Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional Profiling of B19 Virus Nonstructure Protein (NS1) transduced CD36+ Erythoid Progenitor Cells (EPCs)

ABSTRACT: B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA CD36+ EPCs were generated from CD34+ stem cells, and transduced with B19V NS1 or control-lentivirus for 12, 24,and 48 hours. Each sample has triplicates. There are 18 samples analyzed.

ORGANISM(S): Homo sapiens

SUBMITTER: Ning zhi 

PROVIDER: E-GEOD-18906 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Human parvovirus B19 causes cell cycle arrest of human erythroid progenitors via deregulation of the E2F family of transcription factors.

Wan Zhihong Z   Zhi Ning N   Wong Susan S   Keyvanfar Keyvan K   Liu Delong D   Raghavachari Nalini N   Munson Peter J PJ   Su Su S   Malide Daniela D   Kajigaya Sachiko S   Young Neal S NS  

The Journal of clinical investigation 20100920 10

Human parvovirus B19 (B19V) is the only human pathogenic parvovirus. It causes a wide spectrum of human diseases, including fifth disease (erythema infectiosum) in children and pure red cell aplasia in immunocompromised patients. B19V is highly erythrotropic and preferentially replicates in erythroid progenitor cells (EPCs). Current understanding of how B19V interacts with cellular factors to regulate disease progression is limited, due to a lack of permissive cell lines and animal models. Here,  ...[more]

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