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10.4049/jimmunol.2100742 http://scihub22266oqcxt.onion/10.4049/jimmunol.2100742 34819389!8702473!34819389     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2022 ; 208 (1): 74-84 Nephropedia Template TP {{tp|p=34819389|t=2022. ORAI1 Limits SARS-CoV-2 Infection by Regulating Tonic Type I IFN Signaling |pdf=|usr=}}{{34819389}} gab.com Text ORAI1 Limits SARS-CoV-2 Infection by Regulating Tonic Type I IFN Signaling JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34819389 #FOAvip ORAI1 and stromal interaction molecule 1 (STIM1) are the critical mediators of store-operated Ca(2+) entry by acting as the pore subunit and an endoplasmic reticulum-resident signaling molecule, respectively. In addition to Ca(2+) signaling, STIM1 is also involved in regulation of the type I IFN (IFN-I) response. To examine their potential role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we generated ORAI1 and STIM1 knockout human HEK293-angiotensin-converting enzyme 2 cells and checked their responses. STIM1 knockout cells showed strong resistance to SARS-CoV-2 infection as a result of enhanced IFN-I response. On the contrary, ORAI1 deletion induced high susceptibility to SARS-CoV-2 infection. Mechanistically, ORAI1 knockout cells showed reduced homeostatic cytoplasmic Ca(2+) concentration and severe impairment in tonic IFN-I signaling. Transcriptome analysis showed downregulation of multiple antiviral signaling pathways in ORAI1 knockout cells, likely because of reduced expression of the Ca(2+)-dependent transcription factors of the AP-1 family and MEF2C Accordingly, modulation of homeostatic Ca(2+) concentration by pretreatment with ORAI1 blocker or agonist could influence baseline IFNB expression and resistance to SARS-CoV-2 infection in a human lung epithelial cell line. Our results identify a novel role of ORAI1-mediated Ca(2+) signaling in regulating the tonic IFN-I levels, which determine host resistance to SARS-CoV-2 infection. Twit Text FOAVip ORAI1 Limits SARS-CoV-2 Infection by Regulating Tonic Type I IFN Signaling ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34819389 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34819389 #FOAvip English Wikipedia <ref>{{Cite pmid|34819389}}</ref> ORAI1 Limits SARS-CoV-2 Infection by Regulating Tonic Type I IFN Signaling #MMPMID34819389 Wu B; Ramaiah A; Garcia G Jr; Hasiakos S; Arumugaswami V; Srikanth S J Immunol 2022[Jan]; 208 (1): 74-84 PMID34819389show ga ORAI1 and stromal interaction molecule 1 (STIM1) are the critical mediators of store-operated Ca(2+) entry by acting as the pore subunit and an endoplasmic reticulum-resident signaling molecule, respectively. In addition to Ca(2+) signaling, STIM1 is also involved in regulation of the type I IFN (IFN-I) response. To examine their potential role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we generated ORAI1 and STIM1 knockout human HEK293-angiotensin-converting enzyme 2 cells and checked their responses. STIM1 knockout cells showed strong resistance to SARS-CoV-2 infection as a result of enhanced IFN-I response. On the contrary, ORAI1 deletion induced high susceptibility to SARS-CoV-2 infection. Mechanistically, ORAI1 knockout cells showed reduced homeostatic cytoplasmic Ca(2+) concentration and severe impairment in tonic IFN-I signaling. Transcriptome analysis showed downregulation of multiple antiviral signaling pathways in ORAI1 knockout cells, likely because of reduced expression of the Ca(2+)-dependent transcription factors of the AP-1 family and MEF2C Accordingly, modulation of homeostatic Ca(2+) concentration by pretreatment with ORAI1 blocker or agonist could influence baseline IFNB expression and resistance to SARS-CoV-2 infection in a human lung epithelial cell line. Our results identify a novel role of ORAI1-mediated Ca(2+) signaling in regulating the tonic IFN-I levels, which determine host resistance to SARS-CoV-2 infection. |A549 Cells[MESH] |Angiotensin-Converting Enzyme 2/genetics/metabolism[MESH] |COVID-19/immunology/*metabolism[MESH] |Calcium Signaling[MESH] |Clustered Regularly Interspaced Short Palindromic Repeats[MESH] |Disease Resistance[MESH] |Disease Susceptibility[MESH] |Gene Expression Profiling[MESH] |HEK293 Cells[MESH] |Humans[MESH] |Interferon Type I/*metabolism[MESH] |Lung/*immunology/virology[MESH] |MEF2 Transcription Factors/genetics[MESH] |Neoplasm Proteins/genetics/*metabolism[MESH] |ORAI1 Protein/genetics/*metabolism[MESH] |Respiratory Mucosa/*metabolism[MESH] |SARS-CoV-2/*physiology[MESH] |Stromal Interaction Molecule 1/genetics/*metabolism[MESH]ORAI1 Limits SARS-CoV-2 Infection by Regulating Tonic Type I IFN Signa(epmc).pdf DeepDyve Pubget Overpricing