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Homo sapiens
24 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
Monocytes play a critical role during infection with Mycobacterium tuberculosis (Mtb). They are recruited to the lung where they participate in the contention of infection. Alternatively, inflammatory monocytes may help in prolonging inflammation or serve as niches for Mtb infection. Also, monocyte response to infection may vary depending on the particularities of the clinical isolate of Mtb from which they are infected. In this pilot study, using microarrays we have examined the global mRNA profiles of circulating human monocytes from healthy individuals and patients with active tuberculosis (TB).
Publication Title
Infection of Monocytes From Tuberculosis Patients With Two Virulent Clinical Isolates of <i>Mycobacterium tuberculosis</i> Induces Alterations in Myeloid Effector Functions.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We used microarrays to detail the global gene expression signature of PDAC and to identify distinct up- and down-regulated transcripts in these tumors compared to control pancreas. We also established from this dataset the metabolic signature of PDAC in order to define new metabolic therapeutic target for pancreatic cancer.
Publication Title
Cholesterol uptake disruption, in association with chemotherapy, is a promising combined metabolic therapy for pancreatic adenocarcinoma.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Pancreatic Ductal Adenocarcinoma (PDA) is a critical health issue in cancer field with little new therapeutic options. Several evidences support an implication of intra-tumoral microenvironment (stroma) on PDA progression. However, its contribution to the role of neuroplastic changes within pathophysiology and clinical course of PDA, mainly through tumor recurrence and neuropathic pain, remains unknown neglecting a putative therapeutic window. Here, we report that intra-tumoral microenvironment is a mediator of PDA Associated Neural Remodeling (PANR). With laser capture microdissection of stromal/tumoral compartment from human PDA followed by cDNA based microarray analyses we highlighted numerous factors expressed by stromal compartment that could impact on neuroplastic changes; among them, the Slit2/Robo axon guidance pathway. Using co-culture in vitro, we showed that stromal secreted Slit2 increases DRG neurite outgrowth and Schwann cells migration/proliferation by modulating N-Cadherin/-Catenin signaling. Importantly, Slit2/Robo signaling inhibition disrupts this stromal/neural connection. Finally, we revealed in vivo that Slit2 expression is correlated with neural remodeling within Human and mouse PDA. These results demonstrate the implication of microenvironment, through secretion of axon guidance molecule, in PANR. Furthermore, it provides rationale to investigate the disruption of stromal/neural compartment dialogue by using Slit2/Robo pathway inhibitors for treatment of pancreatic cancer recurrence and associated pain.
Publication Title
Stromal SLIT2 impacts on pancreatic cancer-associated neural remodeling.
Sample Metadata Fields
Specimen part, Disease
View Samples- Macaca mulatta
- 78 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The hippocampus is part of a brain network essential for memory function. Paradoxically, the hippocampus is also the brain structure that is most sensitive to hypoxic-ischemic episodes. Here we show that the expression of genes associated with glycolysis and glutamate metabolism in astrocytes and the coverage of excitatory synapses by astrocytic processes undergo significant decreases in the CA1 field of the monkey hippocampus during postnatal development. Given the established role of astrocytes in the regulation of glutamate concentration in the synaptic cleft, our findings indicate that a developmental decrease in astrocytic processes underlies the selective vulnerability of CA1 during hypoxic-ischemic episodes in adulthood, its decreased susceptibility to febrile seizures with age, as well as contribute to the emergence of selective, adult-like memory function.
Publication Title
Developmental regulation of gene expression and astrocytic processes may explain selective hippocampal vulnerability.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 82 Downloadable Samples
Illumina HiSeq 2000
Description
Acute myeloid leukemia (AML) is associated with poor clinical outcome and the development of more effective therapies is urgently needed. G protein-coupled receptors (GPCRs) represent attractive therapeutic targets, accounting for approximately 30% of all targets of marketed drugs. Using next-generation sequencing, we studied the expression of 772 GPCRs in 148 genetically diverse AML specimens, normal blood and bone marrow cell populations as well as cord blood-derived CD34-positive cells. Among these receptors, 30 are overexpressed and 19 are downregulated in AML samples compared with normal CD34-positive cells. Upregulated GPCRs are enriched in chemokine (CCR1, CXCR4, CCR2, CX3CR1, CCR7 and CCRL2), adhesion (CD97, EMR1, EMR2 and GPR114) and purine (including P2RY2 and P2RY13) receptor subfamilies. The downregulated receptors include adhesion GPCRs, such as LPHN1, GPR125, GPR56, CELSR3 and GPR126, protease-activated receptors (F2R and F2RL1) and the Frizzled family receptors SMO and FZD6. Interestingly, specific deregulation was observed in genetically distinct subgroups of AML, thereby identifying different potential therapeutic targets in these frequent AML subgroups. Overall design: Total healthy bone marrow was sorted to isolate distinct cell populations. RNA-Seq analysis was performed on sorted cells to determine gene expression profile of healthy bona marrow subpopulations.
Publication Title
Transcriptome analysis of G protein-coupled receptors in distinct genetic subgroups of acute myeloid leukemia: identification of potential disease-specific targets.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 32 Downloadable Samples
- IlluminaHiSeq2000
Description
As regulators of protein degradation, proteasomes regulate practically all cellular functions. It is therefore logical to assume that replacement of the constitutive proteasome (CP) by its IFN- inducible homolog immunoproteasome (IP) could have far reaching effects on cell function. Accordingly, recent studies have revealed important roles for IPs in immune cells beyond MHC I-peptide processing. Moreover, the expression of IPs in non-immune cells from non-inflamed tissues suggests that the involvement of IPs is not limited to the immune system. We demonstrate here that IP-deficiency affects the transcription of 8104 genes in maturing dendritic cells (DCs). This occurs mainly through non-redundant regulation of key immune-related transcription factors by CPs and IPs. Additionally, IP-deficiency decreases DC''s efficiency to activate CD8+ T cells in vivo. Our study reveals that the broad cellular roles of IPs could rely on transcription regulation and, more importantly, illustrates how IP-deficiency could generate MHC I-peptide processing-independent phenotypes. Overall design: Examination of the transcriptome of WT and immunoproteasome-deficient cells at 4 different time points of dendritic cell maturation, in 4 experimental replicates (total of 32 samples).
Publication Title
Immunoproteasomes shape the transcriptome and regulate the function of dendritic cells.
Sample Metadata Fields
No sample metadata fields
View Samples
SRP056295- Homo sapiens
- 523 Downloadable Samples
- IlluminaHiSeq2000
Description
RNA sequencing of human leukemia Overall design: The goals of this project are to obtain a comprehensive study of mutations and gene expression in human acute myeloid leukemia (AML). Methods: AML cells were thawed. DNA and RNA (polyA) was extracted and sequences were obtained with an illumina HiSeq 2000 sequencer. Results are pending.
Publication Title
RNA-sequencing analysis of core binding factor AML identifies recurrent ZBTB7A mutations and defines RUNX1-CBFA2T3 fusion signature.
Sample Metadata Fields
No sample metadata fields
View Samples SRP048759- Homo sapiens
- 434 Downloadable Samples
- IlluminaHiSeq2000
Description
RNA sequencing of human leukemia Overall design: The goals of this project are to obtain a comprehensive study of mutations and gene expression in human acute myeloid leukemia (AML). Methods: AML cells were thawed. DNA and RNA (polyA) was extracted and sequences were obtained with an illumina HiSeq 2000 sequencer. Results are pending.
Publication Title
RNA-sequencing analysis of core binding factor AML identifies recurrent ZBTB7A mutations and defines RUNX1-CBFA2T3 fusion signature.
Sample Metadata Fields
No sample metadata fields
View Samples SRP033266- Homo sapiens
- 144 Downloadable Samples
- IlluminaHiSeq2000
Description
RNA sequencing of human leukemia Overall design: The goals of this project are to obtain a comprehensive study of mutations and gene expression in human acute myeloid leukemia (AML). Methods: AML cells were thawed. DNA and RNA (polyA) was extracted and sequences were obtained with an illumina HiSeq 2000 sequencer. Results are pending.
Publication Title
RNA-sequencing analysis of core binding factor AML identifies recurrent ZBTB7A mutations and defines RUNX1-CBFA2T3 fusion signature.
Sample Metadata Fields
No sample metadata fields
View Samples SRP056197- Homo sapiens
- 81 Downloadable Samples
- IlluminaHiSeq2000
Description
RNA sequencing of human leukemia Overall design: The goals of this project are to obtain a comprehensive study of mutations and gene expression in human acute myeloid leukemia (AML). Methods: AML cells were thawed. DNA and RNA (polyA) was extracted and sequences were obtained with an illumina HiSeq 2000 sequencer. Results are pending.
Publication Title
RNA-sequencing analysis of core binding factor AML identifies recurrent ZBTB7A mutations and defines RUNX1-CBFA2T3 fusion signature.
Sample Metadata Fields
No sample metadata fields
View Samples