Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA215741 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression of the human choroid plexus epithelium (CPE)
| PRJNA215742 | ENA
Project description:We investigated the gene expression of the human CPE in Braak stadia 0, 3 and 6.We isolated CPE cells with laser dissection microscopy from healthy human donor choroid plexus tissues and from human choroid plexus tissue from brains that were post-mortem staged in Braak 3 and Braak 6 Alzheimer disease stages . Next, we performed RNA isolation, amplification, labeling and hybridization against 44k Agilent microarrays.
2014-12-31 | GSE61196 | GEO
Project description:We investigated the gene expression of the human CPE.We isolated CPE cells from healthy human donor choroid plexus tissues with laser dissection microscopy. Next, we performed RNA isolation, amplification, labeling and hybridization against 44k Agilent microarrays. We performed the microarrays against a common reference sample, namely human RPE/choroid RNA. We performed 7 replicates of human CPE samples from 7 different donors.
2013-09-27 | E-GEOD-49969 | biostudies-arrayexpress
Project description:Choroid plexus carcinomas (CPC) are poorly understood and frequently lethal brain tumors with minimal treatment options. Using a new mouse model of the disease and a large cohort of human CPCs [GSE60892; GSE60899], we performed a cross-species, genome-wide search for novel oncogenes within syntenic regions of chromosome gain. TAF12, NFYC and RAD54L, co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3, were identified as oncogenes that are gained in tumors in both species and required to initiate and progress the disease in mice. TAF12 and NFYC are transcription factors that regulate the epigenome, while RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained, novel oncogenes that cooperate in the formation of CPC and unmask potential new avenues for therapy. CPC mouse model samples of tumors derived from choroid plexus epithelium (CPE) cells that are Tp53/RB/Pten null in FVB mice. Female CD1 nude (host) mice were transfected with postanatal CPE and compared with a medulloblastoma normal mouse embryonic, postnatal and adult controls (loxP TP53/RB/PTEN (no Cre)) Implanted and reimplanted are from the orthotropic transplants of the primary tumor or later tumors
2015-05-01 | E-GEOD-61659 | biostudies-arrayexpress
Project description:Gene expression profiles generated from human tumor cells laser-microdissected from surgical samples of seven choroid plexus papillomas (Grade I WHO) as eight samples of epithelial cells lasermicrodissected from normal choroid plexus obtained at autopsy. Choroid plexus tumors are rare pediatric brain tumors derrived from the choroid plexus epithelium. Gene expression profiles of lasermicrodissected tumor cells from 7 individual choroid plexus tumor samples obtained at surgery were compared to gene expression profiles from non-neoplastic choroid plexus epithelial cells lasermicrodissected from normal non-neoplastic choroid plexus obtained at autopsy (Am J Surg Pathol. 2006 Jan;30(1):66-74.) in order to identfy genes differentially expressed in choroid plexus tumor cells.
2009-02-01 | E-GEOD-14098 | biostudies-arrayexpress
Project description:Choroid Plexus Gene Expression in ApoE3 or ApoE4-Knockin Mouse Choroid Plexuses
| PRJNA339308 | ENA
Project description:We investigated the gene expression of the human CPE.We isolated CPE cells from healthy human donor choroid plexus tissues with laser dissection microscopy. Next, we performed RNA isolation, amplification, labeling and hybridization against 44k Agilent microarrays.
2013-09-27 | GSE49969 | GEO
Project description:The choroid plexus (CP) secretes cerebrospinal fluid and is critical for the development and function of the brain. In the telencephalon, the CP epithelium (CPe) arises from the Wnt- and Bmp- expressing cortical hem. We examined the role of canonical Wnt signaling in CPe development and report that the mouse and human embryonic CPe expresses molecules in this pathway. Either loss of function or constitutive activation of β-catenin, a key mediator of canonical Wnt signaling, causes a profound disruption of mouse CPe development. Loss of β-catenin results in a dysmorphic CPe, while constitutive activation of β-catenin causes a loss of CPe identity and a transformation of this tissue to a hippocampal-like identity. Aspects of this phenomenon are recapitulated in human embryonic stem cell (hESC)-derived organoids. Our results indicate that canonical Wnt signaling is required in a precisely regulated manner for normal CP development in the mammalian brain.
2021-11-01 | GSE162784 | GEO