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ABSTRACT: P15-VP

PROVIDER: PRJNA947938 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23976749_1.fastq.gz	Fastqsanger.gz
	SRR23976749_2.fastq.gz	Fastqsanger.gz

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Tumor selective proteotoxicity of verteporfin inhibits colon cancer progression independent of YAP1

Project description:Verteporfin (VP) inhibts colon cancer growth in vivo and in cell lines by inducing high molecular weight oligomerization of proteins. The antitumor effect of VP is independent of its YAP inhibitor activity. Tumor hypoxia contributes partly to antitumor effect of VP by impairing clearance of VP-induced high molecular weight aggregates.

2015-10-14 | PXD002793 | Pride

Interlocking core regulatory circuits enable viral hijacking in Merkel cell carcinoma

Project description:Merkel Cell carcinoma (MCC) is an aggressive neuroendocrine skin cancer. The conditions and cell type(s) of MCC are unknown. Virus positive MCC (VP-MCC) is driven by T antigens expressed from integrated Merkel cell polyomavirus (MCPyV). We found that VP-MCC required lineage-specific neuroendocrine transcription factors (TFs), including ATOH1, INSM1, ISL1, LHX3, POU4F3, and SOX2 that were central to core regulatory (CR) transcriptional circuitry. MCPyV small T antigen and host CR TFs co-bound VP-MCC super enhancers while T antigen expression was directly regulated by LHX3 and ISL1, establishing an interlocking network between host CR circuitry and the oncovirus. Moreover, MCPyV integration sites were enriched near VP- MCC super enhancers, further suggesting a functional relationship between viral oncogenesis and core neuroendocrine circuitry.

2025-05-24 | GSE261681 | GEO

Global gene expression analysis of vascular progenitors differentiated from human embryonic stem cells or induced pluripotent stem cells and their corresponding donor starting cells

Project description:Global gene expression analysis of CD31+ / CD146 +/- vascular progenitors (VP) derived from (a) human embryonic stem cells (VP-hESC), (b) adult fibroblast derived induced pluripotent stem cells (VP-AdF-iPSC), and (c) stromal primed cord blood CD34+ myeloid progenitor derived iPSC (VP-sp-CB-iPSC), (d) corresponding iPSC, and (e) corresponding starting fibroblasts and myeloid progenitors.

2017-12-31 | GSE44429 | GEO

Project description:p15

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Global gene expression analysis of vascular progenitors differentiated from human embryonic stem cells or induced pluripotent stem cells, corresponding donor starting cells, and mature human endothelial cells

2013-10-17 | GSE44926 | GEO

Transcriptomic landscape of mammalian ventral pallidum at single-cell resolution

Project description:The ventral pallidum (VP) is critical for motivated behaviors. While contemporary work has begun to elucidate the functional diversity of VP neurons, the molecular heterogeneity underlying this functional diversity remains incompletely understood. We used snRNA-seq and in situ hybridization to define the transcriptional taxonomy of VP cell types in mice, macaques, and baboons. We found transcriptional conservation between all three species, within the broader neurochemical cell types. Unique dopaminoceptive and cholinergic subclusters were identified and conserved across both primate species but had no homolog in mice. This harmonized consensus VP cellular atlas will pave the way for understanding the structure and function of the VP and identified key neuropeptides, neurotransmitters, and neuro receptors that could be targeted within specific VP cell types for functional investigations.

2024-10-30 | GSE277465 | GEO

Adaptations in nucleus accumbens neuron subtypes mediate negative affective behaviors in fentanyl abstinence II

Project description:We used RNAseq to evaluate baseline expression of NPAS+ VP translatomes in comparison to bulk VP translatomes.

2022-11-28 | GSE218580 | GEO

Monocyte membrane-coated nanoparticles (MoNP)-Verteporfin (VP) treatment alleviated the TNFalpha-induced inflammatory response in Endothelial cells

Project description:Atherosclerosis, characterized by the buildup of plaque in arteries, is a major cause of cardiovascular mortality worldwide, as there is no efficient strategy for targeted therapy. However, we have developed a new drug delivery platform called MoNP, which is loaded with VP, a potent inhibitor of YAP/TAZ signaling. To investigate the MoNP-VP treatment effect, EC were pretreated with MoNP or MoNP-VP then induced the inflammation by TNFalpha. After TNFalpha treatment, the cells were collected and extracted the RNA for RNA sequencing (RNA-Seq). The results showed that MoNP-VP significantly decreased the expression of YAP/TAZ-targeted genes and inflammatory markers while upregulating atheroprotective genes. Overall, these findings suggest that MoNP-VP has the potential to serve as an effective drug delivery platform for atherosclerosis.

2024-10-23 | GSE229918 | GEO

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Project description:Visceral pain (VP) is a global problem with complex etiologies and limited therapeutic options. Guanylyl cyclase C (GUCY2C), an intestinal receptor producing cyclic GMP which regulates luminal fluid secretion, has emerged as a therapeutic target for VP. Indeed, FDA-approved GUCY2C agonists ameliorate VP in patients with chronic constipation syndromes, although analgesic mechanisms remain obscure. Here, we reveal that intestinal GUCY2C is selectively enriched in neuropod cells, a type of enteroendocrine cell that synapses with submucosal neurons, in mice and humans. GUCY2CHigh neuropod cells associate with co-cultured dorsal root ganglia neurons and induce hyperexcitability, reducing the rheobase and increasing the resulting number of evoked action potentials. Conversely, the GUCY2C agonist linaclotide eliminated neuronal hyperexcitability produced by GUCY2C-sufficient, but not GUCY2C-deficient, neuropod cells, an effect independent of bulk epithelial cells or extracellular cGMP. Genetic elimination of intestinal GUCY2C amplified nociceptive signaling and VP that was comparable to chemically-induced VP but refractory to linaclotide. Importantly, eliminating GUCY2C selectively in neuropod cells also increased nociceptive signaling and VP that was refractory to linaclotide. In the context of loss of GUCY2C hormones in patients with VP, these observations suggest a specific role for neuropod GUCY2C signaling in the pathophysiology and treatment of these pain syndromes.

2023-02-09 | GSE207870 | GEO

Project description:Global gene expression analysis of FACS-purified CD31+CD146+ vascular progenitors (VP) derived from (a) human embryonic stem cells (VP-hESC), (b) adult fibroblast derived induced pluripotent stem cells (VP-AdF-iPSC), (c) stromal primed cord blood CD34+ myeloid progenitor derived iPSC (VP-sp-CB-iPSC), (d) corresponding starting fibroblasts and myeloid progenitors, (e) human umbilical vein endothelial cells, and (f) human dermal microvascular endothelial cells. Total RNA was harvested from (a) adult fibroblasts, (b) human myeloid progenitors: Non-nucloefected CD34+ CB cells that were expanded with growth factors from Day -3 until Day 0 and harvested, (c) FACS-purified CD31+CD146+ vascular progenitors (VP) that were differentiated from human embryonic stem cells (hESC), (d) VP differentiated from low passage stromal-primed episomal iPSC derived from growth-factor activated cord blood myeloid progenitors, (e) VP differentiated from iPSC derived from adult fibroblasts, (f) human umbilical vein endothelial cells, and (g) human dermal microvascular endothelial cells.. Illumina HumanHT-12 V4.0 expression beadchips were used for all analyses in this series. Three or independent samples of each sample type were each run on individual microarrays.

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