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Expression Data from HNF4a RNAi Knockdown in HepG2 cells

ABSTRACT: HNF4a is an important liver transcription factor that regulates at least a thousand genes in the liver. Here we used expression profiling in HepG2 cells, a hepatocellular carcinoma cell line, in which HNF4a was knocked down by RNAi to identify some of those target genes. This dataset accompanies the article in Hepatology 2010 Feb;51(2):642-53. Integrated approach for the identification of human hepatocyte nuclear factor 4alpha target genes using protein binding microarrays by Bolotin E, Liao H, Ta TC, Yang C, Hwang-Verslues W, Evans JR, Jiang T, Sladek FM.

ORGANISM(S): Homo sapiens

PROVIDER: GSE29084 | GEO | 2011/05/05

SECONDARY ACCESSION(S): PRJNA140301

REPOSITORIES: GEO

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Expression Data from HNF4a RNAi Knockdown in HepG2 cells

Project description:HNF4a is an important liver transcription factor that regulates at least a thousand genes in the liver. Here we used expression profiling in HepG2 cells, a hepatocellular carcinoma cell line, in which HNF4a was knocked down by RNAi to identify some of those target genes. This dataset accompanies the article in Hepatology 2010 Feb;51(2):642-53. Integrated approach for the identification of human hepatocyte nuclear factor 4alpha target genes using protein binding microarrays by Bolotin E, Liao H, Ta TC, Yang C, Hwang-Verslues W, Evans JR, Jiang T, Sladek FM. RNA interference (RNAi) against HNF4a2 was performed in HepG2 cells using small, interfering RNAs (siRNAs) corresponding to nucleotides +179 to +197 of human HNF4A (NM_178849, sense siRNA: 5'-UGUGCAGGUGUUGACGAUGdTdT-3', antisense siRNA 5'-CAUCGUCAACACCUGCACAdTdT-3') (Dharmacon, Lafayette, CO). Total RNA was extracted with Trizol (Life Technologies, Carlsbad, CA) and reverse transcribed with the Reverse Transcription System (Promega, Madison, WI). Polymerase chain reaction (PCR) amplification was performed in the linear range (see Supporting Table 3B for a list of PCR primers). Expression profiling analysis was performed with Affymetrix oligonucleotide arrays (HGU133 Plus 2.0) using RNA from control (PGL3 siRNA) or treated (HNF4a siRNA) HepG2 cells

2011-05-05 | E-GEOD-29084 | biostudies-arrayexpress

Identification of heptanal receptors in mouse olfactory epithelium by a high-throughput in vivo method

Project description:We present heptanal receptors identified using a high-throughput in vivo method (Jiang et al., 2015)

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Ares Swanson MBNL mutant study

Project description:MBNL1 is a known splicing factor and is related to Myotonic Dystrophy (DM). This study examines the tissue specific splicing patterns of MBNL1 using a mutant and wild type mouse across three tissues (heart,brain,quadricep) related publications: Aberrant alternative splicing and extracellular matrix gene expression in mouse models of myotonic dystrophy. Du H, etal Nat Struct Mol Biol. 2010 Feb;17(2):187-93. and Muscleblind-like 1 knockout mice reveal novel splicing defects in the myotonic dystrophy brain. Suenaga K, Lee KY, Nakamori M, Tatsumi Y, Takahashi MP, Fujimura H, Jinnai K, Yoshikawa H, Du H, Ares M Jr, Swanson MS, Kimura T. PLoS One. 2012;7(3):e33218. Epub 2012 Mar 13. PMID: 22427994 and Hum Mol Genet. 2006 Jul 1;15(13):2087-97. Failure of MBNL1-dependent post-natal splicing transitions in myotonic dystrophy. Lin X, Miller JW, Mankodi A, Kanadia RN, Yuan Y, Moxley RT, Swanson MS, Thornton CA.

2012-07-31 | GSE28640 | GEO

Soluble ST2 induces cardiac contractile dysfunction by repressing mitochondrial electron transport chain genes in cardiomyocytes during fulminant myocarditis

Project description:Fulminant myocarditis (FM) is an acute fatal disease characterised by myocardial inflammation. Our previous study identified soluble growth stimulation- expressed gene 2 (sST2) as a sensitive and specific biomarker for early diagnosis of FM. However, its function in FM remains unclear.In the present study, we observed a marked elevation of sST2 in the plasma and hearts of mice with FM induced by coxsackievirus B3 (CVB3) and explored the main cellular sources of sST2 in FM. Moreover, using recombinant sST2 protein administration and unbiased transcriptomics analyses, we investigated the role and underlying mechanisms of sST2 in FM. Importantly, we found that sST2 has a novel non-classical function in cardiomyocytes, other than acting as an IL-33 decoy receptor. These findings reveal a novel role and action mechanism of sST2 in FM and suggest that sST2 may be a potential therapeutic target for FM.

2024-03-24 | GSE261940 | GEO

Project description:Jiang-flavored Daqu

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Gene expression profile at single cell level of tissue- associated kidney NKp46+NK1.1+ or NK1.1+ ILC from untreated and poly (I:C) treated RORgt-FM mice

Project description:We next asked whether RORgt-FM+ ILC are transcriptionally similar to the Tnfrsf9+ tILC that we identified in lupus-prone mice. To explore this, we isolated tissue RORgt-FM+ and RORgt-FM- NKp46+ ILC from RORgt-FM mice, some of which were treated with poly(I:C) and analyzed them by scRNA-seq

2024-07-11 | GSE269400 | GEO

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Genomic and physiological responses to strong selective pressure during late organogenesis: how natural Fundulus heteroclitus populations cope with persistent environmental pollution Superfund Site

Project description:This study explores the synergistic effects of two model PAHs, an aryl hydrocarbon receptor (AHR) agonist (M-NM-2-naphthoflavone) and a cytochrome P4501A (CYP1A) inhibitor (M-NM-1-naphthoflavone), on gene expression in stage 31 embryos from two different population. One population (Elizabeth River population) is relatively resistant to the pollutants in its environment. A loop design (Figure 5) was used for the microarray hybridizations where each sample is hybridized to 2 arrays using both Cy3 and Cy5 labeled fluorophores (Kerr and Churchill, 2001). The loop consisted of Cy3 and Cy5 labeled embryo aRNAs from 4 biological samples and six different treatments (T1-T6: control, 1 M-NM-<g/L BNF, 50 M-NM-<g/L ANF, 100 M-NM-<g/L ANF, 1 M-NM-<g/L BNF + 50 M-NM-<g/L ANF, 1 M-NM-<g/L BNF + 100 M-NM-<g/L ANF). In total, 48 biological samples were hybridized to 24 microarrays. Each array had different combinations of biological samples, so that the most direct comparisons (i.e., 50 M-BM-5g/L ANF resistant embryo and 50 M-BM-5g/L sensitive embryo) are hybridized to the same array. The loop formed was T1SM-bM-^FM-^R T1R M-bM-^FM-^R T2SM-bM-^FM-^R T2R M-bM-^FM-^RT3SM-bM-^FM-^R T3RM-bM-^FM-^R T4SM-bM-^FM-^R T4RM-bM-^FM-^R T5SM-bM-^FM-^R T5R M-bM-^FM-^R T6SM-bM-^FM-^RT6RM-bM-^FM-^R T1SM-bM-^FM-^R T2S M-bM-^FM-^R T3S M-bM-^FM-^R T4S M-bM-^FM-^R T5S M-bM-^FM-^R T6S M-bM-^FM-^R T1S M-bM-^FM-^R T1R M-bM-^FM-^R T2R M-bM-^FM-^R T3R M-bM-^FM-^R T4R M-bM-^FM-^R T5R M-bM-^FM-^R T6R, where each arrow represents a separate hybridization (array) with the biological sample at the base of the arrow labeled with Cy3 and the biological pool at the head of the arrow labeled with Cy5. T1-6 is treatment, and S and R represent sensitive and resistant embryos.

2013-09-30 | E-GEOD-47654 | biostudies-arrayexpress

Manual therapy improves fibromyalgia symptoms by downregulating SIK1

Project description:Fibromyalgia (FM), classified by ICD-11 with code MG30.0, is a chronic debilitating disease characterized by wide-spread pain, fatigue, cognitive impairment, sleep and intestinal alterations, among other. FM affects a large proportion of the world-wide population, with increased prevalence among women. The lack of understanding of its etiology and pathophysiology hampers the development of effective treatments. Our group had developed a manual therapy (MT) pressure-controlled custom manual protocol on FM showing hyperalgesia/allodynia, fatigue and patient’s quality of life benefits in a cohort of 38 FM cases (NCT04174300). With the aim of understanding the therapeutic molecular mechanisms triggered by MT, this study interrogated PBMC transcriptomes from FM participants of this clinical trial using RNAseq and RT-qPCR technologies. The results showed that the salt-induced kinase SIK1 gene was consistently downregulated by MT in FM, correlating with improvement of patient symptoms. In addition, the study compared the findings in a non-FM control cohort subjected to the same MT protocol evidencing that changes in SIK1 expression with MT only occurred in individuals with FM. This positions SIK1 as a potential biomarker to monitor response to MT, and as a therapeutic target of FM, to be further explored by continuation studies. Keywords: fibromyalgia; myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS); pressure point threshold (PPT); physiotherapy; manual therapy (MT); NCT04174300; SIK1

2024-09-11 | GSE274134 | GEO

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