PMC:7105343 / 79610-80446 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7105343","sourcedb":"PMC","sourceid":"7105343","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7105343","text":"JAK-signal transducer and activator of transcription (STAT), the suppressor of cytokine signaling protein 1 (SOCS1), and SOCS3.\nIFN-I are major antiviral molecules, and coronaviruses have evolved diverse strategies to counter the IFN-I response during infection.\nThis study uses endoplasmic reticulum stress and IFN-I production after infection with transmissible gastroenteritis virus (TGEV) to understand how coronavirus-elicited ER stress is actively involved in viral replication and manipulates the host IFN-I response.\nIncreased SOCS1 or SOCS3 expression impaired the IFN-I antiviral response, promoting TGEV replication.\nIRE1α is an endoplasmic reticulum stress sensor, which led to the increased expression of negative regulators of JAK-STAT SOCS1 and SOCS3.\nTherefore, IRE1α may be a novel target against 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