Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CHD1 Alters Sensitivity to Aurora Kinase A Inhibitors

ABSTRACT: CHD1 Alters Sensitivity to Aurora Kinase A Inhibitors

PROVIDER: PRJNA774875 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16584045_1.fastq.gz	Fastqsanger.gz
	SRR16584045_2.fastq.gz	Fastqsanger.gz
	SRR16584046_1.fastq.gz	Fastqsanger.gz
	SRR16584046_2.fastq.gz	Fastqsanger.gz
	SRR16584047_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

CHD1 Alters Sensitivity to Aurora Kinase A Inhibitors

Project description:In this study, we sought to understand the impact of CHD1 on sensitivity to Aurora A inhibitors in prostate and other cancers and underlying mechanisms

2023-10-16 | GSE186633 | GEO

BET and Aurora Kinase A Inhibitors Synergize against MYCN-positive Human Glioblastoma Cells

Project description:Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor in adults. Patients usually undergo surgery followed by aggressive radio- and chemotherapy with the alkylating agent temozolomide (TMZ). Still, median survival is only 12-15 months after diagnosis. Many human cancers including GBMs demonstrate addiction to MYC transcription factor signaling and can become susceptible to inhibition of MYC downstream genes. JQ1 is an effective inhibitor of BET Bromodomains, a class of epigenetic readers regulating expression of downstream MYC targets. Here, we show that BET inhibition decreases viability of patient-derived GBM cell lines. We propose a distinct expression signature of MYCN-elevated GBM cells that correlates with significant sensitivity to BET inhibition. In tumors showing JQ1 sensitivity, we found enrichment of pathways regulating cell cycle, DNA damage response and repair. As DNA repair leads to acquired chemoresistance to TMZ, JQ1 treatment in combination with TMZ synergistically inhibited proliferation of sensitive cells. Bioinformatic analyses showed that JQ1-sensitive cells could also respond to Aurora Kinase A inhibition which indeed showed synergistic efficacy in combination with BET inhibition. Collectively, our data suggest that BET inhibition could potentiate the efficacy of TMZ or could be combined with Aurora Kinase inhibitors in MYCN-elevated GBM.

2019-12-05 | GSE138942 | GEO

RNA seq_A375 gSMARCB1 + A549 etoposide, Aurora kinases inhibitors treated

Project description:To study the senescence gene signatures in the cells, which were genetic SMARCB1 depleted or treated with aurora kinase inhibitors or etoposide, we performed next generation RNA sequencing on these cell, and 'FRIDMAN_SENESCENCE_UP' geneset was used to determine the enrichment of senescence-related genes. The RNA sequencing results include (1) A375 cells and SMARCB1 depleted counterparts. (2) A549 cells and aurora kinase inhibitor (Alisertib, barasertib or tozasertib) or etoposide treated counterparts.

2017-09-21 | GSE102639 | GEO

Novel, highly potent PROTACs targeting AURORA-A kinase

Project description:The family of AURORA kinases is essential for cell cycle progression and dysregulation of AURORA-A in cancer led to a large number of clinical and pre-clinical inhibitors. However, ATP competitive AURORA-A inhibitors usually do not target non-catalytic functions that have also been identified as mechanisms promoting tumorigenesis. To target non-catalytic as well as catalytic functions, we developed a series of PROTACs (PROteolysis targeting chimeras) based on the selective AURORA-A kinase inhibitor MK-5108 (VX-689) and the CEREBLON E3-ligase ligands. The most potent PROTAC, JB301, had good physicochemical properties and cell penetration resulting in degradation of AURORA-A in leukemic cells at single digit nM concentration. In the presented datasets, we determined the intracellular degradation specificity of the AURKA PROTAC JB300. We therefore treated MV4-11 cells with JB300 and the corresponding ligand MK-5108, or DMSO and quantified the induced degradation using a label free approach.

2023-09-14 | PXD033239 | Pride

BET and Aurora Kinase A Inhibitors Synergize against MYCN-positive Human Glioblastoma Cells

Project description:BET and Aurora Kinase A Inhibitors Synergize against MYCN-positive Human Glioblastoma Cells

| PRJNA577866 | ENA

Expression profiling, U2OS, Aurora kinase and p38 inhibitor response

Project description:U-2 OS (human osteosarcoma cell line) were treated with ZM447439 (an aurora kinase inhibitor), SB202190 (a p38 inhibitor) or ZM447439+SB202190 and resulting changes in gene expression were profiled.

2017-07-01 | E-MTAB-1210 | biostudies-arrayexpress

Aurora A kinase phosphorylates Hec1 to regulate metaphase kinetochore-microtubule dynamics.

Project description:Precise regulation of kinetochore-microtubules is essential for successful chromosome segregation. Central to this regulation is Aurora B kinase, which phosphorylates kinetochore substrates to promote microtubule turnover. A critical target of Aurora B is the N-terminal “tail” domain of Hec1/NDC80, which is a component of the NDC80 complex, a force-transducing link between kinetochores and microtubules. While Aurora B is regarded as the “master regulator” of kinetochore-microtubule attachment, it is likely that other mitotic kinases contribute to Hec1phosphorylation. Here we show that Aurora A kinase phosphorylates the tail domain of Hec1 at Serine 69, a previously uncharacterized phosphorylation target site, and plays an important role in controlling kinetochore-microtubule attachment dynamics. Using phospho-specific antibodies, Hec1 phospho-deficient mutants, and kinase inhibitors, we demonstrate that Aurora A is required for the regulation of kinetochore-microtubule dynamics of metaphase chromosomes and identify Hec1 Serine 69 as a critical Aurora A substrate for this regulation. Additionally, we demonstrate that Aurora A kinase associates with INCENP during mitosis and that INCENP is competent to drive accumulation of the kinase to the centromere region of mitotic chromosomes. These findings reveal that both Aurora A and Aurora B contribute to kinetochore-microtubule attachment dynamics, and they uncover an unexpected role for Aurora A in mitosis.

2017-11-28 | PXD006892 | Pride

Heteractis aurora

Project description:Heteractis aurora

| PRJNA1138220 | ENA

Histone exchange in wildtype, isw1, chd1, isw1 chd1 and ioc4 yeast strains

Project description:Histone exchange in wildtype, isw1, chd1, isw1 chd1 and ioc4 yeast strains.

2012-07-25 | GSE32043 | GEO

Microarray of CHD1 Knockdown in PC3 cells and CHD1 knockout in LNCaP cells

Project description:We used microarrays to study the global gene expression and identified differentially expressed genes in CHD1 knockdown PC-3 cells and CHD1 KO LNCaP cells, aiming to identify genes and pathways that are regulated by CHD1

2017-02-10 | GSE84970 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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