The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform
Wyne P. Lee - One of the best experts on this subject based on the ideXlab platform.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules termed damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^1–3. The underlying mechanism for PMR, however, is unknown. Here we show that the ill-characterized nerve injury-induced protein 1 (NINJ1)^4–8 — a cell surface protein with two transmembrane regions — plays an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ –/– macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and failed to release numerous intracellular proteins including High Mobility Group Box 1 (HMGB1, a known DAMP) and Lactate Dehydrogenase (LDH, a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to Citrobacter rodentium , suggesting a role for PMR in anti-bacterial host defense. Mechanistically, NINJ1 utilized an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held dogma that cell death-related PMR is a passive Event.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules known as damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^ 1 – 3 . The underlying mechanism of PMR, however, is unknown. Here we show that the cell-surface NINJ1 protein^ 4 – 8 , which contains two transmembrane regions, has an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ −/− macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and were unable to release numerous intracellular proteins including HMGB1 (a known DAMP) and LDH (a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to infection with Citrobacter rodentium , which suggests a role for PMR in anti-bacterial host defence. Mechanistically, NINJ1 used an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held idea that cell death-related PMR is a passive Event. The small transmembrane protein NINJ1 promotes plasma membrane rupture in lytic cell death associated with pyroptosis, necrosis and apoptosis.
George Pearson - One of the best experts on this subject based on the ideXlab platform.
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FIU Libraries: World War I: The Great War: Home
2013Co-Authors: George PearsonAbstract:The 100th Anniversary of the War to End All Wars begins in 2014. This libguide provides resources for the study of this Cataclysmic Event that helped shape the 20th century.
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FIU Libraries: World War I: The Great War: Citation
2013Co-Authors: George PearsonAbstract:The 100th Anniversary of the War to End All Wars begins in 2014. This libguide provides resources for the study of this Cataclysmic Event that helped shape the 20th century.
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FIU Libraries: World War I: The Great War: Get Help
2013Co-Authors: George PearsonAbstract:The 100th Anniversary of the War to End All Wars begins in 2014. This libguide provides resources for the study of this Cataclysmic Event that helped shape the 20th century.
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FIU Libraries: research: World War I: The Great War: Get Help
2013Co-Authors: George PearsonAbstract:The 100th Anniversary of the War to End All Wars begins in 2014. This libguide provides resources for the study of this Cataclysmic Event that helped shape the 20th century.
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FIU Libraries: research: World War I: The Great War: Home
2013Co-Authors: George PearsonAbstract:The 100th Anniversary of the War to End All Wars begins in 2014. This libguide provides resources for the study of this Cataclysmic Event that helped shape the 20th century.
Nobuhiko Kayagaki - One of the best experts on this subject based on the ideXlab platform.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules termed damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^1–3. The underlying mechanism for PMR, however, is unknown. Here we show that the ill-characterized nerve injury-induced protein 1 (NINJ1)^4–8 — a cell surface protein with two transmembrane regions — plays an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ –/– macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and failed to release numerous intracellular proteins including High Mobility Group Box 1 (HMGB1, a known DAMP) and Lactate Dehydrogenase (LDH, a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to Citrobacter rodentium , suggesting a role for PMR in anti-bacterial host defense. Mechanistically, NINJ1 utilized an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held dogma that cell death-related PMR is a passive Event.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules known as damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^ 1 – 3 . The underlying mechanism of PMR, however, is unknown. Here we show that the cell-surface NINJ1 protein^ 4 – 8 , which contains two transmembrane regions, has an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ −/− macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and were unable to release numerous intracellular proteins including HMGB1 (a known DAMP) and LDH (a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to infection with Citrobacter rodentium , which suggests a role for PMR in anti-bacterial host defence. Mechanistically, NINJ1 used an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held idea that cell death-related PMR is a passive Event. The small transmembrane protein NINJ1 promotes plasma membrane rupture in lytic cell death associated with pyroptosis, necrosis and apoptosis.
Opher S. Kornfeld - One of the best experts on this subject based on the ideXlab platform.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules termed damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^1–3. The underlying mechanism for PMR, however, is unknown. Here we show that the ill-characterized nerve injury-induced protein 1 (NINJ1)^4–8 — a cell surface protein with two transmembrane regions — plays an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ –/– macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and failed to release numerous intracellular proteins including High Mobility Group Box 1 (HMGB1, a known DAMP) and Lactate Dehydrogenase (LDH, a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to Citrobacter rodentium , suggesting a role for PMR in anti-bacterial host defense. Mechanistically, NINJ1 utilized an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held dogma that cell death-related PMR is a passive Event.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules known as damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^ 1 – 3 . The underlying mechanism of PMR, however, is unknown. Here we show that the cell-surface NINJ1 protein^ 4 – 8 , which contains two transmembrane regions, has an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ −/− macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and were unable to release numerous intracellular proteins including HMGB1 (a known DAMP) and LDH (a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to infection with Citrobacter rodentium , which suggests a role for PMR in anti-bacterial host defence. Mechanistically, NINJ1 used an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held idea that cell death-related PMR is a passive Event. The small transmembrane protein NINJ1 promotes plasma membrane rupture in lytic cell death associated with pyroptosis, necrosis and apoptosis.
Wendy Sandoval - One of the best experts on this subject based on the ideXlab platform.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules termed damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^1–3. The underlying mechanism for PMR, however, is unknown. Here we show that the ill-characterized nerve injury-induced protein 1 (NINJ1)^4–8 — a cell surface protein with two transmembrane regions — plays an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ –/– macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and failed to release numerous intracellular proteins including High Mobility Group Box 1 (HMGB1, a known DAMP) and Lactate Dehydrogenase (LDH, a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to Citrobacter rodentium , suggesting a role for PMR in anti-bacterial host defense. Mechanistically, NINJ1 utilized an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held dogma that cell death-related PMR is a passive Event.
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NINJ1 mediates plasma membrane rupture during lytic cell death
Nature, 2021Co-Authors: Nobuhiko Kayagaki, Opher S. Kornfeld, Bettina L. Lee, Irma B. Stowe, Karen O’rourke, Wendy Sandoval, Donghong Yan, Jing Kang, Juan Zhang, Wyne P. LeeAbstract:Plasma membrane rupture (PMR) is the final Cataclysmic Event in lytic cell death. PMR releases intracellular molecules known as damage-associated molecular patterns (DAMPs) that propagate the inflammatory response^ 1 – 3 . The underlying mechanism of PMR, however, is unknown. Here we show that the cell-surface NINJ1 protein^ 4 – 8 , which contains two transmembrane regions, has an essential role in the induction of PMR. A forward-genetic screen of randomly mutagenized mice linked NINJ1 to PMR. Ninj1 ^ −/− macrophages exhibited impaired PMR in response to diverse inducers of pyroptotic, necrotic and apoptotic cell death, and were unable to release numerous intracellular proteins including HMGB1 (a known DAMP) and LDH (a standard measure of PMR). Ninj1 ^ –/– macrophages died, but with a distinctive and persistent ballooned morphology, attributable to defective disintegration of bubble-like herniations. Ninj1 ^ –/– mice were more susceptible than wild-type mice to infection with Citrobacter rodentium , which suggests a role for PMR in anti-bacterial host defence. Mechanistically, NINJ1 used an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. The discovery of NINJ1 as a mediator of PMR overturns the long-held idea that cell death-related PMR is a passive Event. The small transmembrane protein NINJ1 promotes plasma membrane rupture in lytic cell death associated with pyroptosis, necrosis and apoptosis.