Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA187374 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We discovered a new tissue specific enhancer originated from the human spesific endogenous retrovirus (hsERV). This enhancer displayed its activity in hippocampus and Tera-1 cell line as opposed to HepG2, A549, NT2/D1 and NGP127 cells. The aim of this study was to find transcription factors responsible for the hsERV enhancer activity. So we attempted to identify a fraction of transcription factor genes that were upregulated in enhancer-positive cells. Total RNA obtained from human hippocampus and Tera-1, HepG2, A549, NT2/D1 and NGP127 cell lines.
2013-01-26 | E-GEOD-43773 | biostudies-arrayexpress
Project description:We discovered a new tissue specific enhancer originated from the human spesific endogenous retrovirus (hsERV). This enhancer displayed its activity in hippocampus and Tera-1 cell line as opposed to HepG2, A549, NT2/D1 and NGP127 cells. The aim of this study was to find transcription factors responsible for the hsERV enhancer activity. So we attempted to identify a fraction of transcription factor genes that were upregulated in enhancer-positive cells.
2013-01-26 | GSE43773 | GEO
Project description:The accurate choice of anti-cancer drugs is important problem of modern medicine. We developed a new method for the selection of targeted drugs based on detection of specific intracellular signaling and metabolic pathways in the bioinformatic system termed OncoFinder before the treatment. We obtained transcriptomic data 12 human cancer cell lines (NT2/D1, Tera-1, NGP, HepG2, BT474, Skov-3, T3M4, HeLa, A549, MCF-7, Jurkat, BxPc1) before a treatment. In our research for gene expression quantile normalization of the experimental data of all 12 cell lines together, we used separately eleven gene expression datasets corresponding to different normal human tissues profiled on Illumina HT-12v3-4 platform, 4-33 samples per dataset (from GEO). Normalization datasets used for the processing of the experimental transcriptomic data: GSE17822 (GSM444688, GSM444689, GSM444690, GSM444691, GSM444692, GSM444693), GSE26852 (GSM661123, GSM661124, GSM661125, GSM661126, GSM661127, GSM661128, GSM661130), GSE32124 (GSM796359, GSM796360, GSM796361, GSM796362, GSM796363, GSM796364, GSM796365, GSM796366, GSM796367, GSM796368, GSM796369, GSM796370, GSM796371, GSM796372, GSM796373, GSM796374, GSM796375, GSM796376, GSM796377, GSM796378, GSM796379, GSM796380, GSM796381, GSM796382, GSM796383, GSM796384, GSM796385, GSM796386, GSM796387, GSM796388, GSM796389, GSM796390, GSM796391), GSE34074 (GSM841415, GSM841419, GSM841423, GSM841427, GSM841431, GSM841435), GSE37013 (GSM908514, GSM908515, GSM908516, GSM908517, GSM908518, GSM908519, GSM908520), GSE40645 (GSM998797, GSM998798, GSM998799, GSM998800, GSM998801, GSM998802, GSM998803, GSM998804, GSM998805, GSM998806, GSM998807, GSM998808, GSM998809, GSM998810), GSE42656 (GSM1047460, GSM1047462, GSM1047463, GSM1047467), GSE52130 (GSM1260102, GSM1260103, GSM1260104, GSM1260105, GSM1260106, GSM1260107, GSM1260108), GSE54563 (GSM1318920, GSM1318921, GSM1318922, GSM1318923, GSM1318924, GSM1318925, GSM1318926, GSM1318927, GSM1318928, GSM1318929, GSM1318930, GSM1318931, GSM1318932, GSM1318933, GSM1318934, GSM1318935, GSM1318936, GSM1318937, GSM1318938, GSM1318939, GSM1318940, GSM1318941, GSM1318945, GSM1318946, GSM1318947), GSE57218 (GSM1380887, GSM1380888, GSM1380956, GSM1380957, GSM1380958, GSM1380959), GSE60709 (GSM1486145, GSM1486146, GSM1486160, GSM1486161, GSM1486162, GSM1486163, GSM1486164, GSM1486165, GSM1486166, GSM1486167, GSM1486168, GSM1486169, GSM1486170, GSM1486171, GSM1486172, GSM1486173). Normalization of the 12 new cell line data was performed independently 11 times together with the data from the GSM ID numbers listed above. For GSM1486145, data for replicate samples 34 and 35 were used. For sample GSM1486146, data for replicate sample 36 was used. Total RNA obtained from NT2/D1, Tera-1, NGP, HepG2, BT474, Skov-3, T3M4, HeLa, A549, MCF-7, Jurkat, BxPc1 cell lines.
2015-01-27 | E-GEOD-65314 | biostudies-arrayexpress
Project description:To identify novel downstream target genes of SOX9, transcriptome analysis of SOX9 transfected human embryonic testicular cell line, NT2/D1, was carried out.
2015-04-30 | E-MTAB-3378 | biostudies-arrayexpress
Project description:Whole transcriptome for PRMT6 knock-out and control NT2/D1 cells with and without ATRA (all-trans retinoic acid) was sequenced. These samples were compared to each other to find differentially regulated genes and PRMT6-dependent transcriptome in pluripotency and differentiating cells.
2018-09-27 | GSE107611 | GEO
Project description:To investigate the role of the testicular germ cell tumor cells in complex traits, we generated ATAC-seq and Promoter Focused Capture C to gain insight into the gene regulatory arcitecture contacting promoters in an testicular cell line NT2-D1 model of testicular cancer
2021-06-01 | GSE175367 | GEO
Project description:To investigate the role of the testicular germ cell tumor cells in complex traits, we generated ATAC-seq and Promoter Focused Capture C to gain insight into the gene regulatory arcitecture contacting promoters in an ttesticular cell line NT2-D1 model of testicular cancer
2021-06-01 | GSE175366 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE16858: Human NTERA2 (NT2/D1) cells lines: shZRF1 vs. shRandom during Retinoic Acid (RA) administration GSE16878: Human NTERA2 (NT2/D1) cells lines: Genomewide distribution of ZRF1 at gene promoters during RA administration Refer to individual Series
2010-12-24 | E-GEOD-16891 | biostudies-arrayexpress
Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Total RNA obtained from NT2/D1-R1 sh control or NT2/D1-R1 sh DNMT3B knockdown cells treated with vehicle or 10 nM 5-aza deoxycytidine for 3 days. Four groups in biological triplicate for total of 12 hybridizations on Illumina HT-12v3 beadarray.
2012-12-01 | E-GEOD-42644 | biostudies-arrayexpress
Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Genomic DNA obtained from NT2/D1-R1 sh control or NT2/D1-R1 sh DNMT3B knockdown cells treated with vehicle or 10 nM 5-aza deoxycytidine for 3 days. Four groups in biological triplicate for total of 12 hybridizations on Illumina HumanMethylation27 BeadChip.
2012-12-01 | E-GEOD-42646 | biostudies-arrayexpress