Research Topics
Genomes and Genes
| Jonathan D AshwellSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
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Detail Information
Publications
T cells in G1 provide a memory-like response to secondary stimulationIvana Munitic
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 174:4010-8. 2005....- Activating p38 MAPK: new tricks for an old kinasePaul R Mittelstadt
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Cell Cycle 4:1189-92. 2005..Here we discuss the structural and functional implications of this alternative p38 activation pathway, which may provide a new target for tissue-specific pharmacologic inhibition... - The many paths to p38 mitogen-activated protein kinase activation in the immune systemJonathan D Ashwell
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Rev Immunol 6:532-40. 2006..These alternative pathways might have particular relevance for cells that participate in immune and inflammatory responses... 
TWEAKing deathJonathan D Ashwell
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Cell Biol 182:15-7. 2008..These findings not only extend our appreciation of how cell death pathways are kept in check in tumors, they reinforce the possible utility of induced cIDE (cIAP deficiency) in the selective elimination of neoplastic cells...- The autoimmune suppressor Gadd45alpha inhibits the T cell alternative p38 activation pathwayJesus M Salvador
Gene Response Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 6:396-402. 2005..Thus, constitutive activation of T cell p38 through the alternative pathway is prevented by Gadd45alpha, the absence of which results in p38 activation, T cell hyperproliferation and autoimmunity... - Tumor necrosis factor receptor 2 signaling induces selective c-IAP1-dependent ASK1 ubiquitination and terminates mitogen-activated protein kinase signalingYongge Zhao
Laboratory of Immune Cell Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 282:7777-82. 2007..Moreover, in the absence of c-IAP1 TNFR2-mediated p38 and JNK activation was prolonged. Thus, the ubiquitin protein ligase activity of c-IAP1 is responsible for regulating the duration of TNF signaling in primary cells expressing TNFR2... - T cell receptor-mediated activation of p38{alpha} by mono-phosphorylation of the activation loop results in altered substrate specificityPaul R Mittelstadt
Laboratory of Immune Cell Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 284:15469-74. 2009..These findings suggest that T cells have evolved a mechanism to utilize p38 in a specialized manner independent of and distinct from the classical p38 MAPK signaling cascade... - Optineurin negatively regulates TNFalpha- induced NF-kappaB activation by competing with NEMO for ubiquitinated RIPGuozhi Zhu
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Curr Biol 17:1438-43. 2007..These results reveal a physiologic role for optineurin in dampening TNFalpha signaling, and this role might provide an explanation for its association with glaucoma... - TNF-alpha induced c-IAP1/TRAF2 complex translocation to a Ubc6-containing compartment and TRAF2 ubiquitinationChuan Jin Wu
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
EMBO J 24:1886-98. 2005..Therefore, the ER plays a key role in the TNF-R-mediated signal transduction cascade by acting as a site of assembly for E2/E3/substrate complexes... - Genetic disruption of p38alpha Tyr323 phosphorylation prevents T-cell receptor-mediated p38alpha activation and impairs interferon-gamma productionLudmila Jirmanova
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Blood 113:2229-37. 2009..Thus, the Tyr323-dependent pathway and not the classic mitogen-activated protein (MAP) kinase cascade is the physiologic means of p38alpha activation through the TCR and is necessary for normal Th1 function but not Th1 generation... - Lack of the T cell-specific alternative p38 activation pathway reduces autoimmunity and inflammationLudmila Jirmanova
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Blood 118:3280-9. 2011..Thus, T cell-specific alternative activation of p38 is an important pathway in T-cell proliferation, Th skewing, and inflammatory autoimmunity, and may be an attractive tissue-specific target for intervention in these processes... - Lys63-linked polyubiquitination of IRAK-1 is required for interleukin-1 receptor- and toll-like receptor-mediated NF-kappaB activationDietrich B Conze
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Mol Cell Biol 28:3538-47. 2008..Thus, K63-linked polyubiquitination of proximal signaling proteins is a common mechanism used by diverse innate immune receptors for recruiting IKK and activating NF-kappaB... - The CD8+ memory T-cell state of readiness is actively maintained and reversibleAtef Allam
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Blood 114:2121-30. 2009..Therefore, sustaining the functional phenotype of T memory cells requires active signaling and maintenance... - Gadd45alpha regulates p38-dependent dendritic cell cytokine production and Th1 differentiationLudmila Jirmanova
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 178:4153-8. 2007..Therefore, Gadd45alpha has tissue-specific and opposing functions on p38 activity, and Gadd45alpha-regulated p38 activation in DCs is a critical event in Th1 polarization in vivo... - Sensing of Lys 63-linked polyubiquitination by NEMO is a key event in NF-kappaB activation [corrected]Chuan Jin Wu
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Nat Cell Biol 8:398-406. 2006..These results provide a mechanism for NEMO's critical role in IKK activation, and a key to understanding the link between cytokine-receptor proximal signalling and IKK and NF-kappaB activation... - NEMO recognition of ubiquitinated Bcl10 is required for T cell receptor-mediated NF-kappaB activationChuan Jin Wu
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 105:3023-8. 2008..Therefore, the regulated ubiquitination of Bcl10 and its recognition by NEMO are a critical link between the CBM complex, IKK recruitment, and NF-kappaB activation... - Wip1 phosphatase-deficient mice exhibit defective T cell maturation due to sustained p53 activationMarco L Schito
Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 176:4818-25. 2006..In contrast, the abnormal thymic phenotype of Wip1-deficient mice was reversed in the absence of p53. These data suggest that Wip1 down-regulates p53 activation in the thymus and is required for normal alphabeta T cell development... - CD70 deficiency impairs effector CD8 T cell generation and viral clearance but is dispensable for the recall response to lymphocytic choriomeningitis virusIvana Munitic
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 190:1169-79. 2013..Therefore, CD70 appears to be an important factor in the initiation of a robust and effective primary response but dispensable for CD8 T cell memory responses... - Alternative p38 activation pathway mediated by T cell receptor-proximal tyrosine kinasesJesus M Salvador
Gene Response Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Nat Immunol 6:390-5. 2005..Thus, phosphorylation of Tyr323 dependent on the tyrosine kinase Lck and mediated by Zap70 serves as an important mechanism for TCR activation of p38 in T cells... - Dynamic regulation of IL-7 receptor expression is required for normal thymopoiesisIvana Munitic
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Blood 104:4165-72. 2004..Therefore, the down-regulation of IL-7R on DP cells is an "altruistic" act required for maintaining an adequate supply of local IL-7 for DN cells... - Balance between NF-κB p100 and p52 regulates T cell costimulation dependenceMaria Letizia Giardino Torchia
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 190:549-55. 2013..Thus, p100 represses and p52 promotes costimulation, and the ratio regulates T cell dependence on costimulatory signals... - Posttranscriptional downregulation of c-IAP2 by the ubiquitin protein ligase c-IAP1 in vivoDietrich B Conze
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Building 37, Room 3002, Bethesda, MD 20892, USA
Mol Cell Biol 25:3348-56. 2005..Thus, the c-IAPs represent a pair of TNFR-associated ubiquitin protein ligases in which one regulates the expression of the other by a posttranscriptional and E3-dependent mechanism... - Thymocyte responsiveness to endogenous glucocorticoids is required for immunological fitnessPaul R Mittelstadt
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
J Clin Invest 122:2384-94. 2012.... - Disruption of glucocorticoid receptor exon 2 yields a ligand-responsive C-terminal fragment that regulates gene expressionPaul R Mittelstadt
Building 10, Room 1B 40, National Institutes of Health, Bethesda, Maryland 20892
Mol Endocrinol 17:1534-42. 2003.... - Non-canonical NF-κB activation and abnormal B cell accumulation in mice expressing ubiquitin protein ligase-inactive c-IAP2Dietrich B Conze
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
PLoS Biol 8:e1000518. 2010..Thus, the c-IAP2/MALT1 fusion protein activates NF-κB by two distinct mechanisms, and loss of c-IAP2 E3 activity in vivo is sufficient to induce abnormalities common to MALT lymphoma... - HIV Tat binds Egr proteins and enhances Egr-dependent transactivation of the Fas ligand promoterYili Yang
Laboratory of Immune Cell Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 277:19482-7. 2002.... - IAPs: what's in a name?Srinivasa M Srinivasula
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Mol Cell 30:123-35. 2008..Here, we review the current understanding of the roles of IAPs in apoptotic and nonapoptotic processes and explore the notion that the latter represents the primary physiologic activities of IAPs... - Identification and characterization of polyclonal αβ-T cells with dendritic cell propertiesMirela Kuka
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Nat Commun 3:1223. 2012.... - A20: more than one way to skin a catSrinivasa M Srinivasula
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Mol Cell 44:511-2. 2011..In this issue of Molecular Cell, Skaug et al. (2011) propose a polyubiquitin-dependent, noncatalytic mechanism by which the deubiquitinase A20 inhibits IκB kinase and NF-κB activation... - TNF-RII and c-IAP1 mediate ubiquitination and degradation of TRAF2Xiaoming Li
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Nature 416:345-7. 2002..These findings identify a physiologic role for c-IAP1 and define a mechanism by which TNF-RII-regulated ubiquitin protein ligase activity can potentiate TNF-induced apoptosis... - Mice lacking the p53-effector gene Gadd45a develop a lupus-like syndromeJesus M Salvador
Gene Response Section, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
Immunity 16:499-508. 2002.... - Positive effects of glucocorticoids on T cell function by up-regulation of IL-7 receptor alphaDenis Franchimont
Lymphocyte Cell Biology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
J Immunol 168:2212-8. 2002..These observations provide a mechanism by which glucocorticoids may have a positive influence on T cell survival and function... - Regulation of constitutive TCR internalization by the zeta-chainUgo D'Oro
Chiron, Siena, Italy
J Immunol 169:6269-78. 2002.... - Mutually antagonistic signals regulate selection of the T cell repertoireGeoffrey L Stephens
Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912-2600, USA
Int Immunol 15:623-32. 2003..Together, these results support a role for endogenous GC in balancing TCR-mediated signals during thymic selection...