Research Topics
Genomes and Genes
| Lixin ZhengSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
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Detail Information
Publications
Quantitating lymphocyte programmed cell death in vitro using simple kill assaysLixin Zheng
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Methods Mol Biol 979:1-14. 2013..The detection methods discussed are generally applicable for assessing cell death in several contexts, expanded upon in further detail in subsequent chapters...
Dominant inhibition of Fas ligand-mediated apoptosis due to a heterozygous mutation associated with autoimmune lymphoproliferative syndrome (ALPS) Type IbLilia L Bi
Center for Biologics Evaluation and Research, FDA, Rockville, Maryland, USA
BMC Med Genet 8:41. 2007....- Competitive control of independent programs of tumor necrosis factor receptor-induced cell death by TRADD and RIP1Lixin Zheng
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, NIH, 9000 Rockville Pike, 10 11D09, Bethesda, MD 20892, USA
Mol Cell Biol 26:3505-13. 2006..These single transducers determine cell fate by triggering NF-kappaB activation, apoptosis, and nonapoptotic death signals through separate and competing signaling pathways... - Critical role for BIM in T cell receptor restimulation-induced deathAndrew L Snow
Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892 1508, USA
Biol Direct 3:34. 2008.... - Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survivalNicolas Bidere
Molecular Development Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nature 458:92-6. 2009..ABC DLBCL cells required CK1alpha for constitutive NF-kappaB activity, indicating that CK1alpha functions as a conditionally essential malignancy gene-a member of a new class of potential cancer therapeutic targets... 
Caspase-8 regulation by direct interaction with TRAF6 in T cell receptor-induced NF-kappaB activationNicolas Bidere
Molecular Development Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Curr Biol 16:1666-71. 2006..Our results suggest that PKCtheta independently controls CARMA1 phosphorylation and BCL10-dependent caspase-8 activation and unveil an essential role for TRAF6 as a critical adaptor linking these two convergent signaling events...- Ribosomal protein S3: a KH domain subunit in NF-kappaB complexes that mediates selective gene regulationFengyi Wan
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
Cell 131:927-39. 2007..Our observations provide insight into how NF-kappaB selectively controls gene expression... - The power and the promise of restimulation-induced cell death in human immune diseasesAndrew L Snow
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunol Rev 236:68-82. 2010..Here, we review how these advances offer a refreshing new perspective on the phenomenon of T-cell apoptosis induced through antigen restimulation, including its relevance to immune homeostasis and potential for therapeutic interventions... - The role of IL-15 in activating STAT5 and fine-tuning IL-17A production in CD4 T lymphocytesPushpa Pandiyan
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 189:4237-46. 2012..Taken together, these data indicate that IL-15 has a negative regulatory role in fine-tuning of IL-17A production and Th17-mediated inflammation... - Interferon-inducible immunity-related GTPase Irgm1 regulates IFN gamma-dependent host defense, lymphocyte survival and autophagyCarl G Feng
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892 8003, USA
Autophagy 5:232-4. 2009..We propose that Irgm1 plays a major role in maintaining T lymphocyte homeostasis during host IFN gamma responses by protecting these cells from autophagy-dependent cell death... - A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responsesFrancis Ka Ming Chan
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 278:51613-21. 2003..Thus, TNF-induced programmed necrosis is facilitated by TNFR-2 signaling and caspase inhibition and may play a role in controlling viral infection... - Amelioration of inflammatory arthritis by targeting the pre-ligand assembly domain of tumor necrosis factor receptorsGuo-Min Deng
Laboratory of Immunology, Building 10, Room 11N311, 10 Center Drive, MSC 1892, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Med 11:1066-72. 2005..Thus, targeting the PLAD may have clinical value in the treatment of human arthritis and other disorders involving receptors of the TNFR superfamily... - Requirement for caspase-8 in NF-kappaB activation by antigen receptorHelen Su
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Science 307:1465-8. 2005..These findings thus explain the paradoxical association of defective apoptosis and combined immunodeficiency in human CED... - NRAS mutation causes a human autoimmune lymphoproliferative syndromeJoao B Oliveira
Department of Laboratory Medicine, Clinical Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 104:8953-8. 2007..Our observations on the effects of NRAS activation indicate that RAS-inactivating drugs, such as farnesyltransferase inhibitors should be examined in human autoimmune and lymphocyte homeostasis disorders... - Congenital B cell lymphocytosis explained by novel germline CARD11 mutationsAndrew L Snow
Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health NIH, Bethesda, MD 20892, USA
J Exp Med 209:2247-61. 2012.... - Termination of autophagy and reformation of lysosomes regulated by mTORLi Yu
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nature 465:942-6. 2010..Thus, an evolutionarily conserved cycle in autophagy governs nutrient sensing and lysosome homeostasis during starvation... - The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-gamma-induced cell deathCarl G Feng
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 9:1279-87. 2008..Our studies identify a feedback mechanism in the T helper type 1 response that limits the detrimental effects of IFN-gamma on effector T lymphocyte survival while promoting the antimicrobial functions of IFN-gamma... - Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiencyHyung J Chun
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nature 419:395-9. 2002..Thus, caspase-8 deficiency in humans is compatible with normal development and shows that caspase-8 has a postnatal role in immune activation of naive lymphocytes... - The molecular mechanisms of regulatory T cell immunosuppressionPushpa Pandiyan
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health Bethesda, MD, USA
Front Immunol 2:60. 2011..2011; Pandiyan et al., 2011). Although these points are at variance to varying degrees with the standard model of T(reg) behavior, we will recount developing findings that support these new concepts... - ALPS-ten lessons from an international workshop on a genetic disease of apoptosisMichael J Lenardo
Molecular Development Section, Laboratory of Immunology, NIAID, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 32:291-5. 2010..Their discussions yielded ten broad messages applicable to genetic and immunological investigations of human disease... - CD4(+)CD25(+)Foxp3(+) regulatory T cells promote Th17 cells in vitro and enhance host resistance in mouse Candida albicans Th17 cell infection modelPushpa Pandiyan
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Immunity 34:422-34. 2011.... - Genetic alterations in caspase-10 may be causative or protective in autoimmune lymphoproliferative syndromeShigui Zhu
Genetics and Molecular Biology Branch, National Human Genome Research Institute, NIH, DHHS, Bethesda, MD 20892, USA
Hum Genet 119:284-94. 2006..05). Thus, different genetic variations in caspase-10 can produce contrasting phenotypic effects... - The death effector domain protein family: regulators of cellular homeostasisMichael D Tibbetts
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 4:404-9. 2003..Thus, the DED defines a family of proteins that may be pivotal to cellular homeostasis by establishing a 'cell renewal set point' that coregulates proliferation and apoptosis in parallel... - CD4+CD25+Foxp3+ regulatory T cells induce cytokine deprivation-mediated apoptosis of effector CD4+ T cellsPushpa Pandiyan
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 8:1353-62. 2007..Thus, cytokine deprivation-induced apoptosis is a prominent mechanism by which T(reg) cells inhibit effector T cell responses... - T helper 2 cells' preferred way to dieLixin Zheng
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Immunity 25:187-8. 2006 - Induction of apoptosis and activation of NF-kappaB by CD95 require different signalling thresholdsPatrick Legembre
The Ben May Institute for Cancer Research, University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA
EMBO Rep 5:1084-9. 2004..Mutations in CD95 may eliminate the tumour-suppressive function of CD95, at the same time allowing induction of survival or proliferative pathways, which could contribute to the increased risk for lymphoma seen in ALPS type Ia patients... - Crystal structure of MC159 reveals molecular mechanism of DISC assembly and FLIP inhibitionJin Kuk Yang
Department of Biochemistry, Weill Medical College of Cornell University, New York, New York 10021, USA
Mol Cell 20:939-49. 2005..This interaction apparently competes with FADD self-association and disrupts higher-order oligomerization required for caspase activation in the DISC... - Role of BCL-XL in photoreceptor survivalYun-Zheng Le
Department of Medicine, Dean A. McGee Eye Institute, Oklahoma City, OK, USA
Adv Exp Med Biol 613:69-74. 2008 - Loss of BCL-XL in rod photoreceptors: Increased susceptibility to bright light stressLixin Zheng
Department of Ophthalmology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
Invest Ophthalmol Vis Sci 47:5583-9. 2006.... - Apelin signaling antagonizes Ang II effects in mouse models of atherosclerosisHyung J Chun
Department of Medicine and Department of Anesthesiology, Stanford University School of Medicine, Stanford, California, USA
J Clin Invest 118:3343-54. 2008..Taken together, these findings indicate that apelin signaling can block Ang II actions in vascular disease by increasing NO production and inhibiting Ang II cellular signaling...