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E-MEXP-2144
Arabidopsis thaliana
6 Downloadable Samples
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Systemic transcriptional responses in Arabidopsis thaliana distal leaves to wounding
Publication Title
The plant NADPH oxidase RBOHD mediates rapid systemic signaling in response to diverse stimuli.
Sample Metadata Fields
Age, Specimen part
View Samples- Arabidopsis thaliana
- 18 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Analysis of the genome wide response of wild type and two mutant arabidopsis thaliana seedlings to norflurazon
Publication Title
Signals from chloroplasts converge to regulate nuclear gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Illumina HiSeq 2500
Description
To study the role Cnot3 in early B cells development, RNASeq analysis of pro-B cells (B220+ and CD43+) was performed in tamoxifen treated Cnot3(fl/fl) RERTCre and Cnot3+/+;RERTCre mice. Overall design: Two individual replicates of Cnot3(fl/fl) RERTCre and Cnot3(+/+) RERTCre mice were tamoxifen treated periodically. Ten days after the initial treatment, B220+CD43+ pro-B cells were sorted from the bone marrow and RNASeq analysis was performed.
Publication Title
Interaction of CCR4-NOT with EBF1 regulates gene-specific transcription and mRNA stability in B lymphopoiesis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Physiologically, Notch signal transduction plays a pivotal role in differentiation; pathologically, Notch signaling contributes to the development of cancer. Transcriptional activation of Notch target genes involves cleavage of the Notch receptor in response to ligand binding, production of the Notch intracellular domain (NICD), and NICD migration into the nucleus and assembly of a coactivator complex. Posttranslational modifications of the NICD are important for its transcriptional activity and protein turnover. Deregulation of Notch signaling and stabilizing mutations of Notch1 have been linked to leukemia development. We found that the methyltransferase CARM1 (coactivator-associated arginine methyltransferase 1; also known as PRMT4) methylated NICD at five conserved arginine residues within the C-terminal transactivation domain. CARM1 physically and functionally interacted with the NICD-coactivator complex and was found at gene enhancers in a Notch-dependent manner. Although a methylation-defective NICD mutant was biochemically more stable, this mutant was biologically less active as measured with Notch assays in embryos of Xenopus laevis and Danio rerio. Mathematical modeling indicated that full but short and transient Notch signaling required methylation of NICD.
Publication Title
Site-specific methylation of Notch1 controls the amplitude and duration of the Notch1 response.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
The NEET proteins mitoNEET (mNT) and nutrient-deprivation autophagy factor-1 (NAF-1) are required for cancer cell proliferation and resistance to oxidative stress. MitoNEET and NAF-1 are also implicated in a number of other human pathologies including diabetes, neurodegeneration and heart disease, as well as in development, differentiation and aging. Previous studies suggested that mNT and NAF-1 could function in the same pathway in cancer cells, preventing the over-accumulation of iron and reactive oxygen species (ROS) in mitochondria. Nevertheless, it is unknown whether these two proteins interact in cells, and how they mediate their function. Here we demonstrate, using yeast two-hybrid, in vivo bimolecular fluorescence complementation (BiFC), direct coupling analysis (DCA), RNA- sequencing, ROS and iron imaging, and single and double shRNA lines with suppressed mNT, NAF-1 and mNT/NAF-1 expression, that mNT and NAF-1 interact in cancer cells and function in the same cellular pathway. We further show using an in vitro cluster transfer assay that mNT can transfer its clusters to NAF-1. Our study suggests that mNT and NAF-1 could function as part of an iron-sulfur (2Fe-2S) cluster relay to maintain the levels of iron and Fe-S clusters under control in the mitochondria of cancer cells, thereby preventing the activation of apoptosis and/or autophagy and thus promoting rapid cellular proliferation. Overall design: Examination of the effect of suppression of mNT in the breast cancer cell line MCF-7. Two sample types were analyzed, MCF-7 suppressed for mNT and MCF-7 Empty vector control, three replicates for each.
Publication Title
Interactions between mitoNEET and NAF-1 in cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- IlluminaHiSeq2000
Description
Nutrient autophagy factor 1 (NAF-1) is an iron-sulfur protein found on the outer mitochondrial membrane and the ER. Recent studies highlighted an important role for NAF-1 in regulating autophagy via interaction with BCL-2. We recently reported that the level of NAF-1 is elevated in cancer cells and that NAF-1 is required for tumor growth. Here we report that shRNA suppression of NAF-1 results in the activation of apoptosis in xenograft tumors and cancer cells grown in culture. Suppression of NAF-1 resulted in a depletion in the cytosolic iron pool, facilitated uptake of iron, and accumulation of iron and ROS in mitochondria, a shift to glycolysis and glutaminolysis, and the activation of cellular stress pathways associated with HIF1a, AMPK and mTOR. Suppression of NAF-1 in breast cancer cells appears therefore to reduce their tumorigenicity by interfering with cellular iron distribution and energy metabolism resulting in the activation of apoptosis. Overall design: Examination of the effect of suppression of NAF-1 in the breast cancer cell line MCF-7. Two sample types were analyzed, MCF-7 suppressed for NAF-1 and MCF-7 Empty vector control, three replicates for each.
Publication Title
Activation of apoptosis in NAF-1-deficient human epithelial breast cancer cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
We report application of RNA-seq to quantify gene expression changes in fasted mouse livers compared to re-fed controls. Overall design: RNA-seq from livers of re-fed and 48h fasted mice.
Publication Title
Histone propionylation is a mark of active chromatin.
Sample Metadata Fields
Sex, Specimen part, Treatment, Subject
View Samples- Mus musculus
- 30 Downloadable Samples
- Illumina HiSeq 3000
Description
Metabolic engagement is intrinsic to immune cell function. Prostaglandin E2 (PGE2) has been shown to modulate macrophage activation, yet how PGE2 might affect metabolism is unclear. Here we show that PGE2 causes mitochondrial membrane potential (??m) to dissipate in interleukin-4 activated macrophages (M(IL-4)). Effects on ??m are a consequence of PGE2-initiated transcriptional regulation of genes in the malate-aspartate shuttle (MAS), particularly GOT1. Reduced ??m causes alterations in the expression of 126 voltage regulated genes (VRGs) including Resistin like molecule-a (RELMa), a key marker of M(IL-4), and genes that regulate cell cycle. The transcription factor ETS variant 1 (ETV1) plays a role in the regulation of 38% of the VRGs. These results reveal ETV1 as a ??m-sensitive transcription factor, and ??m as a mediator of mitochondrial-directed nuclear gene expression. Overall design: RNA-seq was performed on bone marrow derived macrophages (triplicate) exposed to IL-4 alone or in combination with PGE2 or Valinomycin plus no stimulation controls. In addition, RNA-seq was performed on bone marrow derived macrophages stimulated in the same way as before, however the transcription factor ETV1 was knocked down.
Publication Title
Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to Prostaglandin E2.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This study presents transcription profiles for mouse axial progenitors, presomitic mesoderm and tailbud mesoderm. During vertebrate embryonic development, the formation of axial structures is driven by a population of stem-like cells (axial progenitors) that reside in a region of the tailbud called the chordoneural hinge (CNH) where. We have compared the CNH transcriptome with those of surrounding tissues and shown that the CNH and tailbud mesoderm are transcriptionally similar, and distinct from the presomitic mesoderm. Amongst CNH-enriched genes are several that are required for axial elongation, including Wnt3a, Cdx2, Brachyury/T and Fgf8, and androgen/estrogen receptor nuclear signalling components such as Greb1.
Publication Title
<i>Greb1</i> is required for axial elongation and segmentation in vertebrate embryos.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
X-linked inhibitor of apoptosis (XIAP) is the most potent endogenous caspase inhibitor preventing cell death via caspase-9, -7 and -3 (initiator and executioner caspase pathways). Using short hairpin RNA (shRNA) against XIAP, stably expressed in a parent HCT116 human colon cancer cell line, a series of clones have been developed. XIAP mRNA levels were established by RT-PCR, the four X (XIAP knockdown) clonal cell lines show 82-93% reduction in XIAP mRNA when compared to the four L (luciferase control) cell lines. Immunoblot analysis showed a 67-89% reduction in XIAP protein in X cell lines compared to L. RNA was analysed by microarray and XIAP knockdown was confirmed in 7 probe sets, there was no significant compensation of other IAP family members. XIAP knockdown induced a 2-fold increase in the basal level of apoptosis without modification of caspase 3/7 activity. Finally, XIAP knockdown sensitises cells to radiotherapy by 20%, to recombinant TRAIL by a 3-fold factor, and to paclitaxel and docetaxel by >2 fold factor. Future work should focus on targeted agents such as rhTRAIL in combination with strategies to down regulate XIAP. XIAP antisense is now in clinical development in oncology.
Publication Title
Stable XIAP knockdown clones of HCT116 colon cancer cells are more sensitive to TRAIL, taxanes and irradiation in vitro.
Sample Metadata Fields
No sample metadata fields
View Samples