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Time course and dose response analysis of gene expression in BCR or CD40-stimulated DT40 B cell

ABSTRACT: Gene Expression dynamics is important information. To know IKK- or ERK-dependent B cell receptor- or CD40-induced gene expression dynamics, we performed the time course and dose response analysis in wild type or MEK inhibitor treated or IKKbeta inactive DT40 B cells. Two replicated samples were analysed. Unstimulated cells (T0) were control. WT cells or MEK Inh. (MEK inhibitor;U0126 5mM, 30min pretreated) or IKKbetaSA (S176/181A knock-in) Cells were stimulated with 0.1, 1, 10 Âµg/ml of anti-IgM (M4) or 1, 3, 6 Âµg/ml of CD40ligand (CD40L) for 0, 15, 30, 45, 60 or 90min.

ORGANISM(S): Gallus gallus

SUBMITTER: Hisaaki Shinohara

PROVIDER: E-GEOD-59002 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Time course and dose response analysis of gene expression in BCR or CD40-stimulated DT40 B cell

Project description:Gene Expression dynamics is important information. To know IKK- or ERK-dependent B cell receptor- or CD40-induced gene expression dynamics, we performed the time course and dose response analysis in wild type or MEK inhibitor treated or IKKbeta inactive DT40 B cells.

2014-08-01 | GSE59002 | GEO

Novel genes involved in the pathophysiology of gonadotropin-dependent adrenocortical tumorigenesis in mice.

Project description:The inh-alpha/Tag mouse is a murine adrenocortical tumor model that combines gonadotropin-dependent tumorigenesis with SV40Tag expression (which inhibits p53). These mice have been extensively used to study adrenocortical and gonadal tumorigenesis, as they initially present with gonadal tumors. To induce adrenocortical tumorigenesis, the inh-alpha/Tag mice need to be prebubertally gonadectomized. Generally, females develop adrenal tumors faster and larger in size than males, with a very high individual variations of tumor volume and histological appearance. In this study, we used the inh-alpha/Tag mouse model to analyze the molecular basis of the LH-dependent adrenal tumorigenesis. Experimental inh-alpha/Tag and control littermates (C57Bl/6N) mice of both sexes were used as the animal model. inh-alpha/Tag and WT mice were gonadectomized at 21-24 days of age. Mice were sacrificed at the age of 30 weeks (+/-1 week) and adrenals snap-frozen in liquid nitrogen for microarray analysis. Additionally, a group of 27 week-old inh-alpha/Tag mice (+/-1 week) were treated for 3 weeks with GnRH antagonist cetrorelix acetate (#C5249, Sigma-Aldrich) (3mg/kg/48h). Mice were sacrificed at the age of 30 weeks (+/-1 week) and adrenals snap-frozen in liquid nitrogen for microarray analysis.

2017-02-01 | E-MTAB-5310 | biostudies-arrayexpress

Protein profile at different cellular fractions of Mycobacterium tuberculosis strains after exposure to Isoniazid

Project description:Out of the 10 million of tuberculosis (TB) cases estimated in the world, around 14% are isoniazid (INH) resistant among new cases and 29% among previously treated cases in the last decade. INH is one of the oldest but also one of the more potent drugs to eliminate Mycobacterium tuberculosis (Mtb), the causing agent of TB. Because of the efficiency of isoniazid (INH) against Mycobacterium tuberculosis (Mtb), many studies are still focused in better understand its role in different bacterial metabolic pathways. We recently conducted a study that evaluated the changes in the protein abundance at different cellular fractions when clonal strains of Mtb developed INH resistance in the clinical and laboratory setting. Here, we want to establish which of the protein changes occurred or started because of the initial exposure to INH. Additionally, we wanted to evaluate if those changes happen differently in strains that are sensitive or resistant to INH, evaluating different cellular compartments from two different genetic lineages of Mtb. For this purpose, we analyzed the proteome of each cellular compartment (cytosol, cell wall, membrane and secreted proteins) through liquid chromatography (nano-HPLC) coupled to mass spectrometry using the Orbitrap Velos instrument and a t-test to perform the statistical analysis for each pair comparison.

2019-06-17 | PXD007588 | Pride

Isonicotinylation is Isonicotinylation is a histone mark induced by the anti-tuberculosis first-line drug isoniazida histone mark induced by the anti-tuberculosis first-line drug isoniazid

Project description:Isoniazid (INH) is the first-line anti-tuberculosis drug used for nearly seventy years. Metabolites of INH showed hepatotoxicity in human and tumorigenicity in rodents. However, mechanism underlying the side effects of INH is elusive. Histone acylation is known to be modulated by intracellular metabolites. Here, we report INH and its metabolites induces a novel post-translational modification (PTM) on histones, the lysine isonicotinylation (Kinic), also called 4-picolinylation, in cells and mice. INH functions as a donor to promote biosynthesis of isonicotinyl-CoA that is used for a co-factor of intracellular isonicotinylation reaction. Twenty-six isonicotinylation sites were identified on histones in HepG2 cells by mass spectrometry. Acetyltransferases CREB-binding protein (CBP) and P300 were found to catalyze histone Kinic, whilst histone deacetylase HDAC3 functions as a deisonicotinylase. MNase sensitivity assay and RNA-seq analysis showed that histone Kinic relaxes chromatin structure and promotes gene transcription. Importantly, INH-mediated histone Kinic upregulates PIK3R1 gene expression and activates PI3K/Akt/mTOR signaling pathway in liver cancer cells, linking INH to the tumorigenicity in liver. Further, Kinic was found increased in liver cancer patients with concomitant raised PIK3R1 protein level. In addition, histone Kinic also affects TNF and GABAergic synapse signaling pathways that are closely related to INH-caused side effects. Taken together, we demonstrated that lysine isonicotinylation represents the first histone acylation mark with the pyridine ring that may arise broad biological effects. Therefore, INH-induced isonicotinylation is likely a mechanism accounting for side effects in patients who taking long-term INH for anti-tuberculosis therapy and this modification may also increase cancer risk in human.

2021-08-20 | PXD025490 | Pride

Microarray gene expression profiling of transgenic mice with myocardium-specific expression of RKIP or a GRK-specific peptide inhibitor

Project description:The Raf kinase inhibitor protein (RKIP) is a dual inhibitor of the Raf kinase and the G-protein-coupled receptor kinase 2 (GRK2). GRK2 is an indispensable kinase, which exerts a major role in the pathogenesis of heart failure, and inhibition of GRK2 is cardioprotective in experimental models of heart failure. To investigate the cardiac function of RKIP as GRK2 inhibitor, we generated transgenic mice with myocardium-specific expression of RKIP under control of the alpha-MHC promoter. For comparison, mice with myocardium-specific expression of a GRK-specific peptide inhibitor (GRK-Inh) were also generated. Two different transgenic mouse models were established. Transgenic RKIP mice and transgenic GRK-Inh mice were born at Mendelian frequencey and grew to adulthood normally. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) RKIP-transgenic mice, (ii) GRK-Inh-transgenic mice, and (iii) B6 control mice.

2012-12-06 | E-GEOD-42753 | biostudies-arrayexpress

Expression profiling of extensively drug-resistant tuberculosis isolates and H37Rv exposed to anti-TB compounds

Project description:To explore the mechanism of drug resistance, most works focused on resistance associated genetic mutations, whereas concerns for resistance related gene expression are relatively low. Here a global expression analysis was performed between a reference strain H37Rv and two clinical extensively drug-resistant (XDR) strains with three anti-TB drug exposures {isoniazid (INH), capreomycin (CAP), rifampicin (RIF)} Strains were grown in Middlebrook 7H9 broth supplemented with ADC, 0.05% Tween 80 and 0.2% glycerol to an OD600 of 0.5-0.6, and then respectively treated with control (water), 10×MIC INH, 1×MIC RIF and CAP for 6hr.

2014-01-07 | E-GEOD-53843 | biostudies-arrayexpress

Melanoma NRAS - Cooperative induction of apoptosis in nras mutant melanoma by inhibition of mek and rock

Project description:In the present work we propose a new therapy for NRAS mutant melanoma. Simultaneous inhibition of MEK and ROCK caused induction of BimEL , PARP, and Puma, and hence apoptosis. In vivo, MEK and ROCK inhibition suppressed growth of established tumors. Our findings warrant clinical investigation of the effectiveness of combinatorial targeting of MAPK/ERK and ROCK in NRAS mutant melanoma.

2015-03-11 | PXD000528 | Pride

Transcription profiling of chicken B cell lymphoma (DT40) cell lines.

Project description:Global gene expression profiling of the avian B-lymphoma DT40 cell line was used as a model to differentiate among Btk KO and Btk KO cells reconstituted with human Btk. Differences in the gene expression pattern showed statistically significant changes between parental DT40 and all the Btk KO cell populations irrespective of whether they are reconstituted or not. These results imply that in the process of generating a knockout cell line, subclones are selected, which have multiple changes in their gene expression pattern (p<0.01). Experiment Overall Design: DT40 cells along with the mutants were grown at various time points in different batches of fetal calf serum with or without any stimulation. All experiments were repeated ten times and then polled together as one sample. In total 28 samples were used RNA extraction and hybridization on Affymetrix microarrays.

2008-11-13 | E-GEOD-11597 | biostudies-arrayexpress

Targeting β-catenin overcomes resistance to MEK inhibitor in PIK3CA mutant colon cancer

Project description:Mitogen-activated protein kinases (MEK 1/2) are central components of the RAS signaling pathway and attractive targets for cancer therapy. However, PIK3CA mutation, which commonly co-occurs with KRAS mutation, offered resistance to MEK inhibitor through activation of PI3K-AKT signaling. We identified a gene that cooperates with MEK inhibitors to forcefully treat PIK3CA mutant colon cancer cells. -catenin, a key molecule of the WNT pathway, emerged as a candidate by protein/Ab Chip array. MEK inhibitor treatment led to a decrease in -catenin in PIK3CA wild-type colon cancer cells but not in PIK3CA mutant colon cancer cells. Tumor regression was promoted by a combination of MEK inhibitor and NVP-TNS656, which targets the WNT pathway. Furthermore, combined inhibition of MEK and -catenin by NVP-TNS656 promoted tumor regression in colon cancer patient-derived xenograft (PDX) models expressing mutant PIK3CA. Taken together, we propose that inhibition of the WNT pathway, particularly -catenin, may bypass resistance to MEK inhibitor in human PIK3CA mutant colon cancer. Additionally, -catenin is a potential PD marker of MEK inhibitor resistance. In the study, we identified and evaluated biomarker for response to MEK inhibitor on colon cancer cells.

2015-08-13 | E-GEOD-71981 | biostudies-arrayexpress

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Project description:We report the IFN-induced dynamics in murine splenic B cells. Male C57BL/6 mice were injected subcutaneously with 10,000U IFNa and spleens were removed at 90min. B cells were negatively isolated using magnetic beads and profiled for the chromatin configuration by ATAC-seq. Profilings of chromatin configuration by ATAC-seq (0 and 90min, biological duplicate for each).

2015-11-21 | E-GEOD-75262 | biostudies-arrayexpress

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