Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA131859 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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.
2011-07-23 | GSE23102 | GEO
Project description:Magnesium is essential for cellular life, but how it is homeostatically controlled still remains poorly understood. Here we report that members of CNNM family, which have been controversially implicated in both cellular Mg2+ influx and efflux, selectively bind to the TRPM7 channel to stimulate divalent cation entry into cells. Co-expression of CNNMs with the channel markedly increased uptake of divalent cations, which is prevented by an inactivating mutation to the channel’s pore. Knockout of Trpm7 in cells or application of the TRPM7-channel inhibitor NS8593 also interfered with CNNM-stimulated divalent cation uptake. Conversely, knockout of CNNM3 and CNNM4 in HEK-293 cells significantly reduced TRPM7-mediated divalent cation entry, without affecting TRPM7 protein expression or its cell surface levels. Furthermore, we found that cellular overexpression of Phosphatases of Regenerating Liver (PRLs), a known CNNMs binding partner, stimulated TRPM7-dependent divalent cation entry and that CNNMs were required for this activity. Whole-cell electrophysiological recordings demonstrated that deletion of CNNM3 and CNNM4 from HEK-293 cells interfered with heterologously expressed and native TRPM7 channel function. We conclude that CNNMs employ the TRPM7 channel to mediate divalent cation influx and that CNNMs also possess separate TRPM7-independent Mg2+ efflux activities that contribute to CNNMs’ control of cellular Mg2+ homeostasis.
2021-11-15 | PXD026635 | Pride
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
Project description:Expression data from HEK293 cells with or without MIBP1 overexpression
| PRJNA136797 | ENA
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
Project description:TRPM7 is a ubiquitous ion channel and kinase, a unique M-bM-^@M-^XchanzymeM-bM-^@M-^Y, 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. Total RNA was extracted from cells using Qiagen RNAeasy Plus mini Kit. Triplicate samples were made for each wild type clone 3 (WT3) and and TRPM7-/- clone 9 (KO9) mESC
2014-04-15 | E-GEOD-55578 | biostudies-arrayexpress
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO