Background: Interferon regulatory factor 6 functions (IRF6) exhibits tumor-suppression in multiple types of cancer. Here, the antitumor properties and pathways involved in the mechanism of IRF6 investigated in cervical cancer.
Methods: Forty-one pairs of cervical cancer specimens and para-carcinoma tissues were collected to evaluate IRF6 expression using immunohistochemical (IHC) staining and miR-587. Effects of miR-587 and IRF6 in the growth of cervical cancer cells explored by MTT test and HeLa tumor mouse xenograft model. Migration and invasion of cervical cancer cells are monitored using transwell test.
Results: Expression of IRF6 in cervical cancer specimens and cell lines were significantly reduced compared with a suitable control group. In addition, the IRF6 expression negatively correlated with miR-587 in cervical cancer tissue. Bioinformatics algorithms and luciferase tests revealed that IRF6 is a potential target of miR-587 and miR-587 mimic transfection cause significant suppression of the IRF6 protein levels in cervical cancer cells. We also found that the antineoplastic properties of IRF6 can be reversed by overexpressing miR-587 in cervical cancer cells. Upregulation of miR-587 correlated with poor overall survival in cervical cancer. In an experiment in vivo silencing of miR-587 induced tumor growth inhibition HeLa, which was associated with upregulation of IRF6 protein in the tumor.
Conclusion: miR-587 represses posttranscriptionally IRF6 protein expression to cancel the antineoplastic activity of IRF6. The miR-587 / IRF6 signaling pathway plays an important role in the development of cervical cancer and serve as a potential therapeutic target for the treatment of cervical cancer.
Interferon-α2b spray inhalation did not shorten virus shedding time of SARS-CoV-2 in hospitalized patients: a preliminary matched case-control study
a mouse model of SARS-CoV-2 expressing inflammatory role of type I interferon signaling
acute respiratory syndrome-coronavirus 2 (SARS-Cov-2) has led to over 13 million cases of coronavirus disease (COVID-19) with a significant mortality rate. laboratory rat has been a supporter of the development of therapies and vaccines; However, they do not support infection by SARS-CoV virus-2 because of the inability to use the mouse orthologue inclusion of human angiotensin-converting enzyme receptor 2 (hACE2). While hACE2 support infection and pathogenesis of transgenic mice, these mice were limited in availability and are limited to a single genetic background.
Here we report the development of a mouse model of SARS-CoV-2 is based on adeno-associated virus (AAV) -mediated expression of hACE2. These mice support replication of the virus and showed pathological findings were found in 19 patients COVID. In addition, we show that type I interferon does not control the SARS-CoV-2 replication in vivo but is a significant driver of pathological response. Thus, AAV-hACE2 rat models enables rapid deployment for a strong following in-depth analysis of SARS-CoV infection-2 with patient derived virus is authentic in mice genetically diverse backgrounds.
ELISA Kit for Mouse Interferon-stimulated gene 20 kDa protein
Description: Recombinant Interferon gamma is a disulfide-linked homodimeric protein consisting of 134 amino acid residues, and migrates as an approximately 16 kDa protein under non-reducing and reducing conditions in SDS-PAGE. Optimized DNA sequence encoding murine Interferon-gamma mature chain was expressed in E. coli.
Description: Recombinant Interferon gamma is a disulfide-linked homodimeric protein consisting of 134 amino acid residues, and migrates as an approximately 16 kDa protein under non-reducing and reducing conditions in SDS-PAGE. Optimized DNA sequence encoding murine Interferon-gamma mature chain was expressed in E. coli.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β1b in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β1b in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β1b in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β1a in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β1a in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A competitive ELISA for quantitative measurement of Mouse Interferon β1a in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A sandwich ELISA for quantitative measurement of Mouse Interferon ω1 in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A sandwich ELISA for quantitative measurement of Mouse Interferon ω1 in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A sandwich ELISA for quantitative measurement of Mouse Interferon ω1 in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A sandwich ELISA for quantitative measurement of Mouse Interferon alpha in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A sandwich ELISA for quantitative measurement of Mouse Interferon alpha in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Description: A sandwich ELISA for quantitative measurement of Mouse Interferon alpha in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. This is a high quality ELISA kit developped for optimal performance with samples from the particular species.
Toxoplasma encephalitis is an AIDS-defining condition. The decline in CD4 + T cell IFN-γ-producing AIDS is a major factor in silent reactivation of Toxoplasma gondii to replicate the active stage of infection. Therefore, it is important to characterize the CD4-independent mechanisms that limit acute T. gondii infection. We investigated the in vivo regulation of IFN-γ production by CD8 + T cells, DN T cells and NK cells in response to acute T. gondii infection.
Our data suggest that IFN-γ treatment by non-CD4 cells is dependent on both IL-12 and IL-18, and secretion of bioactive IL-18 in response to T. gondii parasite requires sensing inflammasome feasible by multiple redundant sensors in several hematopoietic cell types.
Ricardo
