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GSE81245
Mus musculus
24 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
Spinal muscular atrophy (SMA) is a neurodegenerative disease which exhibits selective motor neuron death caused by a ubiquitous deficiency of the survival motor neuron (SMN) protein. It remains unclear how the ubiquitous reduction of SMN lead to death in selective motor neuron pools. Medial motor neuron columns (MMC) are vulnerable, whereas lateral motor columns (LMC) are resistant to motor neuron death in SMA. Here we performed microarray and pathway analysis comparing cholera toxin subunit B (CTb) labeled vulnerable MMC and resistant LMC of pre-symptomatic SMA with corresponding motor neuron columns of control mice to identify pathways involved in selective motor neuron death in SMA. WT is FVB. SMN is Delta7 (SMN7;SMN2;Smn-) on a FVB background.
Publication Title
Converging Mechanisms of p53 Activation Drive Motor Neuron Degeneration in Spinal Muscular Atrophy.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Differential gene expression profiling in PPP2R2A depleted RT-112 cells was performed using Human Genome U133 Plus 2.0 Array
Publication Title
MKAD-21 Suppresses the Oncogenic Activity of the miR-21/PPP2R2A/ERK Molecular Network in Bladder Cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Differential gene expression profiling in KMT2D-depleted MIA PaCa-2 cells was performed using Human Genome U133 Plus 2.0 Array
Publication Title
Lysine methyltransferase 2D regulates pancreatic carcinogenesis through metabolic reprogramming.
Sample Metadata Fields
Treatment
View Samples- Anopheles gambiae
- 16 Downloadable Samples
- Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)
Description
Insect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle. We used microarrays to identify transcripts that are specific or enriched in circulating hemocytes compared to either neuronal or to the rest of the body.
Publication Title
Discovery of Plasmodium modulators by genome-wide analysis of circulating hemocytes in Anopheles gambiae.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Anopheles gambiae
- 6 Downloadable Samples
- Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)
Description
Insect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle.
Publication Title
Discovery of Plasmodium modulators by genome-wide analysis of circulating hemocytes in Anopheles gambiae.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 5 Downloadable Samples
Illumina HiSeq 2000
Description
Usp22, a component of the SAGA complex, is over expressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of Usp22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGFß and several receptor tyrosine kinase (RTK) pathways. Usp22 deletion in endothelial cells and pericytes induced from embryonic stem cells also hinders these signaling cascades with detrimental effects on cell survival and differentiation as well as ability to form vessels. Our findings provide new insights to Usp22 functions during development that may offer clues to its role in disease states. Overall design: To determine changes in gene expression profile upon Usp22 loss in the developing placenta, RNA from day E9.5 placentas from wild-type and Ups22-/- mice s was isolated for deep sequencing, in triplicates and duplicates respectively. Key genes identified from RNAseq were validated by qRT-PCR using RNA from the same samples that were used for sequencing.
Publication Title
USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Many successful vaccines induce persistent antibody responses that can last a lifetime. The mechanisms by which they do so remain unclear, but emerging evidence suggests that activate dendritic cells (DCs) via Toll-like receptors (TLRs). For example, the yellow fever vaccine YF-17D, one of the most successful empiric vaccines ever developed, activates DCs via multiple TLRs to stimulate pro-inflammatory cytokines. Triggering specific combinations of TLRs in DCs can induce synergistic production of cytokines, which results in enhanced T cell responses, but its impact on antibody responses remain unknown. Learning the critical parameters of innate immunity that programs such antibody responses remains a major challenge in vaccinology. We demonstrated that immunization of mice with synthetic nanoparticles containing antigens plus Toll-like receptor (TLR) ligands 4 (MPL) + 7 (R837) induces synergistic increases in antigen-specific, neutralizing antibodies compared to immunization with a single TLR ligand. To determine whether there was any early programming of B cells, we isolated isotype switched, TCRbeta-CD11b-CD19+IgD-IgG+ B cells by FACS at 7 days post immunization with nanoparticles containing various adjuvants plus OVA, and performed microarray analyses to assess their molecular signatures.
Publication Title
Programming the magnitude and persistence of antibody responses with innate immunity.
Sample Metadata Fields
Specimen part, Time
View Samples- Mus musculus
- 21 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of the transcriptome of mouse models of prostate cancer. NP (Nkx3.1CreERT2/+; Ptenfloxed/floxed) mice develop non-metastatic tumors while NPK (Nkx3.1CreERT2/+; Ptenfloxed/floxed; KrasG12D/+) mice develop metastatic tumors
Publication Title
ETV4 promotes metastasis in response to activation of PI3-kinase and Ras signaling in a mouse model of advanced prostate cancer.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We performed mRNA expression profiling of lung tumors from C/L858R, C/T790M, and C/L+T mice and from corresponding normal lung tissue.
Publication Title
Dual targeting of EGFR can overcome a major drug resistance mutation in mouse models of EGFR mutant lung cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Somatic cell nuclear transfer (SCNT) and induced pluripotent stem cells (iPSCs) represent two major approaches for somatic cell reprogramming. However, little attention has been paid to the ability of these two strategies in rejuvenating cells from donors with aging associated syndrome. Here, we utilized telomerase deficient (Terc-/-) mice to probe this question. SCNT-derived embryonic stem cells (ntESCs) and iPSCs were successfully derived from second generation (G2) and third generation (G3) of Terc-/- mice, and ntESCs showed better differentiation potential and self-renewal ability. Telomeres lengthened extensively in cloned embryos while remained or slightly increased in the process of iPSCs induction. Furthermore, G3 ntESCs exhibited improvement of telomere capping function as evidenced by decreased signal free ends and chromosome end-to-end fusion events. In contrast, there was a further decline of telomere capping function in G3 iPSCs. In addition to telomere dysfunction, mitochondria function was severely impaired in G3 iPSCs as evidenced by oxygen consumption rate (OCR) decline, reactive oxygen species (ROS) accumulation and dramatically increased mitochondria genome mutations while these deficiencies were greatly mitigated in G3 ntESCs. Our data proved the principle that SCNT-mediated reprogramming appears more superior than transcription factors induced reprogramming in terms of the resetting of telomere quality and mitochondria function, and thus, providing valuable information for further improvement of transcription factors mediated reprogramming.
Publication Title
Enhanced telomere rejuvenation in pluripotent cells reprogrammed via nuclear transfer relative to induced pluripotent stem cells.
Sample Metadata Fields
Specimen part
View Samples