Chip seq of in vitro induced senescent myeloid cells treated with HDAC inhibitor
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA924709 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23097402.fastq.gz | Fastqsanger.gz | |||
| SRR23097403.fastq.gz | Fastqsanger.gz | |||
| SRR23097404.fastq.gz | Fastqsanger.gz | |||
| SRR23097405.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:To understand the epigenetic regulations in in vitro induced senescent myeloid cells, we used Romidepsin (regulator of hyston H3) and we analysed how the genes get regulated.
2023-03-02 | GSE223014 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE26789: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (ALL-B and ALL-T) GSE26790: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (TOM-1 and MOLT-4) GSE26791: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (Illumina) GSE26792: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (SNP) Refer to individual Series
2012-04-17 | E-GEOD-26807 | biostudies-arrayexpress
Project description:Chronic Myeloid Leukemia (CML) remains a therapeutic challenge, particularly in patients who develop resistance to standard tyrosine kinase inhibitors (TKIs) such as imatinib. Here, we present the first demonstration of the potent anti-leukemic activity of the histone deacetylase (HDAC) inhibitor martinostat in both TKI-sensitive and TKI-resistant CML. Structural and biochemical analyses confirmed the efficient and selective binding of martinostat to HDAC isoenzyme ligand-binding pockets, resulting in histone and tubulin hyperacetylation in both imatinib-sensitive and resistant CML cells, outperforming vorinostat, a clinically used HDAC inhibitor (HDACi). It selectively impaired CML cell proliferation and viability and induced apoptosis across various CML models, including resistant cell models and patient blasts, with minimal toxicity to healthy cells and low developmental toxicity in zebrafish. In addition to its single-agent efficacy, martinostat demonstrated enhanced anticancer effects when combined with imatinib, both in vitro and in vivo, significantly reducing tumor growth in resistant CML xenograft models. Mechanistically, mRNA-seq data showed that martinostat disrupted key survival signaling pathways and amplified apoptotic responses, thereby contributing to its anticancer activity. These findings highlight the potential of martinostat as a selective, low-toxicity HDACi that, when combined with TKIs, could provide an effective strategy to overcome drug resistance in CML and improve therapeutic outcomes.
2025-07-23 | GSE292088 | GEO
Project description:Schistosomula exposed to HDAC inhibitor (Trichostatin A)
| PRJNA325300 | ENA
Project description:Here, we examined mouse brain trancriptional changes 1 hour after the 10th daily i.p. treament with one of the four following treaments: i) vehicle control (45% saline, 45% PEG-400 and 10% DMSO administered at 7.5mL/kg), ii) Cpd-60, 45mg/kg , administered at 7.5mL/kg or iii) SAHA, 25mg/kg, administered at 5mL/kg) or iv) CI-994, 10mg/kg, administered at 5mL/kg. Cpd-60 is a benzamide HDAC inhibitor with selectivity for class I HDAC subtypes HDAC1 and HDAC2; CI-994 is a benzamide inhibitor with selectivity for HDACs1,2 and 3; SAHA is a hydroxamic acid HDAC inhibitor with selectivity for class I HDAC subtypes 1,2, and 3 and the class II HDAC subtype HDAC 6. We examined transcript differences using the Illumnia WG-6 2.0 whole genome expression array and profiled 3 specific brain regions (prefrontal cortex, nucleus accumbens, hippocampus) from each of 36 mice (n=6 mice / treatment group) . For application to array chips, we pooled two biological replicates from like treatment and brain region-groups such that 36 samples were applied in total: 4 treatment groups x 3 brain regions per treament group x 3 pools of two samples each for each treatment/brain region.
2013-05-29 | GSE47452 | GEO
Project description:H929 human myeloma cells were exposed to aminopeptidase inhibitor (CHR-2797), HDAC inhibitor (CHR-3996), or a combinaion of the two agents, for 24 hours. Following this treatment RNA was extracted and microarrays used to determine gene expression changes. Myeloma cells were exposed to chemotherapeutic agent for 24 hours.
2014-01-24 | E-GEOD-20405 | biostudies-arrayexpress
Project description:H929 human myeloma cells were exposed to aminopeptidase inhibitor (CHR-2797), HDAC inhibitor (CHR-3996), or a combinaion of the two agents, for 24 hours. Following this treatment RNA was extracted and microarrays used to determine gene expression changes.
2014-01-24 | GSE20405 | GEO
Project description:Here, we examined mouse brain trancriptional changes 1 hour after the 10th daily i.p. treament with one of the four following treaments: i) vehicle control (45% saline, 45% PEG-400 and 10% DMSO administered at 7.5mL/kg), ii) Cpd-60, 45mg/kg , administered at 7.5mL/kg or iii) SAHA, 25mg/kg, administered at 5mL/kg) or iv) CI-994, 10mg/kg, administered at 5mL/kg. Cpd-60 is a benzamide HDAC inhibitor with selectivity for class I HDAC subtypes HDAC1 and HDAC2; CI-994 is a benzamide inhibitor with selectivity for HDACs1,2 and 3; SAHA is a hydroxamic acid HDAC inhibitor with selectivity for class I HDAC subtypes 1,2, and 3 and the class II HDAC subtype HDAC 6. We examined transcript differences using the Illumnia WG-6 2.0 whole genome expression array and profiled 3 specific brain regions (prefrontal cortex, nucleus accumbens, hippocampus) from each of 36 mice (n=6 mice / treatment group) . For application to array chips, we pooled two biological replicates from like treatment and brain region-groups such that 36 samples were applied in total: 4 treatment groups x 3 brain regions per treament group x 3 pools of two samples each for each treatment/brain region. Treatment groups: All adult male, C57BL/6 mice (n=6mice/treatment group) were sacrificed by rapid cervical dislocation and decapitation 1 hour after the tenth daily i.p. injection with one of the four following treaments: i) vehicle control (45% saline, 45% PEG-400 and 10% DMSO administered at 7.5mL/kg), ii) Cpd-60, 45mg/kg , administered at 7.5mL/kg or iii) SAHA, 25mg/kg, administered at 5mL/kg) or iv) CI-994, 10mg/kg, administered at 5mL/kg. Brains were removed, frozen immediately on dry ice and stored at -80°C until use. Frozen mouse brains (n = 6/ treatment group) were rapidly dissected at 4°C, isolating medial prefrontal cortex, nucleus accumbens and hippocampus. RNA was isolated using the Qiagen RNeasy Lipid Tissue mini kit, RNA concentration was determined using a NanoDrop spectrophotometer and quality was assessed using Agilent Bioanalyzer PICO chips, with the RNA Integrity Number (RIN) determined at 7.0-8.8 for all samples assayed, indicative of good RNA quality. For microarray experiments on Illumina MouseWG-6 BeadChips, RNA samples were pooled from two biological replicates such that the total number of samples was 36 (3 treatment groups x 3 brain regions x 3 RNA pools representing two mice per pool). All microarray analysis and gene set analysis (GSA) was performed using GeneSpring software (v.11.5.1) with raw signals adjusted using quantile normalization and baseline transformation with the median signal in all samples set to zero. Data were included in subsequent analyses if the normalized signal, thresholded at 0.8, was ‘present’ for 3 of 3 replicates for like treatment and tissue groups.
2013-05-29 | E-GEOD-47452 | biostudies-arrayexpress
Project description:Expression profiling of neonatl rat ventricular cardiomyocytes (NRVMs) upon the treatement of Class IIa HDAC inhibitor
2019-04-23 | GSE130150 | GEO
Project description:Expression data in PC3 prostate cancer cells treated with DMSO, HDAC inhibitor, EZH2 inhibitor, or combined HDAC and EZH2 inhibitors.
| PRJNA630152 | ENA