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The effect of TRPM7 kinase inactivation on expression levels of the genes involved in insulin production and cell cycle regulation in pancreatic islets

ABSTRACT: The effect of TRPM7 kinase inactivation on expression levels of the genes involved in insulin production and cell cycle regulation in pancreatic islets

PROVIDER: PRJNA901956 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22301369.fastq.gz	Fastqsanger.gz
	SRR22301370.fastq.gz	Fastqsanger.gz
	SRR22301371.fastq.gz	Fastqsanger.gz
	SRR22301372.fastq.gz	Fastqsanger.gz
	SRR22301373.fastq.gz	Fastqsanger.gz

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Similar Datasets

The effect of TRPM7 kinase inactivation on expression levels of the genes involved in insulin production and cell cycle regulation in pancreatic islets

Project description:To investigate the function of TRPM7 kinase in the regulation of insulin production and beta cell proliferation, we used a mouse model harboring a single point mutation at the active site of the enzyme Trpm7tm1.1Mkma (K1646R, Trpm7R/R) We then performed gene expression profiling analysis using data obtained from RNA-seq of isolated islets of Trpm7R/R mice and their control littermates after 16 weeks exposure to the obesogenic diet

2023-03-08 | GSE218030 | GEO

Whole-genome profiling of human HAP1 cells after the genetic and pharmacological inactivation of TRPM7

Project description:The project aims to attain deeper insight into the role of TRPM7 in the regulation of cellular pathways. We identified a set of differently expressed genes in HAP1 cells after the genetic or pharmacological inactivation of TRPM7.

2024-07-01 | GSE203013 | GEO

Expression data comparing adult human islets to human embryonic stem cell-derived insulin-positive and insulin-negative cells

Project description:The study was completed to compare expression profiles of primary human beta cells (in the form of adult human islets), to the expression profile of hESC-derived beta-like cells. A HES3 line modified by homologous recombination to express GFP under the insulin promoter allowed us to FACS sort the hESC-derived cells into purified insulin-positive (presumably beta-like cells), and insulin-negative populations. Expression profile of adult human islets from cadaveric donors is compared to insulin-positive and insulin-negative populations of hESC-derived beta-like cells

2012-09-09 | E-GEOD-40709 | biostudies-arrayexpress

Regulated and adaptive in vivo insulin secretion from islets only containing β-cells

Project description:The activity of pancreatic islets’ insulin-producing β-cells is closely regulated by systemic cues and, locally, by adjacent islet hormone-producing “non-β-cells” (namely α-, δ- and γ-cells). Still, it is unclear whether the presence of the non-β-cells is a requirement for accurate insulin secretion. Here, we generated and studied a mouse model in which adult islets are exclusively composed of β-cells, and human pseudoislets containing only primary β-cells. Mice lacking non-β-cells had optimal blood glucose regulation. They exhibited enhanced glucose tolerance, insulin sensitivity and restricted body weight gain under high-fat diet. The insulin secretion dynamics in islets composed of only β-cells was like in intact islets, both in homeostatic conditions and upon extreme insulin demand. Similarly, human β-cell pseudoislets retained the glucose-regulated mitochondrial respiration, insulin secretion and exendin-4 responses of human islets comprising all four cell types. Together, the findings indicate that non-β-cells are dispensable for blood glucose homeostasis and β-cell function. This is particularly relevant in diabetes, where non-β-cells become dysfunctional and worsen the disease’s pathophysiology. These results support efforts aimed at developing diabetes treatments by generating β-like cell clusters devoid of non-β-cells, as for example from human embryonic stem cells and/or by in situ conversion of non-β-cells into insulin producers.

2024-07-19 | GSE226479 | GEO

TRPM7 maintains progenitor-like features of neuroblastoma cells

Project description:Analysis of the effect of shRNA-mediated knockdown of TRPM7 on gene expression levels in SH-SY5Y and SH-EP2 human neuroblastoma cells. Results were used for the identification of neural-crest-associated transcription factors that were affected by TRPM7 knockdown. Total RNA isolated from SH-EP2 and SH-SY5Y human neuroblastoma cells transduced with a scrambled shRNA (control) or TRPM7 shRNA, experiment performed in duplicate.

2014-12-10 | E-GEOD-64000 | biostudies-arrayexpress

Expression profiles from HEK293 cells by overexpression of TRPM7 channel

Project description:The functional activity of TRPM7 is essential for cell viability and growth, and its expression is up-regulated in certain pathological conditions. In order to assess the effects of TRPM7 activity on cellular gene expression, inducible HEK293 cell-lines harboring the wild-type mouse TRPM7 and a mutant lacking the kinase domain were established. By using microarray analysis, we identified genetic profiles altered in transcription significantly and specifically by the expression of the functional TRPM7 channel. Overexpression of TRPM7 channel in HEK cells induce the cell damage and cell death. So we used tetracycline-inducible system for channel expression. However, since the treatment of inducer itself could also affect the transcription profile, we established another cell-line harboring a nonfunctional TRPM7 mutant (TRPM7DKD) as a control in which the entire kinase domain at the C-terminus was deleted. The wild-type and the non-functional TRPM7 channels were induced transiently, and the comparative changes in cellular transcription were investigated

2011-07-22 | E-GEOD-23102 | biostudies-arrayexpress

TRPM7 maintains mesenchymal phenotype of breast cancer cells by tensional regulation of SOX4 (TRPM7 shRNA)

Project description:Analysis of the effect of shRNA-mediated knockdown of TRPM7 on gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of so-called epithelial-mesenchymal transcription factors that were affected by TRPM7 knockdown and for the analysis of overlapping up- and downregulated genes in shT7#1 + shSOX4#1 MDA-MB-231 cells

2015-06-16 | GSE63956 | GEO

Expression profiles from HEK293 cells by overexpression of TRPM7 channel

2011-07-23 | GSE23102 | GEO

TRPM7 maintains progenitor-like features of neuroblastoma cells

2014-12-10 | GSE64000 | GEO

Reduced basal insulin secretion from islets isolated from tafazzin deficient mice is associated with reduced mitochondrial function

Project description:Tafazzin is a transacylase which causes the content and molecular structure of cardiolipin (CL) to be altered in the inner mitochondrial membrane. The enzymatic machinery responsible for oxidative respiration are localized to the inner mitochondrial membrane and require CL for activity. As a result, tafazzin is critical for maintaining mitochondrial function. In beta-cells, which are the insulin secreting cells in pancreatic islets, mitochondrial function is linked to insulin secretion. We previously established that tafazzin knock-down mice were lean and maintained insulin sensitivity compared to the obese insulin resistant control litter mates. However, it was unknown whether tafazzin deficiency also influenced insulin secretion in the establishment of the lean phenotype. Using X week-old mice, we ascertained that the number of beta-cells was similar between genotypes. Ex vivo insulin secretion under low glucose conditions was reduced (52%) from islets isolated from tafazzin knock-down mice. Consistent with this tafazzin knock-down mice exhibited reduced fasting insulin plasma insulin levels. Measurement of mitochondrial oxygen consumption revealed that basal oxygen consumption was reduced (58%) in islets from tafazzin-deficient animals. The addition of etomoxir, an inhibitor of mitochondrial fatty acid translocation, significantly elevated basal mitochondrial respiration (5-fold) in islets from tafazzin knockdown mice, indicating a significant fatty acid-mediated inhibitory effect. In contrast, etomoxir lacked any measurable effect on control wild-type islets. The altered mitochondrial function identified in taffazin knock-down islets was not associated with reduced CL content or elevated oxyCL species. Our experiments indicate that tafazzin plays a key role in regulating normal islet beta-cell function.

2021-07-31 | GSE136242 | GEO

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