Ontology highlight
ABSTRACT:
PROVIDER: PRJNA197365 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression profiles of primary cortical neurons after knocking down Tdp-43
| PRJNA197368 | ENA
Project description:Expression profiles of primary cortical neurons after knocking down Cugbp1
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Project description:Expression profiles of primary cortical neurons after knocking down Fus
| PRJNA152895 | ENA
Project description:To clarify the functional properties of Tdp-43, we established the differentially expressed alternative exons in Tdp-43-silenced primary cortical neurons by using exon-sensitive microarray technology. We analyzed total RNA of primary motor neuron infected with lentivirus expressing shRNA against mouse Tdp-43 or control. RNA was harvested 11 days after transfection.
2013-04-18 | E-GEOD-46146 | biostudies-arrayexpress
Project description:To clarify the functional properties of Tdp-43, we established the differentially expressed alternative exons in Tdp-43-silenced primary cortical neurons by using exon-sensitive microarray technology.
2013-04-18 | GSE46146 | GEO
Project description:We generated total mRNA libraries and ribosome footprint libraries from motor neuron-like cells (MN1) and primary cortical neurons expressing GFPor pure wild type cells as control, human TDP-43 wild type and mutant proteins to identify translational targets of human TDP-43 mutant protein
2018-10-08 | GSE111775 | GEO
Project description:Mutation in TDP-43 is causative to amyotrophic lateral sclerosis (ALS). TDP-43 is a multifunctional ribonucleoprotein and is reproted to regulate thousands of genes in neurons, but how astrocytes contribute to TDP-43 pathogenesis is not known. This study examined how mutant TDP-43 in astrocytes kills motor neurons and causes ALS phenotypes. Primary astrocytes were isolated from transgenic rats expressing mutant TDP-43 or from control rats without mutant TDP-43 expression. Cultured astrocytes were induced to express mutant human TDP-43 and their gene expression profiles were determined by microarray assays. Microarray analysis revealed that hundreds of genes were altered in astrocytes in response to mutant TDP-43 expression.
2013-05-20 | GSE42091 | GEO
Project description:We identify the RNA targets of TAR DNA-binding protein 43 (TDP-43) from cortical neurons by RNA immunoprecipitation followed by deep sequencing (RIP-seq). We identify 4352 highly enriched RNA targets of TDP-43. We determined that the canonical TDP-43 binding site (TG)n was 55.1-fold enriched in our TDP-43 library. Moreover, our analysis shows there is often an adenine in the middle of the motif, (TG)nTA(TG)m. TDP-43 RNA targets are particularly enriched for Gene Ontology terms related to RNA metabolism, neuronal development, and synaptic function. Examination of TDP-43 RNA targets in rat cortical neurons by RIP-seq. Chantelle F. Sephton isolated the TDP-43:RNA complexes and generated the cDNA library for deep sequencing. Email: chantelle.sephton@utsouthwestern.edu Phone: 214-648-4119 Fax: 214-648-1801 ULR: http://www8.utsouthwestern.edu/utsw/cda/dept120915/files/151135.html Organization name: University of Texas Southwestern Medical Center at Dallas Department: Neuroscience Lab: Gang Yu lab Street: 6000 Harry Hines Blvd. City: Dallas State: Texas ZIP: 75390 Country: USA
2010-11-04 | E-GEOD-25032 | biostudies-arrayexpress
Project description:Mutation in TDP-43 is causative to amyotrophic lateral sclerosis (ALS). TDP-43 is a multifunctional ribonucleoprotein and is reproted to regulate thousands of genes in neurons, but how astrocytes contribute to TDP-43 pathogenesis is not known. This study examined how mutant TDP-43 in astrocytes kills motor neurons and causes ALS phenotypes. Primary astrocytes were isolated from transgenic rats expressing mutant TDP-43 or from control rats without mutant TDP-43 expression. Cultured astrocytes were induced to express mutant human TDP-43 and their gene expression profiles were determined by microarray assays. Microarray analysis revealed that hundreds of genes were altered in astrocytes in response to mutant TDP-43 expression. As mutant TDP-43 transgene is under the control of tetracycline-regulated pomoter elements (TRE), mutant TDP-43 expression is subjected to Doxycline regulation. Astrocytes isolated from GFAP-tTA/TRE-TDP43M337V rats were desiginated as M337V groups and astrocytes isolated from GFAP-tTA single transgenic rats were desiginated as tTA control groups. Total RNA was isolated from cultured astrocytes at varying times (3, 4, or 6 days after Dox withdrawal) after mutant TDP-43 was induced in astrocytes. Upon mutant TDP-43 induction in astroyctes, gene expression profiles in astroyctes were determined by Illumina Direct Hybridization Assay and compared between tTA and M337V groups at the varying time points of mutant TDP-43 induction.
2013-05-20 | E-GEOD-42091 | biostudies-arrayexpress
Project description:Dominant mutations in unrelated genes cause fronto-temporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) and include VCP, which is associated with multisystem proteinopathy (MSP). Conditional inactivation of VCP in postnatal forebrain neurons (VCP cKO) caused cortical brain atrophy, neuronal loss, autophago-lysosomal dysfunction, TDP-43 inclusions and hyperactivity. Quantitative proteomics and single nuclei RNA sequencing on VCP cKO brains identified synaptogenesis and the unfolded protein response as the most decreased and increased pathways respectively. Conditional expression of a single MSP disease mutation, VCP-R155C, in cortical neurons similarly recapitulated features of VCP inactivation and FTLD-TDP. Comparison of transcriptomic and proteomic datasets from genetically defined FTD patients revealed that profiles from GRN carriers were similar to VCP insufficiency. These data support a deficiency in VCP dependent functions as the pathogenic mechanism of FTLD-TDP and reveal an unexpected pathogenic similarity with progranulin deficiency. Enhancing VCP function may be therapeutic in MSP and related forms of FTLD-TDP.
2021-08-06 | PXD026685 | Pride