Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

7 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Set1, H3K4A, set1htz1, set1htz1sir2 transcription profiles

ABSTRACT: Relative mRNA abundance of all S. cerevisiae genes was measured in various mutants, compared to wild-type mutant and wild-type grown to log phase, YPAD, 30C, purified mRNA, reverse-transcribed to cDNA, labelled with Cy5/Cy3, hybridized to whole genome ORF microarrays

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Shivkumar Venkatasubrahmanyam

PROVIDER: E-GEOD-4826 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Genome-wide, as opposed to local, antisilencing is mediated redundantly by the euchromatic factors Set1 and H2A.Z.

Venkatasubrahmanyam Shivkumar S Hwang William W WW Meneghini Marc D MD Tong Amy Hin Yan AH Madhani Hiten D HD

Proceedings of the National Academy of Sciences of the United States of America 20071009 42

In Saccharomyces cerevisiae, several nonessential mechanisms including histone variant H2A.Z deposition and transcription-associated histone H3 methylation antagonize the local spread of Sir-dependent silent chromatin into adjacent euchromatic regions. However, it is unclear how and where these factors cooperate. To probe this question, we performed systematic genetic array screens for gene deletions that cause a synthetic growth defect in an htz1Delta mutant but not in an htz1Delta sir3Delta do ...[more]

PMID: 17925448

Similar Datasets

bre1 vs WT transcriptional profile

Project description:Relative mRNA abundance of all S. cerevisiae genes was measured in bre1 compared to wild-type. Arrays done in quadruplicate with dye-swaps.

2010-06-19 | E-GEOD-13701 | biostudies-arrayexpress

RNA co-immunoprecipitations with yeast She proteins

Project description:RNA co-immunoprecipitations with C-terminal protein A-tagged She proteins. One liter of cells were cultured at 30 degrees in YPAD medium and collected during exponential growth by centrifugation. Cells were washed twice and broken mechanically with glass beads. Extracts were incubated with IgG-agarose beads (Sigma). The beads were washed four times, and She proteins were released from the beads by cleavage with TEV-protease (Invitrogen). RNA was isolated by phenol/chloroform extraction and isopropanol precipitation from TEV eluates, which corresponds to the purified fraction, and from extracts (input). Both RNA samples, input and purified, were reverse transcribed and labeled with the fluorescent dyes Cy3 and Cy5 (Amersham), respectively. The samples were mixed and competitively hybridized to yeast DNA microarrays containing all yeast genes Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed

2005-12-20 | E-GEOD-3879 | biostudies-arrayexpress

Gene expression profile of abf1-1 mutant at 36 degrees C

Project description:The abf1-1 mutant and wild type cells were grown at 30 degrees C in YPAD until OD600 reached 1.0-1.2. The same volume of 42 degrees C preheated YPAD was added for each flask. After 45 min incubation at 36 degrees C, cells were harvested and RNA was isolated. Four repeats of microarray results are in this series.

2010-06-09 | E-GEOD-1492 | biostudies-arrayexpress

Calreticulin mutated hematopoietic cells are vulnerable to ATR-CHK1 pathway inhibition

Project description:Disease frameshift mutations of calreticulin (CALR) are the second most prevalent driver mutations in essential thrombocythemia (ET) and primary myelofibrosis (PMF). To identify potential targeted therapies for CALR mutated myeloproliferative neoplasms, we aimed to search for small molecule drugs that selectively inhibit the growth of CALR mutated cells using high-throughput drug screening. We investigated 89,172 compounds using isogenic cell lines and identified several hits targeting the ATR-CHK1 pathway. The selective inhibitory effect of these candidate compounds was validated in a co-culture assay of CALR mutated and wild type cells. Of the tested hit compounds, CHK1 inhibitors potently depleted CALR mutated cells, allowing CALR wild type cell dominance in the co-culture over time. Neither CALR deficient cells nor JAK2V617F mutated cells showed hypersensitivity to the drug treatment, suggesting that the vulnerability to ATR-CHK1 inhibition is specifically caused by the oncogenic activation by the mutant CALR. CHK1 inhibitors induced replication stress in CALR mutated cells revealed by elevated pan-nuclear staining for γH2AX and hyperphosphorylation of RPA2. They also promoted S-phase cell cycle arrest and blocked the completion of DNA replication in CALR mutated cells. Transcriptomic and phosphoproteomic analyses revealed a replication stress signature caused by the oncogenic CALR mutation, suggesting an intrinsic vulnerability of these cells to CHK1 perturbation. This study indicates that ATR-CHK1 pathway is a potential therapeutic target in CALR mutated hematopoietic cells.

2021-09-07 | PXD026803 | Pride

ENCODE Spike-In, Yale Group

Project description:Simulated ChIP DNA labeled by random priming with Klenow; Samples were "Undiluted" and not amplified prior to labeling. Keywords: other For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Systematic analysis of a simulated ChIP-chip experiment

2007-12-27 | E-GEOD-10004 | biostudies-arrayexpress

Comparative Thyroglobulin Interactome Profiling

Project description:Thyroglobulin (Tg) is a secreted iodoglycoprotein serving as the precursor for T3 and T4 hormones. Many characterized Tg gene mutations produce secretion-defective variants resulting in congenital hypothyroidism (CH). Tg processing and secretion is controlled by extensive interactions with chaperones, trafficking, and degradation proteins comprising the secretory proteostasis network. While dependencies on individual pro-teostasis network components are known, the integration of proteostasis pathways mediating Tg protein quality control and the molecular basis of mutant Tg misprocessing remain poorly understood. We employ a multiplexed quantitative affinity purification–mass spectrometry approach to define the Tg proteostasis interactome and changes between WT and several CH-variants. Mutant Tg processing is associated with common imbalances in proteostasis engagement including increased chaperoning, oxidative folding, and routing towards ER-associated degradation components, yet variants are inefficiently degraded. Furthermore, we reveal mutation-specific changes in engagement with N-glycosylation components, suggesting distinct requirements of one Tg variant on dual engagement of both oligosaccharyltransferase complex isoforms for degradation. Modulating dysregulated proteostasis components and pathways may serve as a therapeutic strategy to restore Tg secretion and thyroid hormone biosynthesis.

2020-11-20 | PXD019427 | Pride

Mycobacterium tuberculosis CDC1551 WT/sigI mutant

Project description:Transcription profile of WT compare to sigma factor sigI deletion mutant at OD1 and OD2. This microarray is simple comparison of wild type strain of M. tuberculosis CDC1551 and its sigma factor gene deletion mutant (sigI) at OD1 and OD2, respectively.

2012-01-30 | E-GEOD-35231 | biostudies-arrayexpress

Gene expression profile of abf1-1 mutant at 36 degrees C

2004-06-23 | GSE1492 | GEO

lin-15B(n744) mutants vs. wild type

Project description:Transcriptional profiling of C. elegans first larval stage whole animals comparing lin-15B(n744) mutants and N2 (wild type) at 26 degrees. One-condition experiment, mutant (lin-15B) vs. WT. Biological replicates 4 mutant, 4 wildtype harvested indepedently. One lin-35 replicate and one WT replicate per array.

2011-01-25 | E-GEOD-26823 | biostudies-arrayexpress

lin-35(n745) mutants vs. wild type

Project description:Transcriptional profiling of C. elegans first larval stage whole animals comparing lin-35(n745) mutants and N2 (wild type) at 26 degrees. One-condition experiment, mutant (lin-35) vs. WT. Biological replicates 4 mutant, 4 wildtype harvested indepedently. One lin-35 replicate and one WT replicate per array.

2011-01-25 | E-GEOD-26824 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data