Eucheuma denticulatum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA379657 | ENA |
REPOSITORIES: ENA
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Project description:Endothelial progenitors represent one of the most promising cell-based strategies for vascular repair of ischemic tissue damage, including limb ischemia, myocardial infarction and stroke. We have shown that the transcription factor TAL1 regulates a transcription program that drives the migration and adhesion of ECFCs. Furthermore, treatment of ECFCs with the HDAC inhibitor TSA increases the expression of TAL1-dependent genes and promotes the migration, chemotaxis and adhesion of ECFCs. Finally, ex vivo treatment with TSA also improves the vascular repair properties of ECFCs in vivo when these cells are transplanted in a mouse model of hindlimb ischemia. The goal of this experiment was to test whether TSA treatment of ECFCs affect TAL1 genomic binding. TAL1 ChIP-sequencing was performed from ECFCs that have been treated or not TSA. As negative controls, we performed Mock-ChIP-seq from the same samples using normal IgG instead of the TAL1 antibody. Overall, we find that there is no change in TAL1 genomic binding in ECFCs upon TSA treatment.
2014-05-06 | E-GEOD-53423 | biostudies-arrayexpress
Project description:In order to identify the TSA responsive genes, we performed a gene expression microarray analysis for the RNAs isolated from TSA-untreated and TSA-treated human keratinocytes
2018-12-31 | GSE121902 | GEO
Project description:To explore TSA influence on human breast cancer cells, we attempt to analyze genes differentially expressed between TSA treated and untreated SKBR3 cells, which will hopefully provide clues for TSA target genes.
2017-02-28 | GSE95087 | GEO
Project description:These data were used for prediction of neoantigens and minor histocompatibility mismatch antigens, which were subsequently used for design of a machine-learning algorithm for tumor-specific antigen (TSA) immunogenicity prediction. TSA vaccines are a growing area of study for cancer immunotherapy, but identification of clinically relevant targets remains a challenge. The study associated with these data provides the first description of a computational method for direct prediction of TSA immunogenicity trained entirely from validated TSA immunogenicity scores. This tool has allowed us to 1) predict for clinically efficacious TSA targets, 2) identify genomic correlates of TSA immunogenicity, and 3) demonstrate evidence of alternative out-of-frame TSAs which can promote anti-tumor immunity.
2019-09-03 | GSE136619 | GEO
Project description:Analysis of MDA-MB-231 cells following TSA treatment or not. TSA regulates various miRNA expression in MDA-MB-231 cells.Results provide insight into the role of miRNAs-involved mechanisms underlying TSA-mediated effects on breast cancer stemness.
2022-01-01 | GSE156155 | GEO
Project description:Traditional serrated adenoma (TSA) remains the least understood of all the colorectal adenomas although these lesions have been associated with a significant cancer risk- twice that of the conventional adenoma (CAD) and of the sessile serrated adenoma (SSA/P). This study was performed to investigate the proteomic profiles of the different colorectal adenomas to better assess the pathogenesis of TSA. We performed a global quantitative expression profile of 44 colorectal adenomas (12 TSA, 15 CAD, 17 SSA/Ps) and 17 normal colonic mucosa, conserved as formalin-fixed paraffin-embedded samples, by the label-free quantification (LFQ) method. Unsupervised consensus hierarchical clustering applied to the whole proteomic profile of the 44 colorectal adenomas identified four subtypes. The C1 and C2 were well-individualized clusters composed of most of the CAD (14/15) and most of the SSA (13/17) respectively. This is consistent with the fact that CAD and SSA/Ps are homogeneous but distinct colorectal adenoma entities. In contrast, TSA were subdivided into C3 and C4 clusters that also contained CAD and SSA/Ps, consistent with the more heterogeneous entity of TSA at the morphological and molecular levels. The comparison of the proteome expression profile between the adenoma subtypes and normal colonic mucosa further confirmed the heterogeneous nature of TSA that merged either on CAD or SSA, while CAD and TSA formed homogeneous and distinct entities. Furthermore, we identified LEFTY1 a new potential marker for TSA that may be relevant for the TSA pathogenesis. LEFTY1 is an inhibitor of the Nodal/TGFb pathway that we found to be one of the most overexpressed proteins specifically in the TSA and confirmed by immunohistochemistry. Taken together, our study confirms that CAD and SSA form homogenous but distinct colorectal adenoma entities while TSA are an heterogeneous entity and may arise from either SSA or from normal mucosa that will evolve along the conventional adenoma pathway.
2020-01-21 | PXD014511 | Pride
Project description:Cardiac hypertrophy is characterized by an increase in heart size and profound gene expression changes. Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression. Published literature has linked enzymes that mediates histone acetylation to pathogenesis, however, the role of histone acetylation to define hypertrophic gene regulatory events are not well understood. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (seq) to comprehensively examine genome-wide histone acetylation changes in a pre-clinical model of pathological cardiac hypertrophy by transverse aortic constricted (TAC). We examined the gene targets conferred by the prototypical HDAC inhibitor Trichostatin A (TSA). TSA induces genome-wide histone acetylation and deacetylation in the heart. Alterations to histone acetylation were found on genes involved in cardiac morphology such as cardiac contraction, collagen deposition, inflammation and extracellular matrix. Gene set enrichment analysis identified NF-kappa B (NFKB), as a transcription factor positively correlated with TAC and negatively correlated with TSA by ChIP-seq. Histone acetylation on the promoters of NKFB target genes was increased, consistent with gene activation. In contrast, the promoters of these genes were deacetylated by TSA in hypertrophic animals and reduced expression of NFKB target genes. Our results suggest a potential mechanism for TSA mediated cardioprotection conferred by histone deacetylation of target genes implicating the importance of inflammation. ChIP-seq profiles for histone acetylation in left ventricles of mice that develop cardiac hypertrophy and treated with HDAC inhibitors were generated by deep sequencing, using Illumina GAIIx.
2015-04-25 | E-GEOD-63590 | biostudies-arrayexpress
Project description:We report the differential roles of an HDAC inhibitor-TSA during hESC nerual commitment. In the initiation of hESC differentiation, TSA could inhibit the downregulation of pluripotency genes to maintain pluripotency, whereas in the neural commitment stage, TSA could promote neural gene expression to assist hESC nerual determination.
2015-03-11 | GSE66777 | GEO
Project description:To explore how TSA-MSCexo improves myocardial ischemia-reperfusion injury, miRNA microarray analysis was used to screen differentially expressed miRNAs in MSCexo and TSA-MSCexo.
2022-11-22 | GSE212320 | GEO
Project description:The experiment was designed to study the effects of the Dnmt1 gene knockout on gene expression, as well as to analyze the effects of TSA treatment on both WT (p53-/-) and knockout (p53-/-Dnmt1-/-) cells ; The effect of TSA treatment on knockout and WT cells was tested at two different time points (24 and 48 hs), as well as two weeks after removal of TSA Experiment Overall Design: Seven hybridizations were performed: 1. p53-/- untreated (control), 2. p53-/- +TSA harvested after 24hs of exposure to TSA, 3. p53-/- +TSA 48hs, 4. p53-/-Dnmt1-/- untreated, 5.p53-/-Dnmt1-/- +TSA 24hs 6.p53-/-Dnmt1-/- +TSA 48hs 7.p53-/-Dnmt1-/- two weeks after removal of TSA
2008-06-12 | E-GEOD-3534 | biostudies-arrayexpress