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303篇 您的检索式:作者名="LATZ"
    题名 作者 年代 出处 被引量
1Necroptosis, pyroptosis and apoptosis: an intricate game of cell death显示文摘Cell death is a fundamental physiological process in all living organisms.Its roles extend from embryonic development,organ maintenance,and aging to the coordination of immune responses and autoimmunity.In recent years,our understanding of the mechanisms orchestrating cellular death and its consequences on immunity and homeostasis has increased substantially.Different modalities of what has become known as‘programmed cell death’have been described,and some key players in these processes have been identified.We have learned more about the intricacies that fine tune the activity of common players and ultimately shape the different types of cell death.These studies have highlighted the complex mechanisms tipping the balance between different cell fates.Here,we summarize the latest discoveries in the three most well understood modalities of cell death,namely,apoptosis,necroptosis,and pyroptosis,highlighting common and unique pathways and their effect on the surrounding cells and the organism as a whole.Damien Bertheloot Eicke Latz Bernardo S.Franklin 2021Cellular & Molecular Immunology2021,18,5:84
2HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins显示文摘我们的免疫系统为对主人的任何威胁的快速的察觉基于天生、适应的免疫系统的靠近的合作。导出病原体的分子的识别被委托给特定的编码 germline 的发信号受体。一样的受体现在也作为表明例如,列在后面的织物损坏和房间死亡的错放或改变的自我分子的有效察觉者出现了血供应和随后的组织缺氧的混乱。当免除了垂死的房间时,内长的分子的许多类型被显示了挑起如此的无菌的煽动性的状态。然而,叫作 alarmins 的一组蛋白质有是强烈研究的题目的细胞内部、细胞外的功能。确实, alarmins 也能施加有益的房间家务功能,导致织物修理,或挑起有害不受管束的发炎。这组蛋白质包括高活动性的组盒子 1 蛋白质(HMGB1 ) , interleukin (IL )-1α, IL-33 和 Ca 2+-binding S100 蛋白质。这些双功能的蛋白质分享保存规章的机制,例如能分泌的线路, translational 以后修正并且酶的处理,在时空管理他们的细胞外的功能。从间充质的房间的 alarmins 的版本是有免疫力的房间能被组织损坏,和 alarmins 玩警告的高度相关的机制在急性或长期的煽动性的疾病的发展并且在癌症开发的一个关键角色。Damien Bertheloot Eicke Latz 2017Cellular & Molecular Immunology2017,14,1:40
3Targeting of Vacuolar Membrane Localized Members of the TPK Channel Family显示文摘Arabidopsis thaliana 的双人脚踏车毛孔钾隧道家庭的四个成员(TPK1, 2, 3,和 5 ) 居住在 vacuolar 膜,而 TPK4 是一条血浆膜 K+ 隧道。由构造在 TPK1 和 TPK4 之间的怪物,我们试图识别涉及 trafficking 进程并且发现 TPK1 细胞质的 C 终端域(CT ) 为 ER-是批评的隧道域 -- 象排序 Golgi 步一样。后面的指导地点的 mutagenesis,我们识别了为 TPK1 的嗯出口要求的一个 diacidic 主题(DLE ) 。然而,在 C 终点的这个 diacidic 主题没在 TPK 家庭的另外的成员之中被保存,并且排序的 TPK3 独立于它的 CT。而且, TPK1 的 14-3-3 绑定地点,为隧道激活必要,不涉及隧道排序。Marcel Dunkel Andreas Latz Karin Schumacher Thomas Muller Dirk Becker Rainer Hedrich 2008Molecular Plant2008,1,6:5
4Salt Stress Triggers Phosphorylation of the Arabidopsis Vacuolar K+ Channel TPK1 by Calcium-Dependent Protein Kinases (CDPKs)显示文摘Andreas Latz Norbert Mehlmer Simone Zapf Thomas D. Mueller Bernhard Wurzinger Barbara Pfister Edina Csaszar Rainer Hedrich Markus Teige Dirk Becker 2013Molecular Plant2013,6,4:5
5PKR stirs up inflammasomes显示文摘H James Stunden Eicke Latz 2013Cell Research2013,23,2:3
6How location and cellular signaling combine to activate the NLRP3 inflammasome显示文摘NOD-,LRR-,and pyrin domain-containing 3(NLRP3)is a cytosolic innate immune sensor of cellular stress signals,triggered by infection and sterile inflammation.Upon detection of an activating stimulus,NLRP3 transitions from an inactive homo-oligomeric multimer into an active multimeric inflammasome,which promotes the helical oligomeric assembly of the adaptor molecule ASC.ASC oligomers provide a platform for caspase-1 activation,leading to the proteolytic cleavage and activation of proinflammatory cytokines in the IL-1 family and gasdermin D,which can induce a lytic form of cell death.Recent studies investigating both the cellular requirement for NLRP3 activation and the structure of NLRP3 have revealed the complex regulation of NLRP3 and the multiple steps involved in its activation.This review presents a perspective on the biochemical and cellular processes controlling the assembly of the NLRP3 inflammasome with particular emphasis on structural regulation and the role of organelles.We also highlight the latest research on metabolic control of this inflammatory pathway and discuss promising clinical targets for intervention.Anil Akbal Alesja Dernst Marta Lovotti Matthew S.J.Mangan Róisín M.McManus Eicke Latz 2022Cellular & Molecular Immunology2022,19,11:2
7Further studies with propranolol in psychotic patients显示文摘A. Atsmon I. Blum M. Steiner A. Latz H. Wijsenbeek 1972Psychopharmacologia1972,,3:1
8Innate immune activation in neum- degenerative disease 显示文摘Heneka MT Kummer MP Latz E 2014Nat Rev Immunol2014,14,7:1
9Intracoronary autol- ogous bone marrow cell transfer after myocardial infarction: the BOOST randomized controlled clinical trial 显示文摘Wollert KC Meyer GP Latz J 2004Lan- cet2004,364,9429:1
10Involvement of toll-like receptor(TLR)2 and TLR4 in cell activation by mannuronic acid polymers 显示文摘Flo T H Ryan L Latz E 2002J Biol Chem2002,277,35:1
11The antifungal drug ampho- tericin B promotes inflammatory cytokine release by a Tall-like receptor-and CD14-dependent mechanism显示文摘San K Mambula SS Latz E 2003J Biol Chem2003,278,37:1
12Evidence for the role of G-proteins in flow stimulation ofdinoflagellate bioluminescence显示文摘Chen AK Latz MI Sobolewski P 2007Am J Physiol Regul Integr Comp Physiol2007,,5:1
13TLR-independent type I interferon induction in response to an extracellular bacterial pathogen via intracellular recognition of its DNA显示文摘Charrel-Dennis M Latz E Halmen KA 2008Cell Host Mi- crobe2008,4,6:1
14NLRP3 inflammasomes link inflammation and metabolic disease显示文摘DE NARDO D LATZ E 2011Trends Immunol2011,32,8:1
15Intracoronary autologous bone marrow cell transfer after myocardial infarction:the boost randomized controlled clinical trial显示文摘Wollert KC Meyer GP Latze J 2004Lancet2004,364,9429:1
16The Antifungal Drug Amphotericin B Promotes Inflammatory Cytokine Release by a Toll -like Receptor and CDI4 -dependent Mechanism显示文摘Keya S Salamatu S M Latz E 2003The Journal of Biological Chemistry2003,278,37:1
17Phase I and pharmacokinetic study of pemetrexed with high-dose folie acid supplementation or multivitamin supplementation in patients with locally advanced or metastatic cancer 显示文摘Takimoto CH Hammond-Thelin LA Latz JE 2007Clin Cancer Res2007,13,9:1
18The LPS receptor generates inflammatory signals from the call surface 显示文摘LATZ E VISINTIN A LIEN E 2003J Endotoxin Res2003,,9:1
19Getting closer to the dirty little secret 显示文摘Pelka K Latz E 2011Immuni- ty2011,34,4:1
20Plant diversity improves protection against soil-borne pathogens by fostering antagonistic bacterial communities显示文摘Latz E Eisenhauer N Ralll B C 2012Journal of Ecology2012,,1:1
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