ABSTRACT: Expression data from post natal mouse aortic heart valves treated with all-trans retinoic acid or a retinoic acid receptor antagonist (LE540) relative to DMSO treated controls
Project description:Chick wing buds at Hamburger and Hamilton stage 20 were treated with DMSO, all trans retinoic acid or synthetic retinoid EC23 via ion-exchange beads implanted into the wing buds. The anterior third of treated wing buds of surviving embryos were removed 24 hours after treatment by microdissection and pooled to prepare RNA extracts for microarray analysis.
Project description:Retinoic acid receptors (RARs) ?, ?, and ? heterodimerize with Retinoid X receptors (RXR) ?, ?, and ? and bind the cis-acting response elements known as RAREs to execute the biological functions of retinoic acid during mammalian development. RAR? mediates the anti-proliferative and apoptotic effects of retinoids in certain tissues and cancer cells, such as melanoma and neuroblastoma cells. Furthermore, ablation of RAR? enhanced the tumor incidence of Ras transformed keratinocytes and was associated with resistance to retinoid mediated growth arrest and apoptosis. We used microarray analysis to identify genes, which upon 8 or 24 hr of treatment with all-trans retinoic acid display differential expression in RAR? knockout (RAR?KO) murine embryonic stem cells relative to CCE WT cells. We demonstrate that following RA treatment the majority of inducible transcripts are present at lower levels in RAR?KO ES cells compared to WT ES cells. Murine embryonic stem cells (WT and RAR?KO) were treated with either all-trans retinoic acid (up to 24 hr) or with vehicle control (EtOH).
Project description:ADAR associated proteins of pancreatic cancer cell line by immunoprecipitation in response to different treatment.
Control: File DMSO In response to DMSO treatment.(File DMSO)
Experimental: File ATRA in response to ATRA (all-trans retinoic acid)
Project description:ADAR associated proteins of pancreatic cancer cell line by immunoprecipitation in response to different treatment.
Control: File DMSO In response to DMSO treatment.(File DMSO)
Experimental: File ATRA in response to ATRA (all-trans retinoic acid)
Project description:To investigate the regulatory role of retinoic acid on the macrophages transcriptome depending on their activation status, we treated naïve or IL4-stimulated murine bone marrow-drived macrophages with retinoic acid or vehicle (DMSO) for 6h
Project description:Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 M-NM-<M all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 M-NM-<M ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays. While cytotoxic chemotherapy remains the hallmark of cancer treatment, intensive regimens fall short in many malignancies, including high-risk neuroblastoma. One alternative strategy is to therapeutically promote tumor differentiation. We created a gene expression signature to measure neuroblast maturation, adapted it to a high-throughput platform, and screened a diversity oriented synthesis-generated small-molecule library for differentiation inducers. We identified BRD8430, containing a nine-membered lactam, an ortho-amino anilide functionality, and three chiral centers, as a selective Class I histone deacetylase (HDAC) inhibitor (HDAC1 > 2 > 3). Further investigation demonstrated that selective HDAC1/HDAC2 inhibition using compounds or RNA interference induced differentiation and decreased viability in neuroblastoma cell lines. Combined treatment with 13-cis retinoic acid augmented these effects and enhanced activation of retinoic acid signaling. Therefore, by applying a chemical genomic screening approach we identified selective HDAC1/HDAC2 inhibition as a strategy to induce neuroblastoma differentiation. BE(2)-C cells were treated in triplicate with either vehicle (DMSO), 5 M-NM-<M all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 M-NM-<M ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays [HT-HG_U133A Early Access].
Project description:In SKBR3 cells, simultaneous targeting of RARM-kM-1 with all-trans retinoic acid (ATRA) and HER2 with lapatinib results in synergistic anti-tumor responses. SKBR3 cells were treated with vehicle (DMSO), lapatinib (100 nM), ATRA (100 nM) or lapatinib+ATRA for 36 hours and miRNA expression profile was determined by one-color Agilent microarray experiments.
Project description:The aim of the experiment was to identify genome wide binding sites for retinoic acid receptor beta (RARB) in RARB agonist treated human metastatic pancreatic ductal adenocarcinoma cells (SUIT2). Datasets are prsented for the ChIP-seq analysis for SUIT2 cells after 72 h treatment with either DMSO (vehicle control), 1 µM RAR-β agonist (CD 2314, Tocirs 3824), or 1 µM RAR-β antagonist (LE 135, Tocris 2021).
