Cytokine Signaling Small Molecule Antagonist of Suppressor of Enhancement of Antiviral Immunity by Johnson

Methylation and mRNA expression levels of P15, death-associated protein kinase, and suppressor of cytokine signaling-1 genes in multiple myeloma

Objective(s): The aim of this study was to investigate the methylation status and mRNA expression levels of P15, death-associated protein kinase (DAPK), and suppressor of cytokine signaling-1 (SOCS1) genes in multiple myeloma (MM). Materials and Methods: The bone marrow samples of 54 MM patients were collected and the methylation status of the P15, DAPK, and SOCS1 gene promoter regions was dete...

Genome-wide computational prediction of miRNAs in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) revealed target genes involved in pulmonary vasculature and antiviral innate immunity

The current outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)in China threatened humankind worldwide. The coronaviruses contains the largest RNA genome among all other known RNA viruses, therefore the disease etiology can be understood by analyzing the genome sequence of SARS-CoV-2. In this study, we used an ab-intio based computational tool VMir to scan the complete geno...

Cytokine Signaling 1 Immunity by Targeting Suppressor of Type I IFN Signaling in Antiviral Innate Inducible microRNA-155 Feedback Promotes

HSV-1-induced SOCS-1 expression in keratinocytes: use of a SOCS-1 antagonist to block a novel mechanism of viral immune evasion.

Keratinocytes are important for the acute phase of HSV-1 infection and subsequent persistence in sensory nervous tissue. In this study, we showed that keratinocytes (HEL-30) were refractory to IFN-gamma induction of an antiviral state to HSV-1 infection, while IFN-gamma did induce an antiviral state in fibroblasts (L929). This led us to examine the possible role of suppressor of cytokine signal...

Npgrj_ni_1287 1..7

Suppressor of cytokine signaling 1 (SOCS1) is a critical regulator of cytokine signaling and immune responses. SOCS1-deficient mice develop severe inflammatory disease, but are very resistant to viral infections. Using neutralizing antibody to type I interferon (IFN-a and IFN-b) and mice deficient in interferon-c or type I interferon receptor components (IFNAR1 or IFNAR2), we demonstrate here t...