Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA393355 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5809430_1.fastq.gz | Fastqsanger.gz | |||
| SRR5809430_2.fastq.gz | Fastqsanger.gz | |||
| SRR5809421_1.fastq.gz | Fastqsanger.gz | |||
| SRR5809421_2.fastq.gz | Fastqsanger.gz | |||
| SRR5809431_1.fastq.gz | Fastqsanger.gz |
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Project description:Upstream regulator genes are central hub nodes in a network and their expression may response to upstream trigger factors of a disease and influence expression of hundreds of downstream genes, and further facilitate disease development. Therefore, the identification of upstream regulator genes are vital for understanding the pathophysiology of the disease and seek for potential therapeutic targets for the treatment of the disease. YAP1 was identified as a candidate upstream regulator for Alzheimer's disease (AD) in our study. To test whether expression alterations of YAP1 can lead to AD expression network disturbance and thus promoting AD progression, we knockdown and overexpressed YAP1 in U251 cell line with a stably expression of mutant APP (K670N/M671L) (U251-APP cells). RNA-seq (by IlluminaHiseq 4000) and following analyses were then performed to detect genes whose expression were influenced by YAP1 expression changes. The results indicated that expression alterations of YAP1 can significantly disturbe the whole AD expression network.
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Project description:RPL13 was identified to be downregulated in brain of Alzheimer's disease (AD). To explore the involved pathways in response to RPL13 reduction, we knockdownRPL13 using siRNA in U251 cell line with a stably expressed mutant APP (K670N/M671L, U251-APP cells). RNA-seq (by IlluminaHiseq 4000) and following analyses were then performed to detect genes whose expression were influenced by RPL13 knockdown.
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Project description:We identified a rare coding variant (p.K420Q) in the complement component 7 (C7) gene affecting the risk of Alzheimer's disease. To investigate the cellular effects of the mutant, we performed RNA-seq in cell line overexpression wilt-type and mutant C7. U251 glioma cells with stable expression of mutant APP (K670N/M671L) (U251-APP cells), which produce Aβ42 under Dox inducing, were used as the model cell. Total RNA of U251-APP cells overexpressing wild type and mutant C7 proteins were subjected to transcriptome sequencing using Illumina Hiseq 4000 platform.
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Project description:Identification of downstream genes regulated by YAP1 through knockdown SRSF6 in SW620 cells
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Project description:The multidomain protein BAG3 exerts pleiotropic oncogenic functions in many tumor entities including glioblastoma (GBM). Here we compared BAG3 protein-protein interactions in either adherently cultured or stem-like cultured U251 GBM cells. In line with BAG3´s putative role in stemness, identified interactors in sphere-cultured cells included different stem cell markers (SOX2, OLIG2, NES), while interactomes of adherent BAG3-proficient cells indicated a shift towards involvement of BAG3 in regulation of cilium assembly (ACTR3, ARL3). Applying a set of BAG3 deletion constructs we could demonstrate that none of the domains except the WW domain are required for suppression of cilia formation by full-length BAG3 in U251 and U343 cells. In line with the established regulation of the Hippo pathway by this domain, we could show that the WW mutant fails to rescue YAP1 nuclear translocation. BAG3 depletion reduced activation of a YAP1/AURKA signaling pathway and induction of PLK1. Collectively, our findings point to a complex interaction network of BAG3 with several pathways regulating cilia homeostasis, involving processes related to ciliogenesis and cilium degradation.
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Project description:Overexpression of miR-31 inhibits the migration and invasion ability of glioma cell. We sought to obtain the genes regulated by mir-31 in glioma cell line. The gene expression of U251-mir-31 (U251 over expressing mir-31) and U251-control. U251-Control and U251-mir-31 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Affymetrix.GeneChip.HG-U133_Plus_2.
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Project description:Meningiomas are the most common primary brain tumors in adults. Although generally benign, a subset is of higher grade, recurs even after multiple surgeries, and frequently fatal. Around half of meningiomas harbor inactivating mutations in NF2. While low-grade NF2 mutant meningiomas harbor few additional mutations in addition to NF2 inactivation, high-grade NF2 mutant tumors frequently harbor a highly aberrant genome. We and others have previously shown that NF2 inactivation leads to YAP1 activation and that YAP1 acts as an oncogene in NF2 mutant meningiomas. Here, we show that high-grade NF2 mutant meningiomas downregulate YAP1 signaling, in part through upregulating the expression of the YAP1 competitor VGLL4 and the YAP1 upstream regulators FAT3/4. Overexpression of VGLL4 resulted in the downregulation of YAP activity and the growth inhibition of low-grade NF2 mutant meningioma cells. Our results have important implications for the efficacy of therapies targeting oncogenic YAP1 in high-grade NF2 mutant meningiomas.
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Project description:Pulmonary artery (PA) pressure increases during lung growth after unilateral pneumonectomy (PNX). Mechanosensitive transcriptional co-activator, yes-associated protein (YAP1), in endothelial cells (ECs) is necessary for angiogenesis during post-PNX lung growth. We investigate whether increases in PA pressure following PNX controls angiogenesis through YAP1. When hydrostatic pressure is applied to human pulmonary arterial ECs (HPAECs), the expression of YAP1, transcription factor TEAD1, and angiogenic factor receptor Tie2 increases, while these effects are inhibited when HPAECs are treated with YAP1 siRNA or YAP1S94A mutant that fails to bind to TEAD1. Hydrostatic pressure also stimulates DNA synthesis and cell migration in HPAECs, while YAP1 knockdown or YAP1S94A mutant inhibits the effects. Gene enrichment analysis reveals that the levels of extracellular matrix (ECM) or cell adhesion molecules are altered in post-PNX mouse lung ECs, which interact with YAP1. Exosomes are known to promote tissue regeneration. Proteomics analysis reveals that exosomes isolated from conditioned media of post-PNX mouse lung ECs contain the higher levels of ECM and cell-adhesion proteins compared to those from sham-operated mouse lung ECs. Recruitment of host lung ECs and blood vessel formation are stimulated in the fibrin gel containing exosomes isolated from post-PNX mouse lung ECs or pressurized ECs, while YAP1 knockdown inhibits the effects. These results suggest that increases in PA pressure stimulate angiogenesis through YAP1 during regenerative lung growth.
2022-03-09 | GSE154110 | GEO
Project description:Obesity is a clinical condition characterised by a chronic, low-grade inflammatory state. Adipose-derived mesenchymal stem cells (ADSCs) have a multidirectional differentiation potential to adipocytes. However, the relationship between adipogenesis and inflammation is not yet fully understood.TAZ (WW domain containing transcription regulator 1) can act as a molecular rheostat to fine-tune the osteoblast and adipocyte differentiation balance. In this study, we investigated the role of TAZ in the adipogenesis of Arbas cashmere goat ADSCs (gADSCs). We observed elevated TAZ expression levels during the adipogenesis of gADSCs. Overexpression and knockdown of TAZ were performed in stably transfected gADSCs cell lines, and RNA-seq analysis revealed that TAZ was associated with adipogenesis. TAZ overexpression promoted adipose differentiation of gADSCs, while TAZ knockdown had the opposite effect. In addition, TAZ overexpression and knockdown altered the expression of YAP1 (Yes1 associated transcriptional regulator) and TAZ in the nucleus. TAZ regulated the mRNA expression level and secretion level of tumor necrosis factor (TNF)-α, promoting adipose differentiation of gADSCs. Notably, TNF-α counteracted the inhibitory effect of sh-TAZ on the adipose differentiation of gADSCs. Collectively, these findings suggest that TAZ regulates adipogenesis in gADSCs by modulating TNF-α, which is of particular significance in several metabolic disorders where the amount or function of adipose tissue is altered.
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