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SRP100987
Mus musculus
100 Downloadable Samples
Illumina HiSeq 2500
Description
Objective: Transcriptional profiling of murine HSPC in response to ß-glucan-induced innate immune training Overall design: HSPC mRNA profiles of wild type (WT) mice injected with PBS or ß-glucan. Wild type (WT) C57BL/6 mice were intraperitoneally injected with PBS or 1 mg ß-glucan in PBS. Mice were sacrificed on day 7 or day 28 and long-term heematopoietic stem cells (LT-HSC) and/or multipotent progenitors (MPP) were sorted. In another group, mice were injected with PBS or 1 mg ß-glucan in PBS and on day 7 they were additionally injected with 150 mg/kg 5-fluouracil. Mice were sacrificed on day 14 after 5-FU administration and LT-HSC were sorted.
Publication Title
Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
Illumina HumanHT-12 V3.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Dual role of FoxA1 in androgen receptor binding to chromatin, androgen signalling and prostate cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 16 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
We report the dual role of FoxA1 in androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell line LNCaP-1F5 using ChIP-sequencing. Depletion of FoxA1 reprograms both androgen and glucocorticoid receptor recruitment and subsequent gene expression. The ChIP-seq has been performed using AR, FoxA1, GR, H3K4me2 antibodies. We have also mapped the DNaseI-hypersensitive sites (DHS) using deep sequencing.
Publication Title
Dual role of FoxA1 in androgen receptor binding to chromatin, androgen signalling and prostate cancer.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Transcription factor Stat5 is constitutively active in human prostate cancer but not in normal prostate epithelium. Stat5 activation is associated with prostate cancer lesions of high histological grades, and is present in the majority of castration-resistant recurrent human prostate cancers. The molecular mechnisms underlying constitutive activation of Stat5 in primary and recurrent human prostate cancer are currently unclear.
Publication Title
Stat5 promotes metastatic behavior of human prostate cancer cells in vitro and in vivo.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 48 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The glycopeptide antibiotic vancomycin (VCM) represents one of the last lines of defense against methicillin-resistant Staphylococcus aureus infections. However, vancomycin is nephrotoxic, but the mechanism of toxicity is still unclear.
Publication Title
Gene expression analysis reveals new possible mechanisms of vancomycin-induced nephrotoxicity and identifies gene markers candidates.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We used microarrays to detail the global programme of gene expression after knockdown of Ecdysoneless in hMECs
Publication Title
The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Breast cancers with HER2 overexpression are sensitive to drugs targeting the receptor or its kinase activity. HER2-targeting drugs are initially effective against HER2- positive breast cancer, but resistance inevitably occurs. We previously found that nuclear factor kappa B is hyper-activated in the subset of HER-2 positive breast cancer cells and tissue specimens. In this study, we report that constitutively active NF-B rendered HER2-positive cancer cells resistant to anti-HER2 drugs, and cells selected for Lapatinib resistance up-regulated NF-B. In both circumstances, cells were anti-apoptotic and grew rapidly as xenografts. Lapatinib-resistant cells were refractory to HER2 and NF-B inhibitors alone but were sensitive to their combination, suggesting a novel therapeutic strategy. A subset of NF-B-responsive genes was overexpressed in HER2-positive and triple-negative breast cancers, and patients with this NF-B signature had poor clinical outcome. Anti-HER2 drug resistance may be a consequence of NF-B activation, and selection for resistance results in NF-B activation, suggesting this transcription factor is central to oncogenesis and drug resistance. Clinically, the combined targeting of HER2 and NF-B suggests a potential treatment paradigm for patients who relapse after anti-HER2 therapy. Patients with these cancers may be treated by simultaneously suppressing HER2 signaling and NF-B activation.
Publication Title
NF-κB activation-induced anti-apoptosis renders HER2-positive cells drug resistant and accelerates tumor growth.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Primary T cell activation involves the integration of three distinct signals delivered in sequence: 1) antigen recognition, 2) costimulation, and 3) cytokine-mediated differentiation and expansion. Strong immunostimulatory events such as immunotherapy or infection induce profound cytokine release causing bystander T cell activation, thereby increasing the potential for autoreactivity and need for control. We show that during strong stimulation, a profound suppression of primary CD4+ T cell-mediated immune responses ensued and was observed across preclinical models and patients undergoing high-dose interleukin-2 (IL-2) therapy. This suppression targeted nave CD4+ but not CD8+ T cells and was mediated through transient suppressor of cytokine signaling-3 (SOCS3) inhibition of the STAT5b transcription factor signaling pathway. These events resulted in complete paralysis of primary CD4+ T cell activation affecting memory generation, induction of autoimmunity, as well as impaired viral clearance. These data highlight the critical regulation of nave CD4+ T cells during inflammatory conditions.
Publication Title
Out-of-Sequence Signal 3 Paralyzes Primary CD4(+) T-Cell-Dependent Immunity.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 1 Downloadable Sample
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
S-adenosylmethionine levels regulate the schwann cell DNA methylome.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 22 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
In this study we have analyzed the global gene expression of nave mouse embryonic stem cells in different culture conditions including R2i (PD0325901+SB431542), 2i (PD0325901+CHIR99021), and also PD0325901+LIF and SB431542+LIF to show the similarities and differences between the conditions in maintaining pluripotency.
Publication Title
Inhibition of TGFβ signaling promotes ground state pluripotency.
Sample Metadata Fields
Specimen part, Cell line
View Samples