Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways [BY4741]

ABSTRACT: The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE70168 | GEO | 2015/06/24

SECONDARY ACCESSION(S): PRJNA287786

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways [BY4741]

Project description:The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5. Comparison of 2 transfected yeast cell populations in 2 different growth phases. In total, 4 comparisons were made, each comparison was done in duplo by a colourflip. Every conditions is represented through 2 biol reps.

2015-06-24 | E-GEOD-70168 | biostudies-arrayexpress

The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways [HEK293T]

2015-06-24 | GSE70167 | GEO

The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways [HEK293T]

Project description:The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5. Comparison of two HEK293T transfected cell populations, either with a WT or mutated DFNA5 gene. There are 5 biol reps for the WT transfected cells and 6 biol reps for the mut DFNA5 transfected cells.

2015-06-24 | E-GEOD-70167 | biostudies-arrayexpress

JMJD2A ChIP-chip from HEK293T cells

Project description:JMJD2A was chromatin immunoprecipitated from HEK293T cells overexpressing GFP-JMJD2A. From Van Rechem et al. 2011 JBC

2013-08-01 | GSE48765 | GEO

JMJD2A ChIP-chip from HEK293T cells

Project description:JMJD2A was chromatin immunoprecipitated from HEK293T cells overexpressing GFP-JMJD2A. From Van Rechem et al. 2011 JBC Determination of JMJD2A binding sites by MA2C analysis

2013-08-01 | E-GEOD-48765 | biostudies-arrayexpress

Role of the mRNA-binding protein HuR in the global transcriptomic status of cells stimulated with electrophiles and oxidants

Project description:HuR has been implicated as a stress-responsive protein: cytoplasmic translocation of HuR is promoted by several small-molecule stressors, e.g., H2O2, arsenite, and the cyclopentenone prostaglandin A2 (PGA2), a Michael acceptor RES (Wang et al., 2000; Yang et al., 2004). Treatment with PGA2 also increases the affinity of HuR for p21 mRNA (Wang et al., 2000). Intrigued by these reports, we launched HuR-dependent gene-expression profiling studies in the presence and absence of small-molecule stress signals. HNE—a native RES with a reactive core chemically similar to that of PGA2—was selected as a representative bioactive RES (Jacobs and Marnett, 2009; Schopfer et al., 2011) and H2O2 was selected as a representative ROS. shHuR and shControl HEK293T cells were first generated and then treated with HNE or H2O2 under the conditions where cell viability is largely unaffected. We subsequently sequenced their RNA post ribosomal RNA (rRNA) depletion (see details below). Significant differential expression was evaluated with CuffDiff (Trapnell et al., 2013).

2020-02-10 | GSE127444 | GEO

Strand-oriented RNAseq of LNCaP prostate cancer cells in culture for 24h in the presence of androgen

Project description:The aim of this study was to use NGS RNAseq deep-sequencing in order to characterize the polyadenylated mRNAs and lncRNAs expressed in LNCaP cells treated with androgen hormone compared with untreated LNCaP cells (GSE79301). Trimmed reads were mapped using the hg19 genome with TopHat v.2.0.12 and Bowtie v.2.2.3. The assembly was guided by a custom GTF file created with transcripts fromhuman lncRNA annotations from GENCODE v19 (Harrow, Frankish et al.2012) and those already annotated as lincRNAs in (Cabili, Trapnell et al. 2011; Prensner, Iyer et al. 2011; Hangauer, Vaughn et al. 2013). The diferencial expression was calculated by the sum of exon read count per gene with HTSeq (Anders, Pyl et al. 2015), followed by a DESeq2 analysis (Love, Huber et al. 2014).

2017-12-31 | GSE102305 | GEO

Batrachochytrium dendrobatidis

Project description:DNAseq of Batrachochytrium dendrobatidis (Farrer et al PNAS 2011)

| PRJNA222638 | ENA

A time-course profiling of the effects of maslinic acid on mRNA expression of chemically induced Raji cells.

Project description:Maslinic acid is a novel phytochemical reported to exert prominent anti-cancer effects and it was hypothesized that this compound induces cellular apoptosis through the activation of the mitochondrial apoptotic pathway (Martin et al, 2007) — thereby resulting in significant inhibition of cell proliferation in a dose-dependent manner (Reyes-Zurita et al, 2009). Prior studies on maslinic acid in its function as a time-dependent inhibitor in both tumorigenesis and inflammation events by targeting multiple signaling pathways; particularly the NF-ĸB, MAPK (Li et al, 2010; Yap, et al, 2011) and JNK (Reyes-Zurita et al, 2011) pathways were mostly based on proteomic analyses (Li et al, 2010; Yap et. al., 2011). However, these results may not depict an accurate scenario of the signaling networks involved due to protein degradation, alternate splicing and extensive post-translational processing. Hence, this study aimed to construct a temporal-based global gene expression profile of the effects of maslinic acid by using the microarray technology. The aim of this project is to construct the complete global mRNA profile of the effects of maslinic acid in inhibiting early-antigen formation in Raji cells.

2018-05-02 | GSE39149 | GEO

SeaIce, Espegrend, Microscosm, Mnemi

Project description:454 dataset for Hosia, et al. Torstensson et al. Dinasquet et al.

| PRJEB7907 | ENA