Previous studies in our laboratory have shown that low folate diet (control diet with 2mg folate/kg, low folate diet with 0.3mg folate/kg) can induce intestinal tumors in BALB/c mice. In addition, we reported that C57Bl/6J mice did not form tumors under the same conditions.
Differential gene expression and methylation in the retinoid/PPARA pathway and of tumor suppressors may modify intestinal tumorigenesis induced by low folate in mice.
Sex, Specimen part, Treatment
View SamplesWe exposed wild-type Vibrio cholerae E7496, multiple Vibrio cholerae virulence factor deleted genes with intact hemolysin A gene [CVD109] and without hemolysin A gene [CVD110] in E7946, and E.coli OP50 to wild-type C.elegans N2 for 18 hours. We used microarrays to detail the global gene expression and identified distinct classes of up-regulated and down-regulated genes during this process.
Genomic analysis of immune response against Vibrio cholerae hemolysin in Caenorhabditis elegans.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.
Cell line
View SamplesPrevious studies in our laboratory have shown that low folate diet (control diet with 2mg folate/kg, low folate diet with 0.3mg folate/kg) can induce intestinal tumors in BALB/c mice.
Genes with aberrant expression in murine preneoplastic intestine show epigenetic and expression changes in normal mucosa of colon cancer patients.
Sex, Specimen part, Treatment
View SamplesER17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ER) and initially synthesized to mimic its calmodulin binding site. ER17p was subsequently found to elicit estrogenic responses in E2-deprived ER-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ER17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ER17p induces a massive early (3h) transcriptional activity in breast cancer cell lines SKBR3). Remarkably, about 75% of the significantly modified transcripts were also modified by E2, confirming the pro-estrogenic profile of ER17p. The different ER spectra of the used cell lines allowed us to extract a specific ER17p signature related to ER and its variant ER36. With respect to ER, the peptide activates nuclear (cell cycle, cell proliferation, nucleic acid and protein synthesis) and extranuclear signaling pathways. In contrast, through ER36 it exerts inhibitory events on inflammation and cell cycle and inhibition of EGFR signaling. This is the first work reporting ER36 specific transcriptional effects. The fact that a number ER17p-induced transcripts is different from those activated by E2 revealed that the apoptosis and actin modifying effects of ER17p are independent from the ER-related actions of the peptide.
Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.
Cell line
View SamplesER17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ER) and initially synthesized to mimic its calmodulin binding site. ER17p was subsequently found to elicit estrogenic responses in E2-deprived ER-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ER17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ER17p induces a massive early (3h) transcriptional activity in breast cancer cell line MDA-MB-231.
Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.
Cell line
View SamplesER17p is a synthetic peptide corresponding to the sequence P295LMIKRSKKNSLALSLT311 of the estrogen receptor alpha (ER) and initially synthesized to mimic its calmodulin binding site. ER17p was subsequently found to elicit estrogenic responses in E2-deprived ER-positive breast cancer cells, increasing proliferation and E2-dependent gene transcription. Surprisingly, in E2-supplemented media, ER17p induced apoptosis and modified the actin network, influencing thereby cell motility. Here, we report that ER17p induces a massive early (3h) transcriptional activity in breast cancer cell line T47D.
Whole transcriptome analysis of the ERα synthetic fragment P295-T311 (ERα17p) identifies specific ERα-isoform (ERα, ERα36)-dependent and -independent actions in breast cancer cells.
Cell line
View SamplesTha altered biological pathways in Epidermolysis bulloda simplex, a rare monogenetic skin disease, have not been well characterized. Thus, the goal of this study is to characterize the expression profile of EBS patients compared with normal subjects using genomic expression analyses. Microarray analyses were performed with RNA isolated from skin biopsies. Robust multiarray analysis (RMA) normalization and Smyths moderated t test were used to select differentially expressed genes. Expression profiling comparisons show that 28 genes are differentially expressed in EBS patients compared to control subjects and 41 genes in EBS-DM compared to their matched controls. Nine genes involved in fatty acid metabolism and 2 genes in epidermal keratinisation are common altered expressed genes between the two subgroups. These two biological pathways contribute both to the formation of the cell envelope barrier and seem to be defective in the severe EBS phenotype. This study demonstrates, for the first time, the relevance of metabolic cluster, specifically fatty acid metabolism in EBS biology. Difference of expression for three (AWAT2, ELOVL , and SPRR4 ) of the five selected genes were validated using real-time reverse transcriptionpolymerase chain reaction. To our knowledge, the distinctive pattern of gene expression that characterizes EBS versus healthy skin tissue has never been reported.
Expression signature of epidermolysis bullosa simplex.
Specimen part, Disease, Disease stage
View SamplesWe report a transcriptional response in human OECs that encompasses multiple innate immune networks not previously associated with these cells. Major pathways included immune cell trafficking, and differential cytokine production Overall design: We used RNA-based sequencing technology for high-throughput profiling of innate immune responses in human OECs and the role of Burkholderia in triggering these responses
Burkholderia pseudomallei Capsule Exacerbates Respiratory Melioidosis but Does Not Afford Protection against Antimicrobial Signaling or Bacterial Killing in Human Olfactory Ensheathing Cells.
No sample metadata fields
View SamplesRNA sequencing of human dermal fibroblasts from CAID patients passage 8 and passage 14 Overall design: RNA sequencing was perfomed on 3 wild type controls and 3 CAID patients fibroblast cell lines at cell passages 8 and 14. Sequencing was performed on Illumina Hiseq4000, 8 samples/lanes, paired-end.
Molecular Signature of CAID Syndrome: Noncanonical Roles of SGO1 in Regulation of TGF-β Signaling and Epigenomics.
Specimen part, Subject
View Samples