https://www.zbp.at/en/
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https://www.stjude.org/media-resources/news-releases/2022-medicine-science-news/zbp1-links-interferon-treatment-and-cell-death-during-covid-19.html
Scientists from St. Jude Children's Research Hospital have shown that the innate immune sensor, ZBP1, and its associated inflammatory cell death pathway, PANoptosis, are major contributors to the negative effects of interferon treatment and high interferon levels in some COVID-19 patients. The work was published today in Science Immunology.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5863909/
Recent studies have identified ZBP1 as an innate sensor of viral infections and a target of viral evasion strategies, regulating cell death, inflammasome activation and proinflammatory responses. ZBP1 also functions during development and can trigger perinatal lethality when its RHIM-dependent interactions are not restricted.
https://pubmed.ncbi.nlm.nih.gov/35587515/
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19), continues to cause substantial morbidity and mortality in the ongoing global pandemic. Understanding the fundamental mechanisms that govern innate immune and inflammatory resp
https://pubmed.ncbi.nlm.nih.gov/34686350/
ADAR1 suppresses this PANoptosis by interacting with the Zα2 domain of ZBP1 to limit ZBP1 and RIPK3 interactions. Adar1 fl/fl LysM cre mice are resistant to development of colorectal cancer and melanoma, but deletion of the ZBP1 Zα2 domain restores tumorigenesis in these mice. In addition, treating wild-type mice with IFN-γ and the NEI KPT
https://www.science.org/doi/pdf/10.1126/sciimmunol.aag2045
generation of Zbp1−/− mice (11-13). ZBP1 was of potential interest be-causeofitsunknownroleininnateimmunesensinganditspossiblerole in the regulation of cell
https://www.rcmguide.com/bcbs-prefix-list-zaa-to-zzz/
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https://www.cell.com/cell-reports/pdf/S2211-1247(21)01325-5.pdf
Combining IFNs with NEIs induces ZBP1-mediated inflammatory cell death, PANoptosis. ADAR1 negatively regulates the ZBP1-mediated PANoptosis. Blocking ADAR1 activity unleashes ZBP1-mediated PANoptosis to inhibit tumorigenesis. In mice, IFN-g + KPT-330 dramatically regresses tumors in a ZBP1-dependent manner.
https://journals.aai.org/jimmunol/article/203/5/1348/107474/ZBP1-DAI-Drives-RIPK3-Mediated-Cell-Death-Induced
The perinatal lethality of Ripk1-deficient mice remained largely unexplained for 15 y, until three studies demonstrated that this lethal phenotype could be rescued by the concurrent ablation of both FADD/caspase-8-mediated apoptosis and RIPK3-driven necroptosis pathways (4-6).Mice triply deficient in Ripk1, Ripk3, and either Fadd or Caspase-8 exhibit no overt developmental defects, matured
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https://pubmed.ncbi.nlm.nih.gov/29236673/
Recent studies have identified ZBP1 as an innate sensor of viral infections and a target of viral evasion strategies, regulating cell death, inflammasome activation, and proinflammatory responses. ZBP1 also functions during development and can trigger perinatal lethality when its RHIM-dependent interactions are not restricted.
https://pubmed.ncbi.nlm.nih.gov/31358656/
In this study, we show that Z-form nucleic acid binding protein 1 (ZBP1; also known as DAI) drives IFN-stimulated cell death in settings of RIPK1 deficiency. IFN-activated Jak/STAT signaling induces robust expression of ZBP1, which complexes with RIPK3 in the absence of RIPK1 to trigger RIPK3-driven pathways of caspase-8-mediated apoptosis and
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6902032/
The Manifestation of PAN-optosis (Pyroptosis, Apoptosis, and Necroptosis) Cell death plays key roles in infection and immunity, as programmed cell death is often part of the host anti-microbial strategy (Man and Kanneganti, 2016; Jorgensen et al., 2017; Van Opdenbosch and Lamkanfi, 2019).The innate immune system recognizes microbial infections through its pattern recognition receptors (PRRs
https://journals.aai.org/jimmunol/article/200/4/1489/106514/IRF1-Is-a-Transcriptional-Regulator-of-ZBP1
IFN regulatory factor (IRF)1 was the first member of the IRF family of transcription factors and was initially identified as a regulator of IFNs and IFN-stimulated genes (ISGs) (14, 15).The antiviral functions of IRF1 were revealed after generation of Irf1 −/− mice, and IRF1 was shown to selectively restrict replication of certain classes of viruses ().
https://rupress.org/jem/article/214/8/2217/42511/ZBP1-DAI-ubiquitination-and-sensing-of-influenza
Innate immune sensors activate programmed cell death pathways as an antiviral and antibacterial mechanism to exert host defense (Man and Kanneganti, 2016; Jorgensen et al., 2017).Influenza A virus (IAV) is a negative sense single-stranded RNA virus that belongs to the family Orthomyxoviridae.IAV infection initiates when the virus infects epithelial lining of the respiratory tract.
https://www.scientificarchives.com/article/newly-identified-function-of-caspase-6-in-zbp1-mediated-innate-immune-responses-nlrp3-inflammasome-activation-panoptosis-and-host-defense
Caspases are critical for regulating cell death, immune responses, and homeostasis. These cysteine-dependent endoproteases cleave their substrates after certain aspartic acid residues. So far, thirteen caspases have been discovered in mice and humans. They are composed of an N-terminal pro-domain of variable size and a C-terminal protease domain consisting of one small and one large catalytic
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