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SRP068723
Mus musculus
2 Downloadable Samples
Illumina HiSeq 2000
Description
about 250 genes were significantly changed after Gata4 and Gata6 were specifically deleted in the pancreatic progenitor cells Overall design: 6 pancreatic buds were pooled for the control, and 12 pancreatic buds were pooled for the Pdxcre; Gata4fl/fl; Gata6fl/fl. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq
Publication Title
GATA4 and GATA6 regulate pancreatic endoderm identity through inhibition of hedgehog signaling.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 4000
Description
RNA transcriptome sequencing analysis was performed in SGC-7901 cells that were transfected with ENST00000431060 shRNA or control shRNA Overall design: mRNA profiles of SGC-7901 cells transfected with ENST00000431060 shRNA or control shRNA
Publication Title
lncRNA GCAWKR Promotes Gastric Cancer Development by Scaffolding the Chromatin Modification Factors WDR5 and KAT2A.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2500
Description
Medulloblastoma could be classified into four subtypes: Wnt, Shh, Group 3, and Group 4. Subtypes of medulloblastoma have distinct epigenetic properties. We report that a chromatin regulator SMARCA4/Brg1 controls a transcriptional program that specifically required for Shh-type medulloblastoma identity and proliferation. We show that Brg1 deletion significantly inhibited tumor formation and progression in a mouse medulloblastoma model. Genomic experiments indicate that Brg1 specifically coordinates with key transcription factors including Gli1, Atoh1, and REST to regulate the expression of both oncogenes and tumor suppressors. Shh-type medulloblastoma displays distinct H3K27me3 properties. We demonstrate that Brg1 modulates activities of H3K27me3 modifiers to regulate expression of medulloblastoma genes. Brg1 is important for the growth of a human medulloblastoma cell line and Brg1-regulated pathways are conserved in human Shh-type medulloblastoma. This study reveals a novel epigenetic mechanism that controls medulloblastoma development and provides a rationale for developing subtype-specific treatment strategies. Overall design: Examine differential gene expression in SmoM2 medulloblastoma after Smarca4/Brg1 conditional knockout
Publication Title
SMARCA4/Brg1 coordinates genetic and epigenetic networks underlying Shh-type medulloblastoma development.
Sample Metadata Fields
No sample metadata fields
View Samples- Escherichia coli
- 6 Downloadable Samples
Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
Gene expression in E coli W3110 strains with either ybaO over-expression (W3110/pcutR) or ybaO deletion (W3110/cutR) were measured with cysteine challenge.
Publication Title
Anaerobic Cysteine Degradation and Potential Metabolic Coordination in Salmonella enterica and Escherichia coli.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The identification of gene regulatory modules is an important yet challenging problem in computational biology. While many computational methods have been proposed to identify regulatory modules, their initial success is largely compromised by a high rate of false positives, especially when applied to human cancer studies. New strategies are needed for reliable regulatory module identification.
Publication Title
Multilevel support vector regression analysis to identify condition-specific regulatory networks.
Sample Metadata Fields
Sex, Age, Cell line, Race
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Scope: Soy flour diet (MS) prevented isoflavones from stimulating MCF-7 tumor growth in athymic nude mice, indicating that other bioactive compounds in soy can negate the estrogenic properties of isoflavones. The underlying signal transduction pathways to explain the protective effects of soy flour consumption were studied here.
Publication Title
Isoflavones in soy flour diet have different effects on whole-genome expression patterns than purified isoflavone mix in human MCF-7 breast tumors in ovariectomized athymic nude mice.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
Analysis of transcriptome from AR-deleted CARN-derived lines (ADCA) and controls, AR-positive CARN-derived lines (APCA) ADCA and APCA lines at passage 5 or 6 were grown to approximately 70-80% confluency in the presence of DHT, lysed in Trizol and frozen for subsequent molecular analysis Overall design: Total RNA obtained from ADCA and APCA cell lines. Frozen cells in Trizol were processed for RNA isolation and transcriptome analysis using the MagMAX-96 for Microarray kit (Ambion).
Publication Title
Differential requirements of androgen receptor in luminal progenitors during prostate regeneration and tumor initiation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
The root cap-specific conversion of the auxin precursor indole-3-butyric acid (IBA) into the main auxin indole-3-acetic acid (IAA) generates a local auxin source which subsequently modulates both the periodicity and intensity of auxin response oscillations in the root tip of Arabidopsis, and consequently fine-tunes the spatiotemporal patterning of lateral roots. To explore downstream components of this signaling process, we investigated the early transcriptional regulations happening in the root tip during IBA-to-IAA conversion in Col-0 and ibr1 ibr3 ibr10 triple mutant after 6 hours of IBA treatment.
Publication Title
Root Cap-Derived Auxin Pre-patterns the Longitudinal Axis of the Arabidopsis Root.
Sample Metadata Fields
Age, Specimen part, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
One-third of all ER+ breast tumors treated with endocrine therapy fail to respond, and the remainder are likely to relapse in the future. Almost all data on endocrine resistance has been obtained in models of invasive ductal carcinoma (IDC). However, invasive lobular carcinomas (ILC) comprise up to 15% of newly diagnosed invasive breast cancers diagnosed each year and, while the incidence of IDC has remained relatively constant during the last 20 years, the prevalence of ILC continues to increase among postmenopausal women. We report a new model of Tamoxifen (TAM)-resistant invasive lobular breast carcinoma cells that provides novel insights into the molecular mechanisms of endocrine resistance. SUM44 cells express ER and are sensitive to the growth inhibitory effects of antiestrogens. Selection for resistance to 4-hydroxytamoxifen led to the development of the SUM44/LCCTam cell line, which exhibits decreased expression of estrogen receptor alpha (ER) and increased expression of the estrogen-related receptor gamma (ERR). Knockdown of ERR in SUM44/LCCTam cells by siRNA restores TAM sensitivity, and overexpression of ERR blocks the growth-inhibitory effects of TAM in SUM44 and MDA-MB-134 VI lobular breast cancer cells. ERR-driven transcription is also increased in SUM44/LCCTam, and inhibition of activator protein 1 (AP1) can restore or enhance TAM sensitivity. These data support a role for ERR/AP1 signaling in the development of TAM resistance, and suggest that expression of ERR may be a marker of poor Tamoxifen response.
Publication Title
ERRgamma mediates tamoxifen resistance in novel models of invasive lobular breast cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Mouse embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) exhibit a pluripotent developmental potential, contributing to all embryonic cell types, though rarely to extra-embryonic lineages. Unexpectedly, rare, totipotent-like stem cells have been identified in cultured ESC populations, suggesting the existence of a discrete molecular pathway that regulates the transition between totipotency and pluripotency in vitro. Here, we identify a single miRNA, miR-34a, whose deficiency in mouse pluripotent stem cells expands cell fate potential, giving rise to both embryonic and extra-embryonic lineages in vitro and in vivo. The expression profiles of the totipotent-like miR-34a-knockout murine pluripotent stem cells are characterized by a strong induction of MERVL endogenous retroviruses, a key molecular hallmark shared with totipotent mouse 2-cell blastomeres and totipotent-like mouse ESCs. In all three cell types, a subset of MERVL elements promotes the expression of specific isoforms of the proximal protein-coding genes. We demonstrate that miR-34a represses MERVL expression through transcriptional regulation, at least in part, by directly targeting the transcription factor GATA-binding protein 2 (Gata2). Since MERVL activation correlated precisely with the totipotent-like state, we hypothesized that the miR-34a/Gata2 pathway that regulates MERVL expression in ESCs/iPSCs also regulates the acquisition of totipotency in culture. Consistent with this hypothesis, gata2 knock-down in miR-34a-knockout mouse pluripotent stem cells not only reduced MERVL expression, but also abolished the expanded cell fate potential of these cells both in vitro and in vivo. Taken together, our findings not only provide key insights into the functional importance of miR-34a in restricting the totipotent cell fate potential of pluripotent stem cells, but also elucidate the underlying molecular basis by which miR-34a regulates the developmental potentials of ESCs/iPSCs. Overall design: Wildtype and miR-34a-deficient iPSCs, three biological replicates per group
Publication Title
Deficiency of microRNA <i>miR-34a</i> expands cell fate potential in pluripotent stem cells.
Sample Metadata Fields
No sample metadata fields
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