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10.3390/cells10082022 http://scihub22266oqcxt.onion/10.3390/cells10082022 34440791!8392315!34440791     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34440791&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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cells 2021 ; 10 (8): ä Nephropedia Template TP {{tp|p=34440791|t=2021. The Molecular Interplay between Human Coronaviruses and Autophagy |pdf=|usr=}}{{34440791}} gab.com Text The Molecular Interplay between Human Coronaviruses and Autophagy JO: Cells http://www.kidney.de/pget.php?&tw=1&pmid=34440791 #FOAvip Coronavirus disease 2019 (COVID-19), caused by a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has instantaneously emerged as a worldwide pandemic. However, humans encountered other coronaviruses in the past, and they caused a broad range of symptoms, from mild to life-threatening, depending on the virus and immunocompetence of the host. Most human coronaviruses interact with the proteins and/or double-membrane vesicles of autophagy, the membrane trafficking pathway that degrades and recycles the intracellular protein aggregates, organelles, and pathogens, including viruses. However, coronaviruses often neutralize and hijack this pathway to complete their life cycle. In this review, we discuss the interactions of human coronaviruses and autophagy, including recent data from SARS-CoV-2-related studies. Some of these interactions (for example, viral block of the autophagosome-lysosome fusion), while being conserved across multiple coronaviruses, are accomplished via different molecular mechanisms. Therefore, it is important to understand the molecular interplay between human coronaviruses and autophagy for developing efficient therapies against coronaviral diseases. Twit Text FOAVip The Molecular Interplay between Human Coronaviruses and Autophagy ????Cells http://www.kidney.de/pget.php?&tw=1&pmid=34440791 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34440791 #FOAvip English Wikipedia <ref>{{Cite pmid|34440791}}</ref> The Molecular Interplay between Human Coronaviruses and Autophagy #MMPMID34440791 Shroff A; Nazarko TY Cells 2021[Aug]; 10 (8): ä PMID34440791show ga Coronavirus disease 2019 (COVID-19), caused by a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has instantaneously emerged as a worldwide pandemic. However, humans encountered other coronaviruses in the past, and they caused a broad range of symptoms, from mild to life-threatening, depending on the virus and immunocompetence of the host. Most human coronaviruses interact with the proteins and/or double-membrane vesicles of autophagy, the membrane trafficking pathway that degrades and recycles the intracellular protein aggregates, organelles, and pathogens, including viruses. However, coronaviruses often neutralize and hijack this pathway to complete their life cycle. In this review, we discuss the interactions of human coronaviruses and autophagy, including recent data from SARS-CoV-2-related studies. Some of these interactions (for example, viral block of the autophagosome-lysosome fusion), while being conserved across multiple coronaviruses, are accomplished via different molecular mechanisms. Therefore, it is important to understand the molecular interplay between human coronaviruses and autophagy for developing efficient therapies against coronaviral diseases. |*Autophagy[MESH] |COVID-19/metabolism/physiopathology[MESH] |Coronavirus Infections/metabolism/*physiopathology[MESH] |Coronavirus/*metabolism[MESH] |Humans[MESH] |Lysosomes[MESH]The Molecular Interplay between Human Coronaviruses and Autophagy (epmc).pdf DeepDyve Pubget Overpricing