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10.1099/jgv.0.000623 http://scihub22266oqcxt.onion/10.1099/jgv.0.000623 C5203671!5203671!27902314     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27902314&cmd=llinks): Failed to open stream: HTTP request failed! 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Newcastle disease virus degrades HIF-1? through proteasomal pathways independent of VHL and p53 |pdf=|usr=}}{{27902314}} gab.com Text Newcastle disease virus degrades HIF-1 through proteasomal pathways independent of VHL and p53 JO: J Gen Virol http://www.kidney.de/pget.php?&tw=1&pmid=27902314 #FOAvip Newcastle disease virus (NDV) is a candidate agent for oncolytic virotherapy. Despite its potential, the exact mechanism of its oncolysis is still not known. Recently, we reported that NDV exhibited an increased oncolytic activity in hypoxic cancer cells. These types of cells negatively affect therapeutic outcome by overexpressing pro-survival genes under the control of the hypoxia-inducible factor (HIF). HIF-1 is a heterodimeric transcriptional factor consisting of a regulated ? (HIF-1?) and a constitutive ? subunit (HIF-1?). To investigate the effects of NDV infection on HIF-1? in cancer cells, the osteosarcoma (Saos-2), breast carcinoma (MCF-7), colon carcinoma (HCT116) and fibrosarcoma (HT1080) cell lines were used in the present study. Data obtained showed that a velogenic NDV infection diminished hypoxia-induced HIF-1? accumulation, leading to a decreased activation of its downstream target gene, carbonic anhydrase 9. This NDV-induced downregulation of HIF-1? occurred post-translationally and was partially abrogated by proteasomal inhibition. The process appeared to be independent of the tumour suppressor protein p53. These data revealed a correlation between NDV infection and HIF-1? downregulation, which highlights NDV as a promising agent to eliminate hypoxic cancer cells. Twit Text FOAVip Newcastle disease virus degrades HIF-1 through proteasomal pathways independent of VHL and p53 ????J Gen Virol http://www.kidney.de/pget.php?&tw=1&pmid=27902314 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27902314 #FOAvip English Wikipedia <ref>{{Cite pmid|27902314}}</ref> Newcastle disease virus degrades HIF-1? through proteasomal pathways independent of VHL and p53 #MMPMID27902314 Abd-Aziz N; Stanbridge EJ; Shafee N J Gen Virol 2016[Dec]; 97 (12): 3174-82 PMID27902314show ga Newcastle disease virus (NDV) is a candidate agent for oncolytic virotherapy. Despite its potential, the exact mechanism of its oncolysis is still not known. Recently, we reported that NDV exhibited an increased oncolytic activity in hypoxic cancer cells. These types of cells negatively affect therapeutic outcome by overexpressing pro-survival genes under the control of the hypoxia-inducible factor (HIF). HIF-1 is a heterodimeric transcriptional factor consisting of a regulated ? (HIF-1?) and a constitutive ? subunit (HIF-1?). To investigate the effects of NDV infection on HIF-1? in cancer cells, the osteosarcoma (Saos-2), breast carcinoma (MCF-7), colon carcinoma (HCT116) and fibrosarcoma (HT1080) cell lines were used in the present study. Data obtained showed that a velogenic NDV infection diminished hypoxia-induced HIF-1? accumulation, leading to a decreased activation of its downstream target gene, carbonic anhydrase 9. This NDV-induced downregulation of HIF-1? occurred post-translationally and was partially abrogated by proteasomal inhibition. The process appeared to be independent of the tumour suppressor protein p53. These data revealed a correlation between NDV infection and HIF-1? downregulation, which highlights NDV as a promising agent to eliminate hypoxic cancer cells. äNewcastle disease virus degrades HIF-1? through proteasomal pathways i(epmc).pdf DeepDyve Pubget Overpricing