Mocarski edward (43 risultati)

108 pp.; 21.6 x 19.6 cm.; glue bound; black-and-white & color; edition size unknown; unsigned and unnumbered; offset-printed Exhibition catalogue published in conjunction with show held February 17 - March 14, 1981. Texts by Laurence Dreiband, Peter Plagens, Michael Kurcfeld, and Walter Gabrielson. Artists include Laurence Dreiband, Walter Gabrielson, Peter Plagens, Lita Albuquerque, Peter Alexander, Martha Alf, Chuck Arnoldi, Don Bachardy, Joel Bass, Billy Al Bengston, Tony Berlant, Doug Bond, Paul Brach, William Brice, Jerrold Burchman, Carole Caroompas, Karen Carson, Judy Chicago, Max Cole, Ron Cooper, Mary Corse, Ron Davis, James DeFrance, Tony DeLap, Richard Diebenkorn, Laddie Dill, Paul Dillon, Dan Douke, Bruce Everett, Llyn Foulkes, Sam Francis, Joe Goode, Scott Grieger, D.J. Hall, Marvin Harden, Charles Christopher Hill, Patrick Hogan, Richard Joseph, Craig Kauffman, Claude Kent, Peter Liashkov, Ron Linden, Peter Lodato, John Mandel, Jay McCafferty, David Mocarski, Ed Moses, James Murray, John Okulick, Margit Omar, Edward Ruscha, Miriam Schapiro, Don Sorenson, Masami Teraoka, Joyce Treiman, James Valerio, Guy Williams, Tom Wudl, and Norman Zammitt. Includes images of artworks included in the exhibition as well as photographs of the artists. Good. 1.6 cm. and 6 mm. tears to bottom edges of spine with additional rubbing of spine edges. Rubbing and dust soiling of covers with 1 cm., 1 mm., and 4 mm. areas of soiling to recto. Loosening of glue binding along inside of front and back covers, text block still attached to spine. …

Hardcover. Condizione: new. Hardcover. 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. Shipping may be from multiple locations in the US or from the UK, depending on stock availability.…

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Hardcover. Condizione: new. Hardcover. 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. Shipping may be from our Sydney, NSW warehouse or from our UK or US warehouse, depending on stock availability.…

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Taschenbuch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - 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 likepseudokinase(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.…

Buch. Condizione: Neu. Druck auf Anfrage Neuware - Printed after ordering - 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 likepseudokinase(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.…

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Condizione: New. 1st ed. 2023 edition NO-PA16APR2015-KAP.

Taschenbuch. Condizione: Neu. Alternate Programmed Cell Death Signaling in Antiviral Host Defense | Edward S. Mocarski (u. a.) | Taschenbuch | Current Topics in Microbiology and Immunology | v | Englisch | 2025 | Springer | EAN 9783031452802 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu. …

Condizione: Hervorragend. Zustand: Hervorragend | Sprache: Englisch | Produktart: Bücher | 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.…

Hardcover. Condizione: Brand New. 179 pages. 9.26x6.10x0.55 inches. In Stock.

Hardcover. Condizione: gut. 2023. Alternate Programmed Cell Death Signaling in Antiviral Host Defense In deutscher Sprache. pages.

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Buch. Condizione: Neu. Neuware - This comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein-Barr virus, Kaposi's Sarcoma-associated herpesvirus, cytomegalovirus, HHV6A, 6B and 7, and varicella-zoster virus. The viral diseases and cancers they cause are significant and often recurrent. Their prevalence in the developed world accounts for a major burden of disease, and as a result there is a great deal of research into the pathophysiology of infection and immunobiology. Another important area covered within this volume concerns antiviral therapy and the development of vaccines. All these aspects are covered in depth, both scientifically and in terms of clinical guidelines for patient care. The text is illustrated generously throughout and is fully referenced to the latest research and developments. …

Gebunden. Condizione: New. This definitive and comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein Barr virus, cytomegalovirus and va.

Condizione: New. pp. 1408.

Condizione: New. pp. 1408.

Condizione: New. pp. 1408 242 Illus. (85 Col.).