Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.virol.2020.06.008 http://scihub22266oqcxt.onion/10.1016/j.virol.2020.06.008 32838947!7297182!32838947     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Virology 2020 ; 548 (ä): 59-72 Nephropedia Template TP {{tp|p=32838947|t=2020. N6-methyladenosine regulates PEDV replication and host gene expression |pdf=|usr=}}{{32838947}} gab.com Text N6-methyladenosine regulates PEDV replication and host gene expression JO: Virology http://www.kidney.de/pget.php?&tw=1&pmid=32838947 #FOAvip Methylation of the N6 position of adenosine (m(6)A) is a widespread RNA modification that is critical for various physiological and pathological processes. Although this modification was also found in the RNA of several viruses almost 40 years ago, its biological functions during viral infection have been elucidated recently. Here, we investigated the effects of viral and host RNA methylation during porcine epidemic diarrhea virus (PEDV) infection. The results demonstrated that the m(6)A modification was abundant in the PEDV genome and the host methyltransferases METTL3 and METTL14 and demethylase FTO were involved in the regulation of viral replication. The knockdown of the methyltransferases increased PEDV replication while silencing the demethylase decreased PEDV output. Moreover, the proteins of the YTHDF family regulated the PEDV replication by affecting the stability of m(6)A-modified viral RNA. In particular, PEDV infection could trigger an increasement of m(6)A in host RNA and decrease the expression of FTO. The m(6)A modification sites in mRNAs and target genes were also altered during PEDV infection. Additionally, part of the host responses to PEDV infection was controlled by m(6)A modification, which could be reversed by the expression of FTO. Taken together, our results identified the role of m(6)A modification in PEDV replication and interactions with the host. Twit Text FOAVip N6-methyladenosine regulates PEDV replication and host gene expression ????Virology http://www.kidney.de/pget.php?&tw=1&pmid=32838947 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32838947 #FOAvip English Wikipedia <ref>{{Cite pmid|32838947}}</ref> N6-methyladenosine regulates PEDV replication and host gene expression #MMPMID32838947 Chen J; Jin L; Wang Z; Wang L; Chen Q; Cui Y; Liu G Virology 2020[Sep]; 548 (ä): 59-72 PMID32838947show ga Methylation of the N6 position of adenosine (m(6)A) is a widespread RNA modification that is critical for various physiological and pathological processes. Although this modification was also found in the RNA of several viruses almost 40 years ago, its biological functions during viral infection have been elucidated recently. Here, we investigated the effects of viral and host RNA methylation during porcine epidemic diarrhea virus (PEDV) infection. The results demonstrated that the m(6)A modification was abundant in the PEDV genome and the host methyltransferases METTL3 and METTL14 and demethylase FTO were involved in the regulation of viral replication. The knockdown of the methyltransferases increased PEDV replication while silencing the demethylase decreased PEDV output. Moreover, the proteins of the YTHDF family regulated the PEDV replication by affecting the stability of m(6)A-modified viral RNA. In particular, PEDV infection could trigger an increasement of m(6)A in host RNA and decrease the expression of FTO. The m(6)A modification sites in mRNAs and target genes were also altered during PEDV infection. Additionally, part of the host responses to PEDV infection was controlled by m(6)A modification, which could be reversed by the expression of FTO. Taken together, our results identified the role of m(6)A modification in PEDV replication and interactions with the host. |*Gene Expression Regulation[MESH] |*Virus Replication[MESH] |Adenosine/*analogs & derivatives/metabolism[MESH] |Animals[MESH] |Cell Line[MESH] |Chlorocebus aethiops[MESH] |Coronavirus Infections/*veterinary[MESH] |Genome, Viral[MESH] |Host-Pathogen Interactions/*genetics[MESH] |Methylation[MESH] |Porcine epidemic diarrhea virus/*physiology/ultrastructure[MESH] |Protein Binding[MESH] |RNA, Viral[MESH] |RNA-Binding Proteins/metabolism[MESH] |Swine[MESH] |Swine Diseases/*genetics/*virology[MESH]N6-methyladenosine regulates PEDV replication and host gene expression(epmc).pdf DeepDyve Pubget Overpricing