Bibliography
- JIRAPONGSANANURUK O, LEUNG DYM: Clinical applications of cytokines: new directions in the therapy of atopic diseases. Ann. Allergy Asthma Immunol. (1997) 79:5–20.
- •A good review describing the pathogenesis of allergic inflammation and the role of various cells and cytokines in allergic diseases.
- MENZ G, YING S, DURHAM SR et al.: Molecular concepts of IgE-initiated inflammation in atopic and non-atopic asthma. Allergy (1998) 53:15–21.
- •A short review on the differences between atopic and non-atopic asthma and the role of IgE.
- VON MUTIUS E, MARTINEZ FD, FRITZSCH C et al.: Prevalence of asthma and atopy in two areas of West and East Germany. Am. J. Respir. Grit. Care Med. (1994) 149:358–364.
- STRACHAN D: Socio-economic factors and the develop-ment of allergy. Toxicol. Lett. (1996) 86:199–203.
- STRACHAN DP: Hay fever, hygiene, and household size. Br. Med. J. (1989) 299:1259–1260.
- ROSENWASSER LJ: The genetics of atopy. Allergy (1998) 53 (Suppl.):8–11.
- KAPSENBERG ML, HILKENS CMU, WIERENGA EA, KALINSKI P: The role of antigen-presenting cells in the regulation of allergen-specific T cell responses. Curr. Opin. Immunol. (1998) 10:607–613.
- •Review describing the active role of APCs in atopic individuals during aberrant Th-cell polarisation.
- GRUNIG G, WARNOCK M, WAKIL AE et al.: Requirement for IL-13 independently of IL-4 in experimental asthma. Science (1998) 282:2261–2263.
- ••This paper convincingly shows that IL-13, in addition to IL-4, has a role in a mouse model of asthma. A role for the common IL-4 receptor a chain is shown by the use of knock-out mice.
- WILLS-KARP M, LUYIMBAZI J, XU X et al.: Interleukin-13: central mediator of allergic asthma. Science (1998) 282:2258–2261.
- ••In this paper, a number of mouse studies demonstrate thatIL-13 is necessary and sufficient for the expression of allergic asthma. Moreover, IL-13 was shown to induce the pathological features of asthma in a manner that is independent of IgE and eosinophils.
- RINCON M, ANGUITA J, NAKAMURA T, FIKRIG E, FLAVELLRA: Interleukin (IL)-6 directs the differentiation of IL-4 producing CD4+ T cells. J. Exp. Med. (1997) 185: 461–469.
- TAKEDA K, TSUTSUI H, YOSHIMOTO T et al.: DefectiveNK cell activity and Thl response in IL-18-deficient mice. Immunity (1998) 8:383–390.
- KIMBER I, DEARMAN RJ, CUMBERBATCH M, HUBY RJD:Langerhans cells and chemical allergy. Curr. Opin. Immunol. (1998) 10:614–619.
- •Review describing the interplay between several cytokines and epidermal Langerhans cells in the induction of cutaneous immune responses.
- GASCAN H, GAUCHET JF, RONCAROLO MG et al. HumanB-cell clones can be induced to proliferate and to switch to IgE and IgG4 synthesis by interleukin 4 and a signal provided by activated CD4+ T cell clones. J. Exp. Med. (1991) 173:747–750.
- McKENZIE ANJ, CULPEPPER JA, DE WALA MALEFYT R etInterleukin-13, a novel cell-derived cytokine that regulates human monocyte and B cell function. Proc. Natl. Acad. Sci. USA (1992) 90:3735–3739.
- OKUDAIRA H, MORI A: Simple understanding and optimistic strategy for coping with atopic diseases. Int. Arch. Allergy Immunol (1998) 117:11–19.
- METCALF D, BEGLEY CG, JOHNSON GR et al.: Biologicproperties in vitro of a recombinant human granulo-cyte macrophage colony-stimulating factor. Blood (1986) 67:37–45.
- LOPEZ AF, TO LB, YANG YC et al.: Stimulation of prolif-eration, differentiation, and function of human cells by primate interleukin-3. Proc. Natl. Acad. Sci. USA (1987) 84:2761–2765.
- SCHLEIMER RP, BECK L, SCHWEIBERT L et al.: Inhibitionof inflammatory cell recruitment by glucocorticoids: cytokines as primary targets. In: Topical Glucocorticoids in Asthma: Mechanisms and Clinical Actions. Schleimer RP, Busse WW, O'Byrne P (Eds.), Marcel Dekker, Inc., New York, USA (1997):203–238.
- BARNES PJ, ADCOCK IM: Transcription factors and asthma. Eur. Respir. J. (1998) 12:221–234.
- ••An overview of the signalling pathways which are involvedin the activation of NF-IcB, AP-1, C/EBP, CREB, NF-AT, their interactions and their therapeutic implications. Good illustrations.
- VAYSSIERE BM, DUPONT S, CHOQUART A et al.: Synthetic glucocorticoids that dissociate transactiva-tion and AP-1 transrepression exhibit anti-inflammatory activity in vivo. Mol. Endocrinol. (1997) 11:1245–1255.
- BARNES PJ, GREENING AP, CROMPTON GK: Glucocorti-coid resistance in asthma. Am. J. Respir. Grit. Care Med. (1995) 152:125S–140S.
- SCHREIBER SL, CRABTREE GR: The mechanism of action of cyclosporin A and FK506. Immunol. Today (1992) 13:136–141.
- SOWDEN JM, BERTH-JONES J, ROSS JS et al.: Double-blind, controlled, cross-over study of cyclosporin in adults with severe refractory atopic dermatitis. Lancet (1991) 338:137–140.
- NAGAKAWA H: Tacrolimus ointment for atopic dermatitis. Lancet (1994) 344:883.
- NELSON HS: Beta-adrenergic bronchodilators. New Engl. J. Med. (1995) 333:499–506.
- COLEMAN RA, JOHNSON M, NIALS AT, VARDEY CJ: Exosites: their current status, and their relevance to the duration of action of long-acting beta 2-adrenoceptor agonists. Trends Pharmacol. Sci. (1996) 17:325–330.
- COWARD WR, SAGARA H, CHURCH MK: Asthma, adenosine, mast cells and theophylline. Clin. Exp. Allergy (1998) 28:42–46.
- MONTANA JG, BUCKLEY GM, COOPER N et al.: Aryl sulfonamides as selective PDE4 inhibitors. Bioorg. Med. Chem. Lett. (1998) 8:2635–2640.
- SLATER JW, ZECHNICH AD, HAXBY DG: Second-generation antihistamines: a comparative review. Drugs (1999) 57:31–47.
- PARNHAM MJ: Sodium cromoglycate and nedocromil sodium in the therapy of asthma, a critical comparison. Pulm. Pharmacol (1996) 9:95–105.
- GRISWOLD DE, WEBB EF, BADGER AM et al.: SB 207499 (Ariflo), a second generation phosphodiesterase 4 inhibitor, reduces tumor necrosis factor a and interleukin-4 production in vivo. J. Pharmacol. Exp. Ther. (1998) 287:705–711.
- BACHER E, BOER C, BRAY-FRENCH K et al.:N-arylrolipram derivatives as potent and selective PDE4 inhibitors. Bioorg. Med. Chem. Let. (1998) 8:3229–3234.
- HAY DWP: Pharmacology of leukotriene receptor antagonists. More than inhibitors of bronchoconstric-tion. Chest (1997) 111:35S–455.
- NYCE JW, METZGER WJ: DNA antisense therapy for asthma in an animal model. Nature (1997) 385:721–725.
- BARNES PJ, LIM S: Inhibitory cytokines in asthma. Mol. Med. Today (1998) 4 (1 0):452–458.
- •Review that discusses the therapeutic potential of a number of inhibitory cytokines (including IL-10, IL-12 and IFN-y) in the treatment of asthma.
- LEE JC, LAYDON JT, MCDONNELL PC et al.: A protein kinase involved in the regulation of inflammatory cytokine biosynthesis. Nature (1994) 372:739–746.
- ••This paper demonstrates that a specific p38 MAPK inhibitoris able to inhibit TNF and IL-1 synthesis.
- BLACK RA, RAUCH CT, KOZLOSKY CJ et al.: A met allopro-teinase disintegrin that releases tumour necrosis factor-alpha from cells. Nature (1997) 385:729–733.
- ••Describes the cloning and characterisation of a newprotease which is responsible for the release of soluble TNF from macrophages.
- LI P, ALLEN H, BANERJEE S et al.: Mice deficient in 11-10-converting enzyme are defective in production of mature 11-10 and resistant to endotoxic shock. Cell (1995) 80:401–411.
- ••Describes the generation of knock-out mice for caspase-1and shows that the latter is the key enzyme responsible for the maturation of proIL–1.
- GHAYUR T, BANERJEE S, HUGUNIN M et al.: Caspase-1 processes IFN-gamma-inducing factor and regulates LPS-induced IFN-gamma production. Nature (1997) 386:619–623.
- •This is the first report which demonstrates that caspase-1 also leads to the maturation of IL-18, thus regulating the production of IFN-y in T-cells and natural killer cells.
- THORNBERRY NA, LAZEBNIK Y: Caspases: enemies within. Science (1998) 281:1312–1316.
- RAHMAN I, MACNEE W: Role of transcription factors ininflammatory lung diseases. Thorax (1998) 53:601–612.
- •A thorough review that focuses on recent progress in our understanding of the role of NF-IcB, AP-1, NF-1L6, and NFAT transcription factors in the pathogenesis of inflammatory lung diseases. Also, the interactions with other transcription factors, nuclear receptor co-activators and glucocorticoid receptors is discussed.
- BARNES PJ, KARIN M: Nuclear factor-KB: a pivotaltranscription factor in chronic inflammatory diseases. New Engl. J. Med. (1997) 336:1066–1071.
- BLACKWELL TS, CHRISTMAN JW: The role of nuclearfactor-KB in cytokine gene regulation. Am. J. Respir. Cell Mol Biol. (1997) 17:3–9.
- ZHU Z, TANG W, RAY A et al.: Rhinovirus stimulation ofinterleukin-6 in vivo and in vitro. Evidence for nuclear factor kappa B-dependent transcriptional activation. J. Clin. Invest. (1996) 97:421–430.
- HART LA, KRISHNAN VL, ADCOCK IM, BARNES PJ, CHUNG KF: Activation and localization of transcrip-tion factor, nuclear factor-KB, in asthma. Am. J. Respir. Crit. Care Med. (1998) 158:1585–1592.
- YANG L, COHN L, ZHANG D-H et al.: Essential role of nuclear factor KB in the induction of eosinophilia in allergic airway inflammation. J. Exp. Med. (1998) 188:1739–1750.
- ••This paper demonstrates that mice deficient in the p50subunit of NF-IcB are incapable of mounting eosinophilic airway inflammation compared with wild-type mice. This was correlated with the lack of production of IL-5 and the chemokine eotaxin.
- SNAPPER CM, ZELAZOWSKI P, ROSAS FR et al.: B cells from p50/NF-x13 knock-out mice have selective defects in proliferation, differentiation, germ-line CH transcription and Ig class switching. J. Immunol (1996) 156:183–191.
- •In this report it is shown that B-cells derived from p50 NF-icB knock-out mice show a marked reduction in the switch to IgG3 and IgE.
- TAVARES JC, BAYON Y, CRESPO MS: ImmunoglobulinE-mediated anaphylaxis activates nuclear factor KB in rat small intestine. Inflamm. Res. (1998) 47:265–269.
- STACEY MA, SUN G, VASSALLI G et al. The allergen Derpl induces NF-x13 activation through interference with kik function in asthmatic bronchial epithelial cells. Biochem. Biophys. Res. Commun. (1997) 236:522–526.
- RAY A, PREFONTAINE KE: Physical association and functional antagonism between p65 subunit of transcription factor NF-x13 and the glucocorticoid receptor. Proc. Nati Acad. ScL USA (1994) 91:752–756.
- ••This paper provides a molecular explanation for theanti-inflammatory effect of glucocorticoids.
- SCHEINMAN RI, COGSWELL PC, LOFQUIST AK et al.: Role of transcriptional activation of Ix13-a in mediation of immunosuppression by glucocorticoids. Science (1995) 270:283–286.
- ••This paper provides evidence for a second mechanism ofNF-icB regulation by glucocorticoids.
- SEN R, BALTIMORE D: Multiple nuclear factors interactwith the immunoglobulin enhancer sequences. Cell (1986) 46:705–716.
- BALDWIN AS, JR.: The NF-x13 and la proteins: newdiscoveries and insights. Ann. Rev. Immunol. (1996) 14:649–683.
- BEG AA, SHA WC, BRONSON RT, GHOSH S, BALTIMORE D: Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-03. Nature (1995) 376:167–170.
- ••The results of this paper shows that disruption of the p65NF-icB locus leads to embryonic lethality and massive liver degeneration. It is also shown that p65 controls inducible, but not basal, transcription in NF-icB regulated pathways.
- SHA WC, LIOU H-C, TUOMANEN El, BALTIMORE D: Targeted disruption of the p50 subunit of NF-x13 leads to multifocal defects in immune responses. Cell (1995) 80:321–330.
- ••In this paper it is shown that B-cells from p50 NF-KBknock-out mice do not proliferate in response to lipopoly-saccharide, and are defective in basal and specific antibody production.
- CRAMER P, MULLER CW: A firm hand on NFkappaB: structures of the IkappaBalpha-NFkappaB complex. Structure (1999) 7:R1–6.
- ••In this short review, the crystal structure of an licB-NFicBcomplex is discussed, explaining the mechanism by which licB controls the subcellular localisation and activity of
- DIDONATO J, MERCURIO F, ROSETTE C: Mapping of theinducible bcB phosphorylation sites that signal its ubiquitination and degradation. Mol. Cell. Biol. (1996) 16:1295–1304.
- YARON A, GONEN H, ALKALAY I et al.: Inhibition ofNF-KB cellular function via specific targeting of the bcB-ubiquitin ligase. EMBO J (1997) 16:6486–6494.
- YARON A, HATZUBAI A, DAVIS M et al.: Identification of the receptor component of the Iacc-ubiquitin ligase. Nature (1998) 396:590–594.
- ••This report describes the component of the ubiquitin ligasewhich specifically recognises phosphorylated licB, promoting its ubiquitination. It is shown to belong to a recently distinguished family of I3-transducin repeat-containing protein (I3-TrCP)/Slimb proteins.
- DESTERRO JM, RODRIGUEZ MS, HAY RT: SUMO-1 modification of b(Ba inhibits NF-KB activation. Mol Cell (1998) 2:233–239.
- ••This paper describes an alternative mechanism of NF-KBregulation by IlcB modification.
- ARENZANA-SEISDEDOS F, THOMPSON J, RODRIGUEZ MS et al.: Inducible nuclear expression of newly synthe-sized hcB-a negatively regulates DNA-binding and transcriptional activities of NF-KB. Mol. Cell. Biol. (1995) 15:2689–2696.
- KLEMENT JF, RICE NR, CAR BD et al.: IKB-a deficiency results in a sustained NF-KB response and severe widespread dermatitis in mice. Mol. Cell. Biol. (1996) 16:2341–2349.
- ••Clearly shows the existence of redundancy betweendifferent IlcB family members for cytoplasmic retention of NF-IcB. However, in licB deficient cells, nuclear localisation of NF-icB is prolonged. licBoc knock-out mice develop normally, but die soon after birth. Death is accompanied by severe widespread dermatitis and increased levels of TNF in the skin.
- CHENG JD, RYSECK RP, ATTAR RM, DAMBACH D, BRAVOR: Functional redundancy of the nuclear factor KB inhibitors 1c13-a and bc13-13. J. EXP. MED. (1998) 188:1055–1062.
- MERCURIO F, ZHU H, MURRAY BW: IKK-1 and IKK-2: cytokine-activated IkappaB kinases essential for NF-kappaB activation. Science. (1997) 278:860–866.
- ••This paper describes the cloning and characterisation of thekinases that are responsible for phosphorylation of IlcB.
- LI Q, VAN ANTWERP D, MERCURIO F, LEE KF, VERMA IM: Severe liver degeneration in mice lacking the hcB kinase 2 gene. Science (1999) 284:321–325.
- ••This report shows that IKK-2 is essential for mouse develop-ment and cannot be substituted by IKK-1. Interestingly, mice could be rescued by the inactivation of the gene for TNF receptor–1.
- TAKEDA K, TAKEUCHI O, TSUJIMURA T et al. Limb and skin abnormalities in mice lacking IKK-a. Science (1999) 284:313–316.
- ••It is shown that IKK-1 is not essential for cytokine-inducedactivation of NF-IcB. In contrast, IKK-1 is essential for NF-KB activation in the limb and skin during embryogenesis.
- ROTH WARF DM, ZANDI E, NATOLI G, KARIN M: IKK-y is an essential regulatory subunit of the 1(13 kinase complex. Nature (1998) 395:297–300.
- ••This report describes the cloning and characterisation ofIKK-y as a third component of the licB kinase complex which is essential for NF-icB activation.
- MALININ NL, BOLDIN MP, KOVALENKO AV, WALLACH D: MAP3K-related kinase involved in NF-kappaB induction by TNF, CD95 and IL-1. Nature (1997) 385:540–544.
- LEE FS, HAGLER J, CHEN ZJ et al.: Activation of the bcB-a kinase complex by MEKK1, a kinase of the JNK pathway. Cell (1997) 88:213–222.
- DARNAY BG, AGGARWAL BB: Early events in TNF signaling: a story of associations and dissociations. J. Leuk. Biol. (1997) 61:559–566.
- CARPENTIER I, DECLERCQ W, MALININ NL et al.: TRAF2 plays a dual role in NF-KB dependent gene activation by mediating the TNF-induced activation of p38 MAPK and bcB kinase pathways. FEBS Lett. (1998) 425:195–198.
- •This paper demonstrates the divergence of two protein kinase pathways leading to NF-icB dependent gene expres-sion at the level of TRAF2.
- ARCH RH, GEDRICH RW, THOMPSON CB: Tumor necrosis factor receptor-associated factors (TRAFs)-a family of adapter proteins that regulates life and death. Genes Dev. (1998) 12:2821–2830.
- •Review which gives an overview of the structure and function of all members of the TRAF family.
- HSU H, SHU H, PAN M, GOEDDEL DV: TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways. Cell (1996) 84:299–308.
- ••First report describing the divergence of pro-apoptotic andgene regulatory signalling pathways at the level of TRADD in the TNF receptor complex.
- YEH WC, SHAHINIAN A, SPEISER D et al.: Early lethality, functional NF-kappaB activation, and increased sensitivity to TNF-induced cell death in TRAF2-deficient mice. Immunity (1997) 7:715–725.
- ••This paper describes the generation of TRAF2 deficient cells, and the surprising finding that TRAF2 is not essential for TNF-induced NF-IcB activation.
- KELLIHER MA, GRIMM S, ISHIDA Y et al.: The deathdomain kinase RIP mediates the TNF-induced NF-x13 signal. Immunity (1998) 8:297–303.
- ••The crucial role of RIP in TNF-induced NF-icB activation isdemonstrated by the generation of RIP deficient mice.
- CAO Z, XIONG J, TAKEUCHI M, KURAMA T, GOEDDEL DV: TRAF6 is a signal transducer for interleukin-1. Nature (1996) 383:443–446.
- ••First report on the identification and biological role ofTRAF6 in NF-IcB activation.
- GEDRICH KW, GILFILLIAN MC, DUCKETT CS, VAN DONGEN JL, THOMPSON CB: CD30 contains two binding sites with different specificities for members of the TNF-R-associated factor family of signal transducing proteins. J. Biol. Chem. (1996) 271:12852–12858.
- KUHNE MR, ROBBINS M, HAMBOR JE et al. Assemblyand regulation of the CD40 receptor complex in human B-cells. J. Exp. Med. (1997) 186:337–342.
- NINOMIYA-TSUJI J, KISHIMOTO K, HIYAMA A et al. Thekinase TAK1 can activate the NIK-Ia as well as the MAP kinase cascade in the IL-1 signalling pathway. Nature (1999) 398:252–256.
- UN X, CUNNINGHAM ET, JR., MU Y, GELEZIUNAS R, GREENE WC: The proto-oncogene Cot kinase partici-pates in CD3/CD28 induction of NE-KB acting through the NE-KB-inducing kinase and la kinases. Immunity (1999) 10:271–280.
- THOMASSEN E, BIRD TA, RENSHAW BR, KENNEDY MK, SIMS JE: Binding of interleukin-18 to the interleukin-1 receptor leads to activation of signaling pathways similar to those used by interleukin-1. J. Interferon Cytokine Res. (1998) 18:1077–1088.
- ZHANG FX, KIRSCHNING CJ, MANCINELLI R et al.Bacterial lipopolysaccharide activates nuclear factor-KB through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes. J. Biol. Chem. (1999) 274:7611–7614.
- BENDER K, GOTTLICHER M, WHITESIDE S, RAHMSDORFHJ, HERRLICH P: Sequential DNA damage-independent and-dependent activation of NE-03 by UV. EMBO (1998) 17:5170–5181.
- LI N, KARIN M: Ionizing radiation and short wavelength UV activate NE-03 through two distinct mechanisms. Proc. Natl. Acad. Sci. USA (1998) 95:13012–13017.
- ••This paper provides evidence for the existence ofUV-specific signalling pathways responsible for IlcB degradation.
- McELHINNY JA, TRUSHIN SA, BREN GD, CHESTER N, PAYA CV: Casein kinase II phosphorylates I a a at S-283, S-289, S-293, and T-291 and is required for its degradation. Mol. Cell. Biol. (1996) 16:899–906.
- GHODA L, LIN X, GREENE WC: The 90 kDa ribosomal S6kinase (pp9Orsk) phosphorylates the N-terminal regulatory domain of Iact and stimulates its degrada-tion in vitro. J. Biol. Chem. (1997) 272:21281–21288.
- IMBERT V, RUPEC RA, LIVOLSI A et al.: Tyrosinephosphorylation of IKB-a activates NE-03 without proteolytic degradation of 1a-a. Cell (1996) 86:787–798.
- BERAUD C, HENZEL WJ, BAEUERLE PA: Involvement ofregulatory and catalytic subunits of phosphoinositide 3-kinase in NE-03 activation. Proc. Natl. Acad. Sci. USA (1999) 96:429–434.
- •This paper reports the role of phosphoinositide 3-kinase in NF-IcB activation by the tyrosine phosphorylation-dependent pathway.
- BEYAERT R, CUENDA A, VANDEN BERGHE W et al.: Thep38/RK mitogen-activated protein kinase pathway regulates interleukin-6 synthesis in response to tumour necrosis factor. EMBO J (1996) 15:1914–1923.
- ••First report on the role of p38 MAPK in NF-icB dependentgene expression induced by TNF.
- VANDEN BERGHE W, PLAISANCE S, BOONE E et al.: p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways are required for nuclear factor-KB p65 transactivation mediated by tumor necrosis factor. J. Biol. Chem. (1998) 273:3285–3290.
- GERRITSEN ME, WILLIAMS AJ, NEISH AS et al.:CREB-binding protein/p300 are transcriptional coacti-vators of p65. Proc. Nad Acad. Sci. USA (1997) 94:2927–2932.
- •This paper describes the role of CBP/p300 proteins in the nuclear transactivation of NF-icB.
- DE CESARIS P, STARACE D, RICCIOLI A et al.: Tumor necrosis factor-a induces interleukin-6 production and integrin ligand expression by distinct transduc-tion pathways. J. Biol. Chem. (1998) 273:7566–7571.
- WANG D, BALDWIN AS, JR.: Activation of nuclear factor-KB-dependent transcription by tumor necrosis factor-a is mediated through phosphorylation of RelA/p65 on serine 529.1 Biol. Chem. (1998) 273:29411–29416.
- •An article which describes the role of phosphorylation of the p65 subunit of NF-icB in the transactivating potential of
- ZHONG H, SUYANG H, ERDJUMENT-BROMAGE H, TEMPST P, GHOSH S: The transcriptional activity of NE-03 is regulated by the kB-associated PKAc subunit through a cyclic AMP-independent mechanism. Cell (1997) 89:413–424.
- ZHONG H, VOLL RE, GHOSH S: Phosphorylation of NE-03 p65 by PKA stimulates transcriptional activity by promoting a novel bivalent interaction with the co-activator CBP/p300. Mol Cell (1998) 1:661–671.
- •This paper provides evidence for PEA as the kinase respon-sible for p65 phosphorylation, and further demonstrates that this modification promotes the binding of the co-activators CBP/p300.
- JÄÄTTELA M, MOURITZEN H, ELLING F, BASTHOLM L: A20 zinc finger protein inhibits TNF and IL-1 signaling. Immunol. (1996) 156:1166–1173.
- DE VALCK D, HEYNINCK K, VAN CRIEKINGE W et al.: A20 inhibits NF-kappaB activation independently of binding to 14-3-3 proteins. Biochem. Biophys. Res. Commun. (1997) 238:590–594.
- SONG HY, ROTHE M, GOEDDEL DV: The tumor necrosis factor-inducible zinc finger protein A20 interacts with TRAF1/TRAF2 and inhibits NF-kappaB activation. Proc. Natl. Acad. Sci. USA (1996) 93:6721–6725.
- •This paper gives a molecular explanation for the inhibitory effect of A20 on NF-icB activation by TNF.
- HEYNINCK K, BEYAERT R: The cytokine-inducible zinc finger protein A20 inhibits IL-1-induced NF-x13 activa-tion at the level of TRAF6. FEBS Lett. (1999) 442:147–150.
- •This paper gives a molecular explanation for the inhibitory effect of A20 on NF-icB activation by IL–1.
- ROTHE M, XIONG J, SHU H: I-TRAF is a novel TRAF-interacting protein that regulates TRAF-mediated signal transduction. Proc. Natl. Acad. Scl USA (1996) 93:8241–8246.
- LEE SY, CHO Y: TRAF interacting protein (TRIP): a novel component of the TNF-R-and CD3O-TRAF signaling complexes that inhibits TRAF2-mediated NF-x13 activation. J. Exp. Med. (1997) 185:1275–1285.
- STEIN B, BALDWIN AS, JR., BALLARD DW et al.: Cross-coupling of the NF-x13 p65 and Fos/Jun transcription factors produces potentiated biological function. EMBO J (1993) 12:3879–3891.
- SICA A, DORMAN L, VIGGIANO V et al.: Interaction of NF-kappaB and NFAT with the interferon-gamma promoter. J. Biol. Chem. (1997) 272:30412–30420.
- PAHL HL, KRAUSS B, SCHULZE-OSTHOFF K et al. The immunosuppressive fungal metabolite gliotoxin specifically inhibits transcription factor NF-03. J. Exp. Med. (1996) 183:1829–1840.
- BRETON JJ, CHABOT-FLETCHER MC: The natural product hymenialdisine inhibits interleukin-8 production in U937 cells by inhibition of nuclear factor-KB. J. Pharmacol. Exp. Ther. (1997) 282:459–466.
- WANG P, WU P, SIEGEL MI et al.: Interleukin-10 inhibits NF-x13 activation in human monocytes. J. Biol. Chem. (1995) 270:95558–95563.
- SCHRECK R, RIEBER P, BAEUERLE PA: Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-x13 transcription factor and 11IV-1. EMBO J (1991) 10:2247–2258.
- MIYAJIMA T, KOTAKE Y: Spin trapping agent, phenyl N-tert-butyl nitrone, inhibits induction of nitric oxide synthase in endotoxin-induced shock in mice. Biochem. Biophys. Res. Commun. (1995) 215:114–121.
- JUN DY, CHAE HZ, RHEE SG et al.: Regulatory role for a novel human thioredoxin peroxidase in NF-x13 activa-tion. J. Biol. Chem. (1997) 272:30952–30961.
- SCHENK H, KLEIN M, ERDBRUGGER W et al.: Distinct effects of thioredoxin and antioxidants on the activa-tion of transcription factors NF-x13 and AP-1. Proc. Natl. Acad. Sci. USA (1994) 91:1672–1676.
- KAZMI SM, PLANTERK, VISCONTI V et al.: Suppression of NF-x13 activation and NF-KB dependent gene expression by tepoxalin, a dual inhibitor of cyclooxy-genase and 5-lipoxygenase. J. Cell. Biochem. (1995) 57:299–310.
- PALANKI MS, ERDMAN P, GAYO L: Inhibitors of NF-x13 and AP-1 gene expression: structure activity studies on the pyrimidine portion of SP100030. 213th American Chemical Society National Meeting. San Francisco, USA (1997) Abstract 065.
- PALANKI MS, ERDMAN P, SOTA M: Inhibitors of NF-x13 and AP-1 gene expression: structure activity studies of 2-trifluoromethylpyrimidine-4-citraconamide-5-carb oxylate. 26th National Medicinal Chemistry Symposium. Richmond, USA (1998) Abstract C–4.
- NEURATH MF, PETTERSSON S, MEYER ZUM BUSCHEN-FELDE KH, STROBER W: Local administration of antisense phosphorothioate oligonucleotides to the p65 subunit of NF-x13 abrogates established experi-mental colitis in mice. Nature Med. (1996) 2:998–1004.
- •This paper demonstrates the therapeutic potential of antisense oligonucleotides to NF-IcB.
- WRIGHTON CJ, HOFER-WARBINEK R, MOLL T et al.: Inhibition of endothelial cell activation by adenovirus-mediated expression of IxBa, an inhibitor of transcription factor NF-03. J. Exp. Med. (1996) 183:1013–1022.
- SOARES MP, MUNIAPPAN A, KACZMAREK E et al.: Adenovirus-mediated expression of a dominant negative mutant of p65/Re1A inhibits pro-inflammatory gene expression in endothelial cells without sensitizing to apoptosis. J. Immunol (1998) 161:4572–4582.
- ••This paper provides clear evidence that thepro-inflammatory and anti-apoptotic function of NF-icB can be modulated independently.
- YIN MJ, YAMAMOTO Y, GAYNOR RB: The anti-inflammatory agents aspirin and salicylate inhibit the activity of IKB kinase-p. Nature (1998) 396:77–80.
- •This paper gives a molecular explanation for the anti-inflammatory effect of aspirin and salicylate.
- HEYNINCK K, DE VALCK D, VANDEN BERGHE W et al.: The zinc finger protein A20 inhibits TNF-induced NF-x13 dependent gene expression by interfering with a RIP-or TRAF2-mediated transactivation signal and directly binds to a novel NF-KB inhibiting protein, ABM. J. Cell Biol. [In press].