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RNA sequencing of WNK1 and SLUG co-overexpressed LNCaP cells

ABSTRACT: RNA sequencing of WNK1 and SLUG co-overexpressed LNCaP cells

PROVIDER: PRJNA470608 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7130920_1.fastq.gz	Fastqsanger.gz
	SRR7130920_2.fastq.gz	Fastqsanger.gz
	SRR7130921_1.fastq.gz	Fastqsanger.gz
	SRR7130921_2.fastq.gz	Fastqsanger.gz
	SRR7130922_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of WNK1 and SLUG co-overexpressed LNCaP cells

Project description:Human prostate cancer LNCaP cells Overexpressed with rat WNK 1 and human SLUG cDNA

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WNK1 enforces macrophage lineage fidelity

Project description:The appropriate development of myeloid progenitors into macrophages, the body’s professional phagocyte, is essential for organismal development, especially in mammals1. This dependence is exemplified by the observation that loss-of-function mutation in colony stimulating factor 1 receptor (CSF1R) results in multiple tissue abnormalities including osteopetrosis2. Despite this importance, little is known about the molecular and cell biological regulation of macrophage development. Here, we report the surprising finding that the chloride-sensing kinase With-no-lysine 1 (WNK1) is required for embryonic development of tissue-resident macrophages (TRMs). Myeloid-specific deletion of Wnk1 caused a dramatic loss of TRMs and subsequently disrupted organ development, induced systemic neutrophilia, and resulted in mortality between 3 and 4 weeks of age. Specifically, we observed that WNK1 absence stalled macrophage differentiation at the myeloid multipotent progenitor (MPP) stage, instead skewing MPP differentiation towards granulopoiesis. Mechanistically, the cognate CSF1R cytokine, macrophage-colony stimulating factor (M-CSF), triggers macropinocytosis in myeloid progenitors, which in turn induces phosphorylation of WNK1. Importantly, macropinocytosis by myeloid progenitors increases cytosolic chloride, which is directly sensed by WNK1. Perturbing chloride flux during macropinocytosis, inhibiting WNK1 chloride-sensing, and blocking macropinocytosis each skew progenitor differentiation from macrophage lineage to granulocyte lineage. Thus, we have uncovered a novel mechanism that links a cell biological process to a molecular circuit whereby WNK1 chloride-sensing and chloride flux act downstream of M-CSF-induced macropinocytosis by multipotent progenitors to ensure macrophage lineage fidelity.

2024-02-06 | GSE196336 | GEO

Meiotic completion of the spermatocytes requires the kinase WNK1

Project description:The kinase protein WNK1 is highly expressed and phosphorylated in the testis, suggesting possible functions in regulating male fertility. Indeed, conditional pachytene-spermatocyte Wnk1 knock-out mice generated using the novel Wnt7a-Cre failed to produce functional sperm which resulted from the primary spermatogenic arrest during mid-pachynema. Global transcriptomic approaches identified ‘translation’ as one of the impacted events in Wnk1-depleted spermatocytes.

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Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel

2012-09-21 | GSE41026 | GEO

Slug overexpression

Project description:This SuperSeries is composed of the following subset Series: GSE41026: Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel GSE41027: Chip-chip from HepG2 cells and HepG2 cells with slug overexpression Refer to individual Series

2012-09-21 | E-GEOD-41028 | biostudies-arrayexpress

Analysis of anti-CD3e-induced transcriptional changes in WNK1-deficient thymocytes

Project description:RNAseq was used to analyse transcriptional changes occuring in WNK1-expressing or WNK1-deficient DN3 thymocytes following injection of anti-CD3e

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Expression analysis of HepG2, HepG2-slug and HepG2-slug on Matrigel

Project description:Investigation of whole genome gene expression level changes in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Whole genome gene expression level changes have been compared in hepatocellular carcinoma cell line hepG2 in regular culture, hepG2-slug in regular culture and hepG2-slug on Matrigel. Roche NimbleGen micro-array analysis was employed to assess global genome expression in HepG2 in regular culture, HepG2-slug in regular culture and HepG2-slug on Matrigel. The results demonstrated that the up-regulated genes and the down-regulated genes increased significantly when HepG2-slug cells with VM forming ablity were cultured on Matrigel and formed VM.

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Project description:We performed RNA-seq in JJN3 human multiple myeloma cells with or without WNK1 knockdown to profile global transcriptomic changes

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Slug-dependent UVR induction of cytokines and chemokines

Project description:Studies of the zinc finger transcription factors Slug and Snail have largely focused on their important role in modulating epithelial-mesenchymal transition during embryonic development and tumor progression. However, these transcription factors also appear to regulate local inflammation. In previous studies, we showed that Slug knockout mice were resistant to sunburn, an acute cutaneous inflammatory response, compared to wild type mice. In the present studies, we used Slug knockout, chimeric Slug knockout/wild type, conditional Slug knockout, and Slug transgenic mice to study the role of Slug in ultraviolet radiation (UVR)-induced cutaneous inflammation. We demonstrated, using immunohistochemistry, in vivo imaging, and neutrophil migration studies, that it was Slug expression in the epidermis rather than in neutrophils that modulated the UVR response. Microarray analysis indicated that this modulation was effected by the production of epidermal cytokines, including CCL3, CCL4, oncostatin, and interleukin-1β, that recruited neutrophils to UVR-exposed skin. The pattern of pro-inflammatory gene regulation by Slug suggested a central role for NF-κB in mediating gene induction. Immunohistochemical analysis of UVR-induced NF-κB activation demonstrated reduced activation in Slug knockout and enhanced activation in Slug transgenic epidermis. Slug thus appears to modulate NF-κB activation in response to UVR.

2016-08-27 | GSE86107 | GEO

WNK1 enforces macrophage lineage fidelity

Project description:WNK1 enforces macrophage lineage fidelity

| PRJNA804425 | ENA