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10.1016/j.virol.2004.06.020 http://scihub22266oqcxt.onion/10.1016/j.virol.2004.06.020 15327892!?!15327892 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=15327892&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Virology 2004 ; 327 (1): 1-7 Nephropedia Template TP {{tp|p=15327892|t=2004. Hypoxia enhances human B19 erythrovirus gene expression in primary erythroid cells |pdf=|usr=}}{{15327892}} gab.com Text Hypoxia enhances human B19 erythrovirus gene expression in primary erythroid cells JO: Virology http://www.kidney.de/pget.php?&tw=1&pmid=15327892 #FOAvip Human B19 erythrovirus replicates in erythroid progenitors present in bone marrow and fetal tissues where partial oxygen tension is low. Here we show that infected human primary erythroid progenitor cells exposed to hypoxia (1% O2) in vitro increase viral capsid protein synthesis, virus replication, and virus production. Hypoxia-inducible factor-1 (HIF-1), the main transcription factor involved in the cellular response to reduced oxygenation, is shown to bind an HIF binding site (HBS) located in the distal part of the B19 promoter region, but the precise mechanism involved in the oxygen-sensitive upregulation of viral gene expression remains to be elucidated. Twit Text FOAVip Hypoxia enhances human B19 erythrovirus gene expression in primary erythroid cells ????Virology http://www.kidney.de/pget.php?&tw=1&pmid=15327892 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15327892 #FOAvip English Wikipedia <ref>{{Cite pmid|15327892}}</ref> Hypoxia enhances human B19 erythrovirus gene expression in primary erythroid cells #MMPMID15327892 Pillet S; Le Guyader N; Hofer T; NguyenKhac F; Koken M; Aubin JT; Fichelson S; Gassmann M; Morinet F Virology 2004[Sep]; 327 (1): 1-7 PMID15327892show ga Human B19 erythrovirus replicates in erythroid progenitors present in bone marrow and fetal tissues where partial oxygen tension is low. Here we show that infected human primary erythroid progenitor cells exposed to hypoxia (1% O2) in vitro increase viral capsid protein synthesis, virus replication, and virus production. Hypoxia-inducible factor-1 (HIF-1), the main transcription factor involved in the cellular response to reduced oxygenation, is shown to bind an HIF binding site (HBS) located in the distal part of the B19 promoter region, but the precise mechanism involved in the oxygen-sensitive upregulation of viral gene expression remains to be elucidated. |*Cell Hypoxia[MESH] |*Gene Expression Regulation, Viral[MESH] |*Transcription Factors[MESH] |*Up-Regulation[MESH] |Base Sequence[MESH] |Cells, Cultured[MESH] |DNA-Binding Proteins/metabolism[MESH] |Erythroid Precursor Cells/*virology[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit[MESH] |Molecular Sequence Data[MESH] |Nuclear Proteins/metabolism[MESH] |Parvovirus B19, Human/*genetics/metabolism/physiology[MESH] |Viral Proteins/genetics/metabolism[MESH]Hypoxia enhances human B19 erythrovirus gene expression in primary ery(epmc).pdf DeepDyve Pubget Overpricing