Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling by array of chicken wild type and tumor supressor 53Bp1 knockout lymphoblast cells

ABSTRACT: Effect of abrogation of the tumour supressor 53Bp1 on gene expression in the chicken DT40 model system

ORGANISM(S): Gallus gallus

SUBMITTER: Noel Lowndes

PROVIDER: E-MEXP-2721 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling by array of chicken wild type and tumor supressor Dot1L knockout lymphoblast cells

Project description:Effect of abrogation of the histone methyltransferase Dot1L on gene expression in the chicken DT40 model system

2011-05-07 | E-MEXP-2722 | biostudies-arrayexpress

Gene expression profiling in proximal versus distal mouse colon

Project description:Analysis of gene expression in proximal versus distal part of the mouse large intestine. Three (3) animals (biological replicates) were used to isolate tissue from proximal and distal areas of the large intestine.

2015-01-01 | E-GEOD-64423 | biostudies-arrayexpress

Expression data from exposure of BAT and WAT at 6 and 28 degrees C

Project description:We run microarrays from three per group Sv129 female mice, ten weeks old, which were maintained at 28M-BM-0C (warm conditions) or 6M-BM-0 C (cold stimulated) for ten days, while standard animal house temperature is 22 M-BM-0C. After ten days, three types of tissue were collected: Brown Adipose Tissue (BAT), Mesenteric (visceral) White Adipose Tissue (MES) and Posterior Subcutaneous White Adipose Tissue (WAT) Different adipose tissue depots were taken for RNA extraction and hybridization on Affymetrix microarrays. We sought to determine the differences between white and brown adipose tissues at different temperatures

2014-03-01 | E-GEOD-51080 | biostudies-arrayexpress

Transcription profiling of chicken Bcl6 deficient DT40 B cell line to investigate the targets of Bcl6 which is required for germinal center formation

Project description:The transcription factor Bcl6 is required for germinal center formation and deregulated expression of Bcl6 has been observed in lymphomas. To gain insight to the function of Bcl6 in terminal differentiation of B cells to plasma cells and to investigate the targets of Bcl6, we established a Bcl6 deficient DT40 B cell line.

2010-02-17 | E-MEXP-2062 | biostudies-arrayexpress

FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance.

Project description:Glucocorticoid excess is linked to central obesity, adipose tissue insulin resistance and type 2 diabetes mellitus. The aim of our study was to investigate the effects of dexamethasone on gene expression in human subcutaneous and omental adipose tissue, in order to identify potential novel mechanisms and biomarkers for glucocorticoid-induced insulin resistance in adipose tissue. Dexamethasone changed the expression of 527 genes in both subcutaneous and omental adipose tissue. FKBP5 and CNR1 were the most responsive genes in both depots (~7-fold increase). Dexamethasone increased FKBP5 gene and protein expression in a dose-dependent manner in both depots, but FKBP5 protein levels were 10-fold higher in omental than subcutaneous adipose tissue. FKBP5 gene expression in subcutaneous adipose tissue was positively correlated with serum insulin, HOMA-IR and subcutaneous adipocyte diameter, while fold change in gene expression by dexamethasone was negatively correlated with clinical markers of insulin resistance, i.e. HbA1c, BMI, HOMA-IR and serum insulin. Only one gene, SERTM1, clearly differed in response to dexamethasone between the two depots. Dexamethasone at high concentrations, influences gene expression in both subcutaneous and omental adipose tissue in a similar pattern and promotes gene expression of FKBP5, a gene that may be implicated in glucocorticoid-induced insulin resistance. Paired human subcutaneous (sc) and omental (om) adipose tissue samples obtained from 4 non-diabetic adipose tissue donors (4 M; BMI: 20.8-27.5 Kg/m2) were incubated without (Ctr) or with dexamethasone (Dex, 3 M-NM-<M) for 24 h.

2014-08-18 | E-GEOD-42902 | biostudies-arrayexpress

Expression profiling of lesional and non-lesional bulge cells from Lichen planopilaris patients

Project description:Lichen planopilaris (LPP) is a chronic inflammatory disease of unknown pathogenesis that leads to permanent hair loss. Whilst destruction of epithelial hair follicle stem cells (eHFSCs) that reside in an immunologically protected niche of the HF epithelium, the bulge, is a likely key event in LPP pathogenesis, this remains to be demonstrated. Laser capture microdissection of bulge cells from biopsies of lesional and non-lesional scalp skin from adult LPP patients were analyzed by microarray analysis.

2013-07-04 | E-MEXP-3859 | biostudies-arrayexpress

SRC1 gene regulation in endocrine resistant breast cancer cells

Project description:The development of breast cancer resistance to endocrine therapy results from an increase in cellular plasticity leading to the development of a steroid independent tumour. The p160 steroid coactivator protein SRC-1, through interactions with developmental proteins and other non-steroidal transcription factors drives this tumour adaptability. Here, using discovery studies we identify ADAM22, a non-protease member of the ADAMs family, as a direct target of SRC-1, independent of estrogen receptor(ER). Molecular, cellular, in vivo and clinical studies confirmed SRC-1 as a regulator of ADAM22 and established a role for ADAM22 in endocrine resistant tumour progression. ADAM22 has the potential to act as a therapeutic drug target and a companion predictive biomarker in the treatment of endocrine resistant breast cancer. 14 samples representing 4 conditions were analysed. Samples were transfected with either a siRNA targetting SRC1 or a control scrambled siRNA. Samples were subject to tamoxifen treatment or untreated.

2012-01-11 | E-GEOD-28645 | biostudies-arrayexpress

The TAB1-p38α complex aggravates myocardial injury and can be targeted by small molecules

Project description:There is considerable evidence that inhibition of p38α mitogen-activated protein kinase diminishes cardiac damage during myocardial ischemia. During myocardial ischemia p38α interacts with TAB1, a scaffold protein, which promotes p38α autoactivation; active p38α (pp38α) then trans-phosphorylates TAB1. Previously, we solved the X-ray structure of the p38α-TAB1(384-412) complex. Here we further characterize the interaction by resolving the structure of the pp38α-TAB1(1-438) complex in the active state. Based on this information we created a global knock-in mouse with substitution of four residues on TAB1 (V390A, Y392A, V408G, M409A) we show are required for docking onto p38α. Whereas ablating p38α or TAB1 results in early embryonal lethality, the TAB1 KI mice are viable, develop normally and have no appreciable alteration in their lymphocyte repertoire or myocardial transcriptional profile. Nonetheless, following in vivo regional myocardial ischemia, infarction volume is significantly reduced and the trans- phosphorylation of TAB1 is disabled. Unexpectedly, the activation of myocardial p38α during ischemia is only mildly attenuated in TAB1 KI hearts, an effect most likely due to the removal of the steric hindrance to MAP2K3 binding. We conclude that it is the phosphorylation of TAB1 by pp38α during ischemia that is associated with cardiac damage. The data reveal that it is possible to selectively inhibit signalling downstream of p38α to attenuate ischemic injury. Our findings validate the p38α-TAB1 complex as a therapeutic target that may circumvent the toxicity associated with ATP-competitive inhibitors of p38α.

2018-08-27 | E-MTAB-6460 | biostudies-arrayexpress

Adaptive evolution of Corynebacterium glutamicum resistant to oxidative stress and its global gene expression profiling

Project description:Corynebacterium glutamicum was adapted in a chemostat for 1,900 h with gradually increasing H2O2 stress to understand the oxidative stress response of an industrial host. After 411 generations of adaptation, C. glutamicum developed the ability to grow under stress of 10 mM H2O2, whereas the wild-type did not. The adapted strain also showed increased stress resistance to diamide and menadione, SDS, Tween 20, HCl, NaOH, and ampicillin. A total of 1,180 genes in the RNA-seq transcriptome analysis of the adapted strain were up-regulated twice or higher (corresponding to 38.6 % of the genome), and 126 genes were down-regulated half or less (4.1 % of genome) under 10 mM H2O2-stress conditions compared with those of the wild-type under a no stress condition. Especially the aromatic compound-degrading gene clusters (vanRABK, pcaJIRFLO, and benABCDRKE) were more than threefold up-regulated. Plausible reasons for the H2O2-stress tolerance of the adapted strain are discussed as well as the potential strategy for development of oxidative stress-tolerant strain. Comparison of global gene expression profiling using RNA-seq data of wild-type strain under normal condition (WT_MCGC) vs. 10 mM H2O2-adapted strain under oxidative stress condition Global gene expression profiling_WT vs. H2O2 adapted C. glutamicum strains

2013-01-06 | E-GEOD-41232 | biostudies-arrayexpress

Transcription profiling by array of mouse wild type or srx knockouts after lipopolysaccharide-induced endotoxic shock

Project description:Role of sulfiredoxin in the tolerance to lipopolysaccharide-induced endotoxic shock

2011-01-01 | E-MEXP-2856 | biostudies-arrayexpress