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GSE19441
Homo sapiens
6 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
CK1-alpha-LS was knocked down in human coronary artery smooth muscle cells. Gene level and exon level changes in expression were assessed.
Publication Title
Protein kinase CK1alphaLS promotes vascular cell proliferation and intimal hyperplasia.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 12 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Previous results suggest that Bmh might inhibit the activity of the transcription factor Adr1 after binding to Adr1-dependent promoters. In a strain lacking the two major histone deacetylases, Hda1 and Rpd3 (hdac), Adr1 is bound to its target promoters recruiting what appears to be an inactive RNA ploymerase II preinitiation complex (PIC). To determine whether Bmh activity inhibits this inactive PIC and the generality of this effect on glucose-repressed gene expression, the mRNA profiles of wild type, bmh mutant, hdac mutant, and bmh hdac mutant cells grown in high glucose medium were compared.
Publication Title
14-3-3 (Bmh) proteins regulate combinatorial transcription following RNA polymerase II recruitment by binding at Adr1-dependent promoters in Saccharomyces cerevisiae.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 220 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) results in the condition called ER stress which induces the unfolded protein response (UPR) which is a complex cellular process that includes changes in expression of many genes. Failure to restore homeostasis in the ER is associated with human diseases. To identify the underlying changes in gene expression in response to ER stress, we induced ER stress in human B-cells and then measured gene expression at 10 time-points. We followed up those results by studying cells from 60 unrelated people. We rediscovered genes that were known to play a role in ER stress response and uncovered several thousand genes that are not known to be involved. Two of these are VLDLR and INHBE which showed significant increase in expression following ER stress in B-cells and
Publication Title
Gene expression and genetic variation in response to endoplasmic reticulum stress in human cells.
Sample Metadata Fields
Cell line, Subject, Time
View Samples- Homo sapiens
- 31 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (<a href="http://cit.ligue-cancer.net" target="_blank">http://cit.ligue-cancer.net</a>). 104 samples; Affymetrix U133A micro-arrays.<br></br> <br></br> Ninety two patients with T-ALL were diagnosed and treated at Saint-Louis hospital, Paris. Seven patients were studied at diagnosis and relapse (total 99 T-ALL samples). There were 56 children (median age 9 years old; range 1 to 16), and 36 adults (median age 27; range 17 to 66). Informed consent was obtained from the patients and/or relatives. T-ALL diagnosis was based on morphological and immunophenotypical criteria using flow cytometry and an extended monoclonal antibody panel.<br></br> <br></br> Using a combination of molecular cytogenetic and large-scale expression analysis in human T-ALL, we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus. Specific quantitative PCR analysis showed that the expression of the whole HOXA gene cluster was dramatically dysregulated in the HOXA-rearranged cases, and also in MLL and CALM-AF10-related T-ALL cases, strongly suggesting that HOXA genes are oncogenic in these leukemias. Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALL based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biological networks with the TLX1 and TLX3-related cases. Since T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic sub-populations. Inappropriate utilization or perturbation of specific molecular networks involved in thymic differentiation was detected. Moreover, we found a significant association between T-ALL oncogenic subgroups and ectopic expression of a limited set of genes, including several developmental genes, namely HOXA, TLX1, TLX3, NKX3-1, SIX6 and TFAP2C. These data strongly support the view that the abnormal expression of developmental genes, including the prototypical homeobox genes HOXA, is critical in T-ALL oncogenesis.<br></br> <br></br> Project Leader: <br></br> FranC'ois Sigaux<br></br> Institut Universitaire d'Hematologie<br></br> Hopital Saint Louis, Paris, France<br></br> <br></br> Data submission:<br></br>Fabien Petel
Publication Title
HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 33 Downloadable Samples
Illumina HiSeq 2500
Description
In order to understand the underlying mechanisms, which ensure that disease progression is prevented in EC, a comprehensive analysis of clinical phenotypes coupled to genetics and biomolecular mechanisms is required. The rapidly increasing accessibility of genetic and biomolecular expression data from new high-throughput technologies is the foundation to shift the traditional phenotype-first approach to explorative genetic or molecular data-first approaches. In this study, we aimed to explore a comprehensive analysis of host transcriptomics and proteomics data coupled to clinical phenotypes in a well-defined Swedish EC cohort with up to 20 years of clinical follow-up data.
Publication Title
Transcriptomics and Targeted Proteomics Analysis to Gain Insights Into the Immune-control Mechanisms of HIV-1 Infected Elite Controllers.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Treatment, Race
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
The causative role of activated Hedgehog signaling in liver fibrosis was investigated in vivo.
Publication Title
Hepatic expression of Sonic Hedgehog induces liver fibrosis and promotes hepatocarcinogenesis in a transgenic mouse model.
Sample Metadata Fields
Sex, Specimen part
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- Rattus norvegicus
- 9 Downloadable Samples
- Affymetrix Rat Gene 2.0 ST Array (ragene20st)
Description
The goal of this experiment was to investigate the molecular mechanism of how Set-beta regulates neurite growth. Set-betas subcellular localization is regulated by posttranslational modifications. We found that Set-beta suppresses neurite growth of purified postnatal rat retinal ganglion cell (RGC) primary neurons when it is overexpressed in the nucleus, whereas recruiting Set-beta to cellular membrane by fusing myr-tag to its N-terminus promotes neurite growth. Here, we transfected purified by immunopanning postnatal rat RGC with wild-type Set-beta which localizes to the nucleus, myr-Set-beta which is recruited to cellular membranes, and mCherry control, and analyzed with microarrays Set-betas subcellular localization-dependent effects on gene expression. We found that wild-type Set- regulated expression of significantly more genes than myr-Set-, consistent with wild-type Set-s nuclear localization and previously described roles in regulating transcription. These data reveal potential downstream gene effectors regulating neurite growth, and specific candidate genes could be validated and tested in future experiments.
Publication Title
Regulating Set-β's Subcellular Localization Toggles Its Function between Inhibiting and Promoting Axon Growth and Regeneration.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Neuroendocrine tumors (NETs) often harbor loss-of-function mutations in Daxx gene. Daxx interacts with several partners to regulate cellular processes and gene expression.
Publication Title
Menin and Daxx Interact to Suppress Neuroendocrine Tumors through Epigenetic Control of the Membrane Metallo-Endopeptidase.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Multiple endocrine neoplasia type1 (MEN1), an inherited autosomal dominant syndrome characterized by the development of endocrine tumors including NETs, results from mutation in the MEN1 gene that encodes the protein menin. In mouse models, heterozygous loss of Men1 leads to multiple endocrine tumors with loss of heterozygocity at the Men1 locus. Men1 interacts with several partners to regulate cellular processes and gene expression through regulating histone modification.
Publication Title
Menin and Daxx Interact to Suppress Neuroendocrine Tumors through Epigenetic Control of the Membrane Metallo-Endopeptidase.
Sample Metadata Fields
Specimen part
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