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10.1007/s11033-021-07071-9 http://scihub22266oqcxt.onion/10.1007/s11033-021-07071-9 35028855!8758217!35028855     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35028855&cmd=llinks): Failed to open stream: HTTP request failed! 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Mini review ATF4 and GRP78 as novel molecular targets in ER-Stress modulation for critical COVID-19 patients |pdf=|usr=}}{{35028855}} gab.com Text Mini review ATF4 and GRP78 as novel molecular targets in ER-Stress modulation for critical COVID-19 patients JO: Mol Biol Rep http://www.kidney.de/pget.php?&tw=1&pmid=35028855 #FOAvip Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in more than 4.4 million deaths worldwide as of August 24, 2021. Viral infections such as SARS-CoV2 are associated with endoplasmic reticulum (ER) stress and also increased the level of reactive oxygen species. Activating transcription factor 4 (ATF4) is preferentially translated under integrated stress conditions and controls the genes involved in protein homeostasis, amino acid transport and metabolism, and also protection from oxidative stress. The GRP78, regulated either directly or indirectly by ATF4, is an essential chaperone in the ER and overexpressed and appears on the surface of almost all cells during stress and function as a SARS-CoV2 receptor. In this mini-review article, we briefly discuss the effects of SARS-CoV2 infection on the ER stress, and then the stress modulator functions of ATF4 and GRP78 as novel therapeutic targets were highlighted. Finally, the effects of GRP78 inhibitory components as potential factors for targeted therapies for COVID-19 critical cases were discussed. Twit Text FOAVip Mini review ATF4 and GRP78 as novel molecular targets in ER-Stress modulation for critical COVID-19 patients ????Mol Biol Rep http://www.kidney.de/pget.php?&tw=1&pmid=35028855 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35028855 #FOAvip English Wikipedia <ref>{{Cite pmid|35028855}}</ref> Mini review ATF4 and GRP78 as novel molecular targets in ER-Stress modulation for critical COVID-19 patients #MMPMID35028855 Shahriari-Felordi M; Alikhani HK; Hashemian SR; Hassan M; Vosough M Mol Biol Rep 2022[Feb]; 49 (2): 1545-1549 PMID35028855show ga Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in more than 4.4 million deaths worldwide as of August 24, 2021. Viral infections such as SARS-CoV2 are associated with endoplasmic reticulum (ER) stress and also increased the level of reactive oxygen species. Activating transcription factor 4 (ATF4) is preferentially translated under integrated stress conditions and controls the genes involved in protein homeostasis, amino acid transport and metabolism, and also protection from oxidative stress. The GRP78, regulated either directly or indirectly by ATF4, is an essential chaperone in the ER and overexpressed and appears on the surface of almost all cells during stress and function as a SARS-CoV2 receptor. In this mini-review article, we briefly discuss the effects of SARS-CoV2 infection on the ER stress, and then the stress modulator functions of ATF4 and GRP78 as novel therapeutic targets were highlighted. Finally, the effects of GRP78 inhibitory components as potential factors for targeted therapies for COVID-19 critical cases were discussed. |Activating Transcription Factor 4/*metabolism[MESH] |COVID-19/*metabolism[MESH] |Endoplasmic Reticulum Chaperone BiP/*metabolism[MESH] |Endoplasmic Reticulum Stress/*physiology[MESH] |Humans[MESH]Mini review ATF4 and GRP78 as novel molecular targets in ER-Stress mod(epmc).pdf DeepDyve Pubget Overpricing