Project description:Differentially expressed microRNAs (miRNAs) were detected to explore the molecular mechanisms of diapause termination. The total small RNA (sRNA) of diapause-destined silkworm eggs and HCl-treated eggs was extracted and then sequenced using HiSeq/MiSeq high-throughput method. 44 novel miRNAs were discovered. Compared to those in the diapause-destined eggs, 61 miRNAs showed significant changes in the acid-treated eggs, with 23 being up-regulated and 38 being down-regulated. The potential target genes of differentially expressed miRNAs were predicted by miRanda. Gene Ontology and KEGG pathway enrichment analysis of these potential target genes revealed that they were mainly located within cells and organelles, involved in cellular and metabolic processes, and participated in protein production, processing and transportation. Two differentially expressed genes, Bombyx mori SDH (BmSDH) and Bmo-miR-2761-3p, were further analyzed with qRT-PCR. BmSDH was significantly up-regulated in the HCl-treated eggs, while Bmo-miR-2761-3p was down-regulated. These results suggested that these two genes were well coordinated in silkworm eggs. Dual luciferase reporter (DLR) assay demonstrated that Bmo-miR-2761-3p inhibited the expression of BmSDH.

2017-09-05 | GSE95576 | GEO

Effect of cinacalcet HCL on gene expression in mouse kidney

Project description:In order to identify renal pathways regulated by activation of the calcium sensing receptor (CaSR) we performed a microarray on RNA isolated from kidneys of mice not treated or treated with conacalcet HCL

2019-01-01 | GSE112831 | GEO

Effect of Chlorpromazine HCl on Rat Primary Hepatocytes.

Project description:This study provides an evaluation of changes in gene expression associated with chlorpromazine HCl treatment of rat hepatocytes in vitro. Primary rat hepatocytes were treated for 24 and 48 hours with two doses (0.8 uM and 20 uM) of chlorpromazine HCl and 1% DMSO vehicle control. Five replicates of each treatment were performed. Cells were then extracted and RNA processed for microarray analysis. This series is part of a SuperSeries in which primary rat hepatocytes were treated with two doses of ten chemical compounds (and corresponding vehicle controls) for 24 and 48 hours. Each compound/vehicle treatment group was an individual study performed at different times. Each study was analyzed separately and themes common between studies were reported. Time Course/Dose Response

2012-08-28 | E-GEOD-40341 | biostudies-arrayexpress

BRCA1-mimetic compound NSC35446.HCl inhits IKKB expression by reducing estrogen receptor alpha occupancy in the IKKB promoter and inhibts NF-κB activity in anti-estrogen resitant human breast cells

Project description:We previously identified small molecules that fit into a BRCA1-binding pocket within estrogen receptor-alpha (ER), mimic the ability of BRCA1 to inhibit ER activity (“BRCA1-mimetics”), and overcome antiestrogen resistance. One such compound, the hydrochloride salt of NSC35446 (“NSC35446.HCl”), also inhibited growth of antiestrogen-resistant LCC9 tumor xenografts. The purpose of this study was to investigate the down-stream effects of NSC35446.HCl and its mechanism of action. Methods: Here, we studied antiestrogen-resistant (LCC9, T47DCO, MCF-7/RR, LY2), ER-negative (MDA-MB-231, HCC1806, MDA-MB-468), and antiestrogen-sensitive (MCF-7) cell lines. Techniques utilized include RNA-seq, qRT-PCR, cell growth analysis, cell-cycle analysis, Western blotting, luciferase reporter assays, TUNEL assays, in-silico analysis of the IKKB gene, and ChIP assays. Results: NSC35446.HCl inhibited proliferation and induced apoptosis in antiestrogen resistant LCC9, T47DCO, MCF-7/RR, and LY2 cells but not in ER-negative breast cancer cell lines. IKKB (IKKβ, IKBKB), an upstream activator of NF-B, was identified as a BRCA1-mimetic-regulated gene, based on an RNA-seq analysis; and NSC35446.HCl inhibited IKKB mRNA and protein expression in LCC9 cells. NSC35446.HCl also inhibited NF-B activity and expression of NF-B target genes. In-silico analysis of the IKKB promoter identified nine estrogen response element (ERE) half-sites and one ERE-like full-site. ChIP assays revealed that ER was recruited to the ERE-like full-site and five of the nine half-sites and that ER recruitment was inhibited by NSC35446.HCl in LCC9 and T47DCO cells. Conclusions: These studies identify functional EREs in the IKKB promoter and identify IKKB as an NSC35446.HCl-regulated gene; and they suggest that NF-B and IKKB, which were previously linked to antiestrogen resistance, are targets for NSC35446.HCl in reversing antiestrogen resistance.

2017-07-21 | GSE101691 | GEO

Expression data from human lung cancer cancer treated with TXA1.Hcl

Project description:The antitumour activity of a hit tioxanthone is associated with alterations in cholesterol localization We used microarrays to detail the global programme of gene expression underlying treatment of lung cancer with TXA1.Hcl

2018-12-24 | GSE110825 | GEO

Effec of lactic acid or HCl on the Lactiplantibacillus plantarum gene expression

Project description:To characterize the effect of lactic acid on the L. plantarum growth and adaptation, we investigated the transcriptome under hydrochloride (HCl) or lactic acid at the early stage of the growth.

2023-06-14 | GSE211635 | GEO

Responses of Staphylococcus aureus exposed to HCl and organic acid stress.

Project description:Staphylococcus aureus is an important food poisoning bacterium. In food preservation, acidification is a well-known method. Permeant weak organic acids, like lactic and acetic acids, are known to be more effective against bacteria than inorganic strong acids (e.g., HCl). Growth experiments and metabolic and transcriptional analyses were used to determine the responses of a food pathogenic S. aureus strain exposed to lactic acid, acetic acid, and HCl at pH 4.5. Lactic and acetic acid stress induced a slower transcriptional response and large variations in growth patterns compared with the responses induced by HCl. In cultures acidified with lactic acid, the pH of the medium gradually increased to 7.5 during growth, while no such increase was observed for bacteria exposed to acetic acid or HCl. Staphylococcus aureus increased the pH in the medium mainly through accumulation of ammonium and the removal of acid groups, resulting in increased production of diacetyl (2,3-butanedione) and pyrazines. The results showed flexible and versatile responses of S. aureus to different types of acid stress. As measured by growth inhibition, permeant organic acid stress introduced severe stress compared with the stress caused by HCl. Cells exposed to lactic acid showed specific mechanisms of action in addition to sharing many of the mechanisms induced by HCl stress. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-87

2011-04-15 | E-BUGS-87 | biostudies-arrayexpress

Drug target identification of compound M1.HCl

Project description:Whole Genome Sequencing data of Plasmodium falciparum resistant to compound M1.HCl / Gamhépathiopine

| PRJEB61247 | ENA