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

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

PROVIDER: PRJNA838016 | ENA |

REPOSITORIES: ENA

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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

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

RNA-seq analysis of Trpm7-deficient muscle satellite cells

Project description:Muscle satellite cells (MuSCs), skeletal muscle-resident stem cells, are crucial for regeneration of myofibers. Molecular factors such as cations that trigger the transition of MuSCs from a quiescent to an active state remain largely unidentified. In this study, we identified TRPM7, a Mg2+-permeable ion channel, as a critical determinant for myofiber regeneration. We investigated gene profiles of Trpm7-deficient MuSCs to understand the role of TRPM7 during myogenesis. Our results suggest that TRPM7 governs the myogenesis, cell-cycle progression and mitochondrial biosynthesis in satellite cells to regulate crucial events (ie, activation, proliferation, and myogenesis) during skeletal muscle regeneration.

2025-04-04 | GSE290352 | GEO

TRPM7 maintains progenitor-like features of neuroblastoma cells

2014-12-10 | GSE64000 | GEO

Profiling of villi transcriptome in Trpm7 gene deficient mice and control littermates.

Project description:To attain deeper insight into metabolic alterations in Trpm7 gene deficient mice we used microarrays for profiling of transcripts in villi of Trpm7 ko and control mice. We identified a set of gene networks up- or down-regulated in villi of Trpm7 gene deficient mice.

2019-02-01 | GSE110613 | GEO

Essential Role of Mg2+ for Mouse Preimplantation Embryo Development Revealed by TRPM7 Chanzyme Deficient Gametes

Project description:TRPM7 (transient receptor potential cation channel subfamily M member 7) is a chanzyme with channel and kinase domains essential for embryo development. Using gamete-specific Trpm7-null lines, we report that TRPM7-mediated Mg2+ influx is indispensable for reaching the blastocyst stage. TRPM7 was expressed dynamically from gametes to blastocysts, displaying stage-specific and distinct localizations on the plasma membrane, cytoplasm, and nucleus, and undergoes cleavage that produces C- terminal kinase fragments. TRPM7 underpinned Mg2+ homeostasis throughout this time, and excess Mg2+ but not Zn2+ or Ca2+ overcame the arrest of Trpm7-null embryos; expressing Trpm7 mRNA restored development, but mutant versions failed or were less effective. Transcriptomic analyses of embryos lacking Trpm7 revealed an abundance of oxidative stress-pathway genes, confirmed by mitochondrial dysfunction, and a reduction of transcription factor networks essential for proliferation; Mg2+ supplementation corrected these defects. Hence, TRPM7 underpins Mg2+ homeostasis in preimplantation embryos, prevents oxidative stress, and promotes gene expression patterns necessary for developmental progression and cell lineage specification.

2024-01-22 | GSE241487 | GEO

Genome-wide comparative analysis of gene expression in wild type (WT3) and TRPM7-/- (K09) mouse embryonic stem cells

Project description:TRPM7 is a ubiquitous ion channel and kinase, a unique ‘chanzyme’, required for proper early embryonic development. In order to assess the effects of TRPM7 activity on cellular gene expression, mouse embryonic stem cells with TRPM7 gene deletion (TRPM7-/- mESC) were established. By using microarray analysis, we identified genes with transcription significantly different in TRPM7-deficient mESC.

2014-04-15 | GSE55578 | GEO

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