Similar Datasets
Project description:We knocked out the CAMTA1 gene in SH-SY5Y cells and detected differences in RNA seq in wild-type and CAMTA1 KO cells
2022-09-28 | GSE205687 | GEO
Project description:The CAMTA1 mutant and Col-0 were studied under water and drought condition. The camta1 showed stunted primary root growth under osmotic stress. The expression analysis revealed drought recovery as major indicative pathway along with membrane and chloroplast related protein in camta1 under drought stress. Large number of positively regulated genes were related to osmotic balance, transporters, AP2 and ABA. We used Affymetrix expression analysis to validate the role of CAMTA1 under drought stress. The RNA of Col-0 and camta1 mutant were isolated in water and drought condition.The ATH1 gene chip was used for expression analysis.
2012-08-12 | E-GEOD-40061 | biostudies-arrayexpress
Project description:The CAMTA1 mutant and Col-0 were studied under water and drought condition. The camta1 showed stunted primary root growth under osmotic stress. The expression analysis revealed drought recovery as major indicative pathway along with membrane and chloroplast related protein in camta1 under drought stress. Large number of positively regulated genes were related to osmotic balance, transporters, AP2 and ABA. We used Affymetrix expression analysis to validate the role of CAMTA1 under drought stress.
2012-08-13 | GSE40061 | GEO
Project description:TAZ-CAMTA1 is a defining genetic aberration in the vascular cancer epithelioid hemangioendothelioma. We studied the transcriptome of TAZ-CAMTA1 and compared it to that of control or activated TAZ (TAZ4A)-expressing endothelial cells. We utilized an immortalized, mouse endothelial cell line known as MS1. We present and make available the first RNA-sequencing data of TAZ-CAMTA1's transcriptome in endothelial cells
2021-05-23 | GSE156801 | GEO
Project description:TAZ-CAMTA1 is a defining genetic aberration in the vascular cancer epithelioid hemangioendothelioma. We generated a novel transgenic mouse that expresses TAZ-CAMTA1 in endothelial cells. These mice develop vascular tumors in the lung and die by average on day 40. We isolated GFP + endothelial cells from three five-week old TRE-TAZ-CAMTA1;Cdh5-tTA;TRE-GFP mice and subjected these endothelial cells to scRNA-seq via the 10X genomics platform
2021-05-23 | GSE156803 | GEO
Project description:To identify potential mechanisms underlying the role of UBR4 in cargo trafficking, we used quantitative mass spectrometry to analyze the proteomes of wild-type and ubr4 KO HEK293T cells.
2022-03-24 | PXD020630 | Pride
Project description:Ubiquitin Specific Peptidase 7 (USP7) is a deubiquitinase of several important regulatory proteins, and important regulator of TGFb pathway. To investigate their role in cell signaling, we analyzed global mRNA levels in HEK293T cells that were knocked down with shRNAs against USP7 and non-targeting control (CTRL).
2020-10-18 | GSE139094 | GEO
Project description:To identify ZNF506 genome-wide target sites, we performed ChIP-seq assay and found that ZNF506 binding sites enriched at PBS-Pro-containing ERV subfamilies (ERVPs) and further motif calling analysis showed that ZNF506 binds to PBS-Pro sequences, promoting formation of H3K9me3 modifications at binding regions. And ChIP-seq assay also indicated that the distinction of H3K9me3 signals closed to ZNF506 peak regions between ZNF506 overexpressing (OE) HEK293T cells and ZNF506 Knockout (KO) HEK293T cells was correlated with the different recruitment of corepressor KAP1. The ChIP-seq experiments using GFP antibodies and H3K9me3 antibodies on ZNF506-GFP OE HEK293T cell lines, and ZNF417-GFP OE HEK293T cell lines were used as controls for H3K9me3 ChIP. Also, the ChIP-seq experiments were performed using H3K9me3 antibodies and KAP1 antibodies on ZNF506 KO HEK293T cells and ZNF506 OE HEK293T cells.
2023-07-26 | GSE209826 | GEO
Project description:To investigate the depletion of altLAMA3, we established HEK293T cell lines in which alt-LAMA3 gene has been knocked out by CRISPR-Cas9. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells
2022-06-17 | GSE205869 | GEO
Project description:The formation of long-term memory requires signaling from the synapse to the nucleus to mediate neuronal activity-dependent gene transcription. Synapse-to-nucleus communication is initiated by influx of calcium ions through synaptic NMDA receptors and/or L-type voltage-gated calcium channels and involves the activation of transcription factors by calcium/calmodulin signaling in the nucleus. Recent studies have drawn attention to a new family of transcriptional regulators, the so-called calmodulin-binding transcription activator (CAMTA) proteins. CAMTAs are expressed at particularly high levels in the mouse and human brain, and we reasoned that, as calmodulin-binding transcription factors, CAMTAs may regulate the formation of long-term memory by coupling synaptic activity and calcium/calmodulin signaling to memory-related transcriptional responses. This hypothesis is supported by genetic studies that reported a correlation between CAMTA gene polymorphisms or mutations and cognitive capability in humans. Here, we show that acute knock-down of CAMTA1, but not CAMTA2, in the hippocampus of adult mice results in impaired performance in two memory tests, contextual fear conditioning and object-place recognition test. Short-term memory and neuronal morphology were not affected by CAMTA knock-down. Gene expression profiling in the hippocampus of control and CAMTA knock-down mice revealed a number of putative CAMTA1 target genes related to synaptic transmission and neuronal excitability. Patch clamp recordings in organotypic hippocampal slice cultures provided further evidence for CAMTA1-dependent changes in electrophysiological properties. In summary, our study provides experimental evidence that confirms previous human genetic studies and establishes CAMTA1 as a regulator of long-term memory formation.
2016-05-20 | GSE62122 | GEO