Alternate Programmed Cell Death Signaling in Antiviral Host Defense [[electronic resource] /] / edited by Edward S. Mocarski, Pratyusha Mandal

• Record Nr.: UNINA9910770261503321
• Autore: Mocarski Edward S
• Pubbl/distr/stampa: Cham : , : Springer International Publishing : , : Imprint : Springer, , 2023
• ISBN: 3-031-45278-X
• Edizione: [1st ed. 2023.]
• Descrizione fisica: 1 online resource (175 pages)
• Collana: Current Topics in Microbiology and Immunology, , 2196-9965 ; ; 442
• Altri autori (Persone): MandalPratyusha
• Disciplina: 616.9101
• Soggetti: Immunology; Medical microbiology; Virology; Medical Microbiology
• Lingua di pubblicazione: Inglese
• Formato: Materiale a stampa
• Livello bibliografico: Monografia
• Nota di contenuto: Programmed Necrosis in Host Defense -- ZBP1/DAI-dependent Cell Death Pathways in Influenza A Virus Immunity and Pathogenesis -- Pyroptosis in Antiviral Immunity -- Manipulation of Host Cell Death Pathways by Herpes Simplex Virus -- Subversion of Programed Cell Death by Poxviruses -- Cell Killing by Reovirus: Mechanisms and Consequences -- Outcomes of RIP kinase signaling during neuroinvasive viral infection.
• Sommario/riassunto: This volume provides a comprehensive review of programmed cell death pathways and their fundamental role in antiviral host defense. The book deep-dives into the molecular functions and regulation of necroptosis and discusses how viruses induce and manipulate this potent innate cellular sensing system. Initially, understanding of necroptosis emerged from studies on tumor necrosis factor (TNF) signaling that showed the key role of receptor interacting protein kinase 1 (RIPK1) in the activation of receptor interacting protein kinase 3 (RIPK3) which then phosphorylates mixed lineage kinase domain like pseudokinase (MLKL) to execute cells via plasma membrane leakage of cytosolic contents. Since its discovery, multiple facets of the RIPK3-dependent necroptotic machinery have evolved where the requirements ; for execution of death varies depending on the stimulus. Virus-induced necroptosis was discovered over 10 years ago in studies on murine cytomegalovirus (MCMV) where a virus-encoded inhibitor was shown to prevent the recruitment of RIPK3 (RIP3). This transformative evidence identified a novel pathway acting independent of TNF, interferon or RIPK1 that can stop virus from infecting its natural mouse host by killing off infected cells to halt replication. Over the past decade influenza A virus (IAV), herpes simplex virus (HSV) and poxvirus vaccinia (VACV) have all been shown to trigger the pathway. Herpesviruses and poxviruses also encode inhibitors of caspase-8 whose elaboration unleashes the necroptosis pathway. IAV and other RNA viruses do not encode programmed cell death inhibitors. RIPK3 is also known to induce apoptosis by recruiting RIPK1 as shown nearly a decade ago and this dual apoptosis/necroptosis induction occurs naturally during influenza A virus infection. RIPK3 is also able to induce an inflammatory response independently of programmed cell death that can predominate to drive inflammatory disease outcomes. This volume is a must-read for researchers and advanced students in immunology and virology.

Courting Death : The Supreme Court and Capital Punishment / / Carol S. Steiker, Jordan M. Steiker

• Record Nr.: UNINA9910136111403321
• Autore: Steiker Carol S.
• Pubbl/distr/stampa: Cambridge, MA : , : Harvard University Press, , 2016
• ISBN: 9780674974838; 0674974832; 9780674974852; 0674974859
• Descrizione fisica: 390 pages ; 25 cm
• Altri autori (Persone): SteikerJordan M (Author)
• Disciplina: 345.73/0773
• Soggetti: Capital punishment - United States; Judicial review - United States; Discrimination in capital punishment - United States; Capital punishment - United States - History
• Lingua di pubblicazione: Inglese
• Formato: Materiale a stampa
• Livello bibliografico: Monografia
• Note generali: Includes Index (pp. 377-390)
• Nota di bibliografia: Includes Bibliographical References (pp. 325-372)
• Nota di contenuto: Frontmatter -- Contents -- Introduction -- 1. Before Constitutional Regulation -- 2. The Supreme Court Steps In -- 3. The Invisibility of Race in the Constitutional Revolution -- 4. Between the Supreme Court and the States -- 5. The Failures of Regulation -- 6. An Unsustainable System? -- 7. Recurring Patterns in Constitutional Regulation -- 8. The Future of the American Death Penalty -- 9. Life after Death -- Notes -- Acknowledgments -- Index
• Sommario/riassunto: Unique among Western democracies in refusing to eradicate the death penalty, the United States has attempted instead to reform and rationalize state death penalty practices through federal constitutional law. Courting Death traces the unusual and distinctive history of top-down judicial regulation of capital punishment under the Constitution and its unanticipated consequences for our time. In the 1960s and 1970s, in the face of widespread abolition of the death penalty around the world, provisions for capital punishment that had long fallen under the purview of the states were challenged in federal courts. The U.S. Supreme Court intervened in two landmark decisions, first by ; constitutionally invalidating the death penalty in Furman v. Georgia (1972) on the grounds that it was capricious and discriminatory, followed four years later by restoring it in Gregg v. Georgia (1976). Since then, by neither retaining capital punishment in unfettered form nor abolishing it outright, the Supreme Court has created a complex regulatory apparatus that has brought executions in many states to a halt, while also failing to address the problems that led the Court to intervene in the first place. While execution chambers remain active in several states, constitutional regulation has contributed to the death penalty’s new fragility. In the next decade or two, Carol Steiker and Jordan Steiker argue, the fate of the American death penalty is likely to be sealed by this failed judicial experiment. Courting Death illuminates both the promise and pitfalls of constitutional regulation of contentious social issues.