
We sequenced mRNA according to several library prep protocols with known mixtures of two species of Drosophila in order to establish linear response in each protocol. Overall design: For each library prep protocol, mixtures with 0%, 5%, 10%, and 20% D. virilis total RNA was prepared, then libraries prepared according to instructions.
Publication Title
Low-cost, low-input RNA-seq protocols perform nearly as well as high-input protocols.
Sample Metadata Fields
Subject
View Samples- Mus musculus
- 113 Downloadable Samples
- Illumina HiSeq 2500
Description
To study role of Lin28/let-7 axis on nephrogenesis, we profiled kidney transcriptom of LIN28 OE, let-7 KO, and their wild-type littermate control mice. Overall design: RNA-seq on kidneys from LIN28B OE, let-7 KO, and their wild-type littermate controls at P3.
Publication Title
Lin28 and let-7 regulate the timing of cessation of murine nephrogenesis.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 37 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing kidney. The central thesis is straightforward. The combination of laser capture microdissection (LCM) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing kidney. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene in laser capture microdissected components of the developing kidney. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone.
Publication Title
Analysis of early nephron patterning reveals a role for distal RV proliferation in fusion to the ureteric tip via a cap mesenchyme-derived connecting segment.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Our laboratory's interest is in understanding the molecular principles that underlie the regional organization of the mammalian metanephric kidney. Our goal is to generate a detailed spatial map of the cellular expression of selected regulatory genes during mammalian kidney development. The goal of this study is to identify a population of genes that are enriched in the renal vesicle (RV) and its derivatives using Wnt4 mutants.
Publication Title
Analysis of early nephron patterning reveals a role for distal RV proliferation in fusion to the ureteric tip via a cap mesenchyme-derived connecting segment.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
beta-catenin is an essential mediator of canonical Wnt signaling and a central component of the cadherin-catenin epithelial adhesion complex. Dysregulation of beta-catenin expression has been described in pancreatic neoplasia. Newly published studies have suggested that beta-catenin is critical for normal pancreatic development although these reports reached somewhat different conclusions. In addition, the molecular mechanisms by which loss of beta-catenin affects pancreas development are not well understood. The goals of this study then were; 1] to further investigate the role of beta-catenin in pancreatic development using a conditional knockout approach and 2] to identify possible mechanisms by which loss of beta-catenin disrupts pancreatic development. A Pdx1-cre mouse line was used to delete a floxed beta-catenin allele specifically in the developing pancreas, and embryonic pancreata were studied by immunohistochemistry and microarray analysis.
Publication Title
Wnt/beta-catenin signaling is required for development of the exocrine pancreas.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Alternative 3-terminal exons, which use intronic polyadenylation sites, are generally unconserved and lowly expressed, while the main gene products end in the last exon of genes. In this study, we discover a class of human genes, where the last exon appeared recently during evolution, and the major gene product uses an alternative 3-terminal exon corresponding to the ancestral last exon of the gene. This novel class of alternative 3-terminal exons are down-regulated on a large scale by doxorubicin, a cytostatic drug targeting topoisomerase II, and play a role in cell cycle regulation, including centromere-kinetochore assembly. The RNA-binding protein, HuR/ELAVL1 is a major regulator of this specific set of alternative 3-terminal exons. HuR binding to the alternative 3-terminal exon in the pre-messenger RNA promotes its splicing, and is reduced by topoisomerase inhibitors. These findings provide new insights into the evolution, function and molecular regulation of alternative 3-terminal exons.
Publication Title
A recently evolved class of alternative 3'-terminal exons involved in cell cycle regulation by topoisomerase inhibitors.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Loss of function of the tumor suppressor BRCA1 (Breast Cancer 1) protein is responsible for numerous familial and sporadic breast cancers. We previously identified PABP1 as a novel BRCA1 partner and showed that BRCA1 modulates translation through its interaction with PABP1. We showed that the global translation was diminished in BRCA1-depleted cells and increased in BRCA1-overexpressing cells. Our findings raised the question whether BRCA1 affects translation of all cytoplasmic cellular mRNAs or whether it specifically targets a subset of mRNAs.
Publication Title
BRCA1-Dependent Translational Regulation in Breast Cancer Cells.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Immuno-chemotherapy regimens elicit high response rates in B-cell non-Hodgkin lymphoma but heterogeneity in response duration is observed, with some patients achieving cure and others showing refractory disease or relapse. Using a transcriptome-powered targeted proteomics screen, we discovered a gene regulatory circuit involving the nuclear factor CYCLON which characterizes aggressive disease and resistance to the anti-CD20 monoclonal antibody, Rituximab, in high-risk B-cell lymphoma. CYCLON knockdown was found to inhibit the aggressivity of MYC-overexpressing tumors in mice and to modulate gene expression programs of biological relevance to lymphoma. Furthermore, CYCLON knockdown increased the sensitivity of human lymphoma B cells to Rituximab in vitro and in vivo. Strikingly, this effect could be mimicked by in vitro treatment of lymphoma B cells with a small molecule inhibitor for BET bromodomain proteins (JQ1). In summary, this work has identified CYCLON as a new MYC cooperating factor that drives aggressive tumor growth and Rituximab resistance in lymphoma. This resistance mechanism is amenable to next-generation epigenetic therapy by BET bromodomain inhibition, thereby providing a new combination therapy rationale for high-risk lymphoma.
Publication Title
Identification of a novel BET bromodomain inhibitor-sensitive, gene regulatory circuit that controls Rituximab response and tumour growth in aggressive lymphoid cancers.
Sample Metadata Fields
Specimen part, Cell line
View Samples