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Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter

ABSTRACT: Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter

PROVIDER: PRJNA798724 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17335940_1.fastq.gz	Fastqsanger.gz
	SRR17335940_2.fastq.gz	Fastqsanger.gz
	SRR17335941_1.fastq.gz	Fastqsanger.gz
	SRR17335941_2.fastq.gz	Fastqsanger.gz
	SRR17335942_1.fastq.gz	Fastqsanger.gz

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Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter [WGS]

Project description:Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter [WGS]

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Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter [RNA-seq]

Project description:Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter [RNA-seq]

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Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter [WGS]

Project description:Alzheimer’s disease (AD) is the first leading cause of dementia which afflicts tens of millions of people worldwide. Despite many scientific progresses to dissect the molecular basis of AD from studies on various mouse models, it has been suffered from evolutionary species differences between mice and humans. Here, we report generation of a non-human primate, common marmoset (marmoset; Callithrix jacchus) model that ubiquitously expresses Amyloid-beta precursor protein (APP) transgenes with the Swedish (KM670/671NL) and Indiana (V717F) mutations. We generated two female transgenic marmosets (TG1 and TG2), whose transgene integration was thoroughly investigated by genomic PCR, whole genome sequencing (WGS) and Fluorescence in situ hybridization (FISH) analyses. Using the reprogramming technology, we confirmed the validity of the transgene expression in induced neurons in vitro. Moreover, we discovered structural changes in specific brain regions of transgenic marmosets by magnetic resonance imaging (MRI) analysis, including in the entorhinal cortex and hippocampus. In postmortem histological analysis, we detected increased Aβ plaque formation in the TG1 cerebrum at the age of 7 years, although evident neuronal loss or glial inflammation was not observed. Thus, this study summarizes our attempt to establish a non-human primate model of AD, which may be beneficial for drug development and further disease modeling in combination with other genetically engineered models.

2022-03-01 | GSE194005 | GEO

Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter [RNA-seq]

2022-03-01 | GSE192674 | GEO

Multimodal analyses of a non-human primate model harboring mutant amyloid precursor protein transgenes driven by the human EF1α promoter

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-01 | GSE194006 | GEO

Transcriptomic analysis of the spinal cords of knock-in adult mice carrying the ATXN2/TDP-43 human transgenes

Project description:Intermediate-length repeat expansions in ATAXIN-2 (ATXN2) are a strong genetic risk factor for amyotrophic lateral sclerosis (ALS). At the molecular level, ATXN2 intermediate expansions enhance TDP-43 toxicity and pathology. However, whether this triggers ALS pathogenesis at the cellular and functional level remains unknown. To investigate gene expression changes and deregulated pathways caused by ataxin-2 intermediate repeat expansions in presence/absence of mutant TDP-43, we performed RNA sequencing of whole spinal cords from knock-in mice harboring ATXN2 and TDP-43 human transgenes as well as non-transgenic mice (NTg)

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Characterization of Oncolytic Vaccinia Virus Harboring the Human IFNB1 and CES2 Transgenes.

Project description:PurposeThe purpose of this study was to assess characteristics of SJ-815, a novel oncolytic vaccinia virus lacking a functional thymidine kinase-encoding TK gene, and instead, having two human transgenes: the IFNB1 that encodes interferon ?1, and the CES2 that encodes carboxylesterase 2, which metabolizes the prodrug, irinotecan, into cytotoxic SN-38.Materials and methodsViral replication and dissemination of SJ-815 were measured by plaque assay and comet assay, respectively, and compared to the backbone of SJ-815, a modified Western Reserve virus named WI. Tumor cytotoxicity of SJ-815 (or mSJ-815, which has the murine IFNB1 transgene for mouse cancers) was evaluated using human and mouse cancer cells. Antitumor effects of SJ-815, with/without irinotecan, were evaluated using a human pancreatic cancer-bearing mouse model and a syngeneic melanoma-bearing mouse model. The SN-38/ irinotecan ratios in mouse melanoma tissue 4 days post irinotecan treatment were compared between groups with and without SJ-815 intravenous injection.ResultsSJ-815 demonstrated significantly lower viral replication and dissemination, but considerably stronger in vitro tumor cytotoxicity than WI. The combination use of SJ-815 plus irinotecan generated substantial tumor regression in the human pancreatic cancer model, and significantly prolonged survival in the melanoma model (hazard ratio, 0.11; 95% confidence interval, 0.02 to 0.50; p=0.013). The tumor SN-38/irinotecan ratios were over 3-fold higher in the group with SJ-815 than those without (p < 0.001).ConclusionSJ-815 demonstrates distinct characteristics gained from the inserted IFNB1 and CES2 transgenes. The potent antitumor effects of SJ-815, particularly when combined with irinotecan, against multiple solid tumors make SJ-815 an attractive candidate for further preclinical and clinical studies.

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2019-05-15 | GSE40974 | GEO

Transcriptomic changes mediated by β-amyloid in human aortic endothelial cells (HAOEC)

Project description:We found that β-amyloid accumulation is modulated in HAOEC cells by overexpression or blocking of lncRNA BACE1-AS, which in turn regulates both BACE1 mRNA and protein expression. BACE1 is key-enzyme in the synthesis of β-amyloid from Amyloid Precursor Protein (APP). The transcriptomic changes mediated by 400nM β-amyloid was investigated in HAOEC cells.

2018-12-31 | GSE84620 | GEO

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