H Wajant

Summary

Affiliation: University of Stuttgart
Country: Germany

Publications

  1. ncbi request reprint Dominant-negative FADD inhibits TNFR60-, Fas/Apo1- and TRAIL-R/Apo2-mediated cell death but not gene induction
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    Curr Biol 8:113-6. 1998
  2. ncbi request reprint Targeting the FLICE Inhibitory Protein (FLIP) in cancer therapy
    Harald Wajant
    Department of Molecular Medicine Medical Polyclinic, University of Wuerzburg Roentgenring 11, 97070 Wuerzburg, Germany
    Mol Interv 3:124-7. 2003
  3. ncbi request reprint TRAIL and NFkappaB signaling--a complex relationship
    Harald Wajant
    Department of Molecular Internal Medicine Medical Polyclinic, University of Wurzburg, D 97070 Wurzburg, Germany
    Vitam Horm 67:101-32. 2004
  4. ncbi request reprint CD95 and TRAF2 promote invasiveness of pancreatic cancer cells
    Anna Trauzold
    Molecular Oncology Unit, University Hospital Schleswig Holstein, Campus Kiel, Kiel, Germany
    FASEB J 19:620-2. 2005
  5. ncbi request reprint TNF receptor associated factors in cytokine signaling
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Cytokine Growth Factor Rev 10:15-26. 1999
  6. ncbi request reprint Tumor necrosis factor signaling
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring, Germany
    Cell Death Differ 10:45-65. 2003
  7. ncbi request reprint Non-apoptotic Fas signaling
    Harald Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, Germany
    Cytokine Growth Factor Rev 14:53-66. 2003
  8. ncbi request reprint TNF-related apoptosis inducing ligand (TRAIL) and its receptors in tumor surveillance and cancer therapy
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    Apoptosis 7:449-59. 2002
  9. ncbi request reprint The Fas signaling pathway: more than a paradigm
    Harald Wajant
    Institute of Cell Biology and Immunology, Allmandring 31, University of Stuttgart, 70 569 Stuttgart, Germany
    Science 296:1635-6. 2002
  10. ncbi request reprint Tumor necrosis factor receptor-associated factor (TRAF) 2 and its role in TNF signaling
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, Stuttgart 70569, Germany
    Int J Biochem Cell Biol 33:19-32. 2001

Collaborators

Detail Information

Publications51

  1. ncbi request reprint Dominant-negative FADD inhibits TNFR60-, Fas/Apo1- and TRAIL-R/Apo2-mediated cell death but not gene induction
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    Curr Biol 8:113-6. 1998
    ....
  2. ncbi request reprint Targeting the FLICE Inhibitory Protein (FLIP) in cancer therapy
    Harald Wajant
    Department of Molecular Medicine Medical Polyclinic, University of Wuerzburg Roentgenring 11, 97070 Wuerzburg, Germany
    Mol Interv 3:124-7. 2003
    ..Thus, FLIP, which normally prevents inappropriate apoptosis, may become a tumor progression factor. Strategies to overcome this FLIP-mediated blockade of programmed cell death in tumors might become useful for positive prognoses...
  3. ncbi request reprint TRAIL and NFkappaB signaling--a complex relationship
    Harald Wajant
    Department of Molecular Internal Medicine Medical Polyclinic, University of Wurzburg, D 97070 Wurzburg, Germany
    Vitam Horm 67:101-32. 2004
    ..Third, the TRAIL death receptors can activate the NFkappaB pathway. This chapter summarizes basic knowledge regarding the understanding of the NFkappaB pathway and focuses on its multiple roles in TRAIL signaling...
  4. ncbi request reprint CD95 and TRAF2 promote invasiveness of pancreatic cancer cells
    Anna Trauzold
    Molecular Oncology Unit, University Hospital Schleswig Holstein, Campus Kiel, Kiel, Germany
    FASEB J 19:620-2. 2005
    ..Thus, TRAF2 overexpression does not only block apoptosis induction by CD95 but also converts this death receptor into a mediator of invasiveness...
  5. ncbi request reprint TNF receptor associated factors in cytokine signaling
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Cytokine Growth Factor Rev 10:15-26. 1999
    ..Some of the activities of the individual TRAF family members may be redundant although transgenic knockout animal models have already shown that crucial signaling pathways for single TRAF molecules in vivo can be defined...
  6. ncbi request reprint Tumor necrosis factor signaling
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring, Germany
    Cell Death Differ 10:45-65. 2003
    ..In particular, the multiple facets of crosstalk between the various signalling pathways engaged by TNF will be addressed...
  7. ncbi request reprint Non-apoptotic Fas signaling
    Harald Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, Germany
    Cytokine Growth Factor Rev 14:53-66. 2003
    ..This review is focused on the non-apoptotic functions of the FasL/Fas system. In particular, the similarities and differences of the molecular mechanisms of apoptotic and non-apoptotic Fas signaling are addressed...
  8. ncbi request reprint TNF-related apoptosis inducing ligand (TRAIL) and its receptors in tumor surveillance and cancer therapy
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    Apoptosis 7:449-59. 2002
    ..In particular, we debate controversial data in the literature concerning the cytotoxicity of different TRAIL derivatives on primary human cells...
  9. ncbi request reprint The Fas signaling pathway: more than a paradigm
    Harald Wajant
    Institute of Cell Biology and Immunology, Allmandring 31, University of Stuttgart, 70 569 Stuttgart, Germany
    Science 296:1635-6. 2002
    ....
  10. ncbi request reprint Tumor necrosis factor receptor-associated factor (TRAF) 2 and its role in TNF signaling
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, Stuttgart 70569, Germany
    Int J Biochem Cell Biol 33:19-32. 2001
    ....
  11. ncbi request reprint Inhibition of death receptor-mediated gene induction by a cycloheximide-sensitive factor occurs at the level of or upstream of Fas-associated death domain protein (FADD)
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 275:24357-66. 2000
    ..Thus, a novel functional role of cFLIP as a negative regulator of gene induction by death receptors became apparent...
  12. ncbi request reprint p53 upregulates cFLIP, inhibits transcription of NF-kappaB-regulated genes and induces caspase-8-independent cell death in DLD-1 cells
    T Bartke
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    Oncogene 20:571-80. 2001
    ..Moreover, induction of p53 interfered with TNF-induced NF-kappaB activation independently from apoptosis-induction...
  13. ncbi request reprint The TNF-receptor-associated factor family: scaffold molecules for cytokine receptors, kinases and their regulators
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany
    Cell Signal 13:389-400. 2001
    ..In this review, we address the structural and molecular basis of TRAF protein functions and highlight their role in cytokine signalling...
  14. ncbi request reprint Fas-associated death domain protein (FADD) and caspase-8 mediate up-regulation of c-Fos by Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via a FLICE inhibitory protein (FLIP)-regulated pathway
    D Siegmund
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 276:32585-90. 2001
    ..Together these data demonstrate the existence of a death receptor-induced, FADD- and caspase-8-dependent pathway leading to c-Fos induction that is inhibited by the long splice form FLIP-L...
  15. ncbi request reprint TRAIL/Apo2L activates c-Jun NH2-terminal kinase (JNK) via caspase-dependent and caspase-independent pathways
    F Muhlenbeck
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 273:33091-8. 1998
    ....
  16. ncbi request reprint Differential activation of TRAIL-R1 and -2 by soluble and membrane TRAIL allows selective surface antigen-directed activation of TRAIL-R2 by a soluble TRAIL derivative
    H Wajant
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    Oncogene 20:4101-6. 2001
    ..We conclude that antibody targeting-dependent activation can be used to design selective therapeutics derived of those ligands of the TNF family that are biologically inactive in their soluble form...
  17. pmc NF-kappaB inducers upregulate cFLIP, a cycloheximide-sensitive inhibitor of death receptor signaling
    S Kreuz
    Institute of Cell Biology and Immunology, University of Stuttgart, 70569 Stuttgart, Germany
    Mol Cell Biol 21:3964-73. 2001
    ..In conclusion, these data suggest a key role for cFLIP in the antiapoptotic response of NF-kappaB activation...
  18. ncbi request reprint Protein kinase Cmu downregulation of tumor-necrosis-factor-induced apoptosis correlates with enhanced expression of nuclear-factor-kappaB-dependent protective genes
    F J Johannes
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Eur J Biochem 257:47-54. 1998
    ..The dominant negative action of the kinase-negative mutant further suggest a regulatory role of PKCmu for NF-kappaB-dependent gene expression...
  19. pmc Potent antitumoral activity of TRAIL through generation of tumor-targeted single-chain fusion proteins
    B Schneider
    Institute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany
    Cell Death Dis 1:e68. 2010
    ..Cell Death and Disease (2010) 1, e68; doi:10.1038/cddis.2010.45; published online 26 August 2010...
  20. ncbi request reprint Tumor necrosis factor (TNF) and phorbol ester induce TNF-related apoptosis-inducing ligand (TRAIL) under critical involvement of NF-kappa B essential modulator (NEMO)/IKKgamma
    D Siegmund
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 276:43708-12. 2001
    ..The capability of the NF-kappaB pathway to induce the potent death ligand TRAIL may explain the reported proapoptotic features of this typically antiapoptotic pathway...
  21. pmc The type 1 receptor (CD120a) is the high-affinity receptor for soluble tumor necrosis factor
    M Grell
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Proc Natl Acad Sci U S A 95:570-5. 1998
    ..In accordance with this reasoning, the lower signaling capability of homotrimeric lymphotoxin, compared with TNF, correlates with a lower stability of the lymphotoxin-TNF-R1 complex at 37 degrees C...
  22. ncbi request reprint Activation of CD95L fusion protein prodrugs by tumor-associated proteases
    I Watermann
    Institute of Cell Biology and Immunology, University of Stuttgart, Stuttgart, Germany
    Cell Death Differ 14:765-74. 2007
    ..In a xenotransplantation tumor model, local application of the prodrug reduced the growth of target antigen-expressing, but not antigen-negative tumor cells, verifying targeted CD95L prodrug activation in vivo...
  23. ncbi request reprint Restoration of membrane TNF-like activity by cell surface targeting and matrix metalloproteinase-mediated processing of a TNF prodrug
    J Gerspach
    1Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Cell Death Differ 13:273-84. 2006
    ..MMP-2-sensitive TNF prodrugs represent novel cytokine-based reagents for targeted cancer therapy, which should be exploitable for MMP-overexpressing tumors...
  24. ncbi request reprint TNF receptor type 2 mediates thymocyte proliferation independently of TNF receptor type 1
    M Grell
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Eur J Immunol 28:257-63. 1998
    ....
  25. ncbi request reprint Organization of the human tumour necrosis factor receptor-associated factor 1 (TRAF1) gene and mapping to chromosome 9q33-34
    K Siemienski
    Institute of Cell Biology and Immunology, Stuttgart, Germany
    Gene 195:35-9. 1997
    ..The putative promotor region of the TRAFI gene was isolated by use of a PCR-based genomic walking approach. Fluorescence in situ hybridization was used to map this gene to chromosome 9q33-34...
  26. ncbi request reprint Hydroxynitrile lyases in stereoselective catalysis
    F Effenberger
    Institut für Organische Chemie der Universität Stuttgart, Pfaffenwaldring 55, D 70569 Stuttgart, Germany
    Curr Opin Biotechnol 11:532-9. 2000
    ..The enantioselectivity of chiral metal-complex-catalyzed additions of trimethylsilyl cyanide to aldehydes has been improved, but is, by far, not yet competitive with the HNL-catalyzed reactions...
  27. ncbi request reprint CD95L/FasL and TRAIL in tumour surveillance and cancer therapy
    Harald Wajant
    Department of Molecular Internal Medicine, Medical Polyclinic, University of Wuerzburg, Roentgenring 11, 97070 Wuerzburg, Germany
    Cancer Treat Res 130:141-65. 2006
    ..This chapter focuses on the relevance of CD95L/FasL and TRAIL for the tumour surveillance function of natural killer cells and cytotoxic T-cells and discuss current concepts of utilizing these ligands in tumour therapy...
  28. ncbi request reprint Role of caspases in CD95L- and TRAIL-induced non-apoptotic signalling in pancreatic tumour cells
    Daniela Siegmund
    Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, and Division of Molecular Oncology, Clinic for General Surgery and Thoracic Surgery, University Hospital Schleswig Holstein, Kiel, Germany
    Cell Signal 19:1172-84. 2007
    ..Consequently, an NFkappaB and ERK stimulating, caspase-dependent factor must operate downstream of the DISC in Colo357-BclxL cells...
  29. ncbi request reprint Sustained JNK activation in response to tumor necrosis factor is mediated by caspases in a cell type-specific manner
    Andreas Wicovsky
    Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wurzburg, Rontgenring 11, 97070 Wurzburg, Germany
    J Biol Chem 282:2174-83. 2007
    ..Thus, sustained JNK activation by TNF has no obligate role in TNF-induced cell death and is mediated by caspases and reactive oxygen species in a cell type-specific manner...
  30. ncbi request reprint Implication of TNF-related apoptosis-inducing ligand in inflammatory intestinal epithelial lesions
    Bernadette Begue
    INSERM U793, Faculte de Medecine Necker, Universite Paris V, Paris, France
    Gastroenterology 130:1962-74. 2006
    ..In this work, we analyzed the potential implication of tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) in these inflammatory lesions...
  31. pmc Death receptor-induced signaling pathways are differentially regulated by gamma interferon upstream of caspase 8 processing
    Daniela Siegmund
    Department of Molecular Internal Medicine, Medical Polyclinic, University of Wurzburg, Rontgenring 11, 97070 Wurzburg, Germany
    Mol Cell Biol 25:6363-79. 2005
    ..Overexpression of FLIP(L) and FLIP(S) inhibited Fas- as well as TRAIL-mediated NF-kappaB activation and apoptosis induction in IFN-gamma-primed cells suggesting that both responses are coregulated at the level of the DISC...
  32. pmc The extracellular domains of FasL and Fas are sufficient for the formation of supramolecular FasL-Fas clusters of high stability
    Frank Henkler
    Department of Molecular Internal Medicine, Medical Polyclinic, University of Wuerzburg, 97070 Wuerzburg, Germany
    J Cell Biol 168:1087-98. 2005
    ....
  33. ncbi request reprint Tumor therapeutics by design: targeting and activation of death receptors
    Harald Wajant
    Department of Internal Molecular Medicine, Medical Polyclinic, University of Wuerzburg, Germany
    Cytokine Growth Factor Rev 16:55-76. 2005
    ....
  34. ncbi request reprint Enhanced basal AP-1 activity and de-regulation of numerous genes in T cells transgenic for a dominant interfering mutant of FADD/MORT1
    Svetla Chaneva
    Institute for Medical Microbiology, Immunology and Hygiene, Technical University Munich, Munich, Germany
    Eur J Immunol 34:3006-15. 2004
    ..The constitutive activation of AP-1 may thus serve to precondition resting T cells for an enhanced expression of many immunologically relevant genes during activation...
  35. pmc NFkappaB activation by Fas is mediated through FADD, caspase-8, and RIP and is inhibited by FLIP
    Sebastian Kreuz
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    J Cell Biol 166:369-80. 2004
    ..Thus, protection against Fas-induced apoptosis in a FLIP-independent manner converted a proapoptotic Fas signal into an inflammatory NFkappaB-related response...
  36. ncbi request reprint Apoptotic crosstalk of TNF receptors: TNF-R2-induces depletion of TRAF2 and IAP proteins and accelerates TNF-R1-dependent activation of caspase-8
    Mariola Fotin-Mleczek
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Cell Sci 115:2757-70. 2002
    ..Hence, TNF-R2 triggering can interfere with TNF-R1-induced apoptosis by inhibition of NF-kappaB-dependent production of anti-apoptotic factors and by blocking the action of anti-apoptotic factors at the post-transcriptional level...
  37. ncbi request reprint Endogenous membrane tumor necrosis factor (TNF) is a potent amplifier of TNF receptor 1-mediated apoptosis
    Monika Weingärtner
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 277:34853-9. 2002
    ..Moreover, we give evidence that this mechanism circumvents the need of the prolonged presence of exogenous soluble TNF for TNF-R1-mediated apoptosis induction...
  38. ncbi request reprint Rocaglamide derivatives are potent inhibitors of NF-kappa B activation in T-cells
    Bernd Baumann
    Department of Physiological Chemistry, Ulm University, Germany
    J Biol Chem 277:44791-800. 2002
    ..Our data suggest that rocaglamide derivatives could serve as lead structures in the development of anti-inflammatory and tumoricidal drugs...
  39. ncbi request reprint Intracellular localization and transcriptional regulation of tumor necrosis factor (TNF) receptor-associated factor 4 (TRAF4)
    Heike Glauner
    Institute of Cell Biology and Immunology and Institute of Industrial Genetics, University of Stuttgart, Germany Institute of Immunology, Christian Albrechts University of Kiel, Germany
    Eur J Biochem 269:4819-29. 2002
    ..These data suggest that activation of the NF-kappaB pathway is involved in up-regulation of TRAF4 in T-cells...
  40. pmc Selective inhibition of FLICE-like inhibitory protein expression with small interfering RNA oligonucleotides is sufficient to sensitize tumor cells for TRAIL-induced apoptosis
    Daniela Siegmund
    Institute of Cell Biology and Immunology, University of Stuttgart, Germany
    Mol Med 8:725-32. 2002
    ..The expression of the cellular FLICE-like inhibitory protein (cFLIP) is regarded as a major cause of TRAIL resistance. We therefore analyzed the usefulness of targeting FLIP to sensitize tumor cells for TRAIL-induced apoptosis...
  41. ncbi request reprint Caspase-mediated cleavage converts the tumor necrosis factor (TNF) receptor-associated factor (TRAF)-1 from a selective modulator of TNF receptor signaling to a general inhibitor of NF-kappaB activation
    Frank Henkler
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 278:29216-30. 2003
    ....
  42. ncbi request reprint Tumor necrosis factor receptor-associated factor (TRAF) 1 regulates CD40-induced TRAF2-mediated NF-kappaB activation
    Mariola Fotin-Mleczek
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 279:677-85. 2004
    ....
  43. doi request reprint Activity of soluble OX40 ligand is enhanced by oligomerization and cell surface immobilization
    Nicole Muller
    Department of Molecular Internal Medicine, Medical Clinic and Polyclinic II, University of Wuerzburg, Germany
    FEBS J 275:2296-304. 2008
    ..Trimeric single chain OX40L fusion proteins therefore represent a novel type of OX40L-derived immunostimulatory molecule with potentially reduced systemic side effects...
  44. doi request reprint Anti-tumor necrosis factor therapy inhibits pancreatic tumor growth and metastasis
    Jan Hendrik Egberts
    Division of Molecular Oncology, Department of General Surgery and Thoracic Surgery, University Hospital of Schleswig Holstein, Campus Kiel, Kiel, Germany
    Cancer Res 68:1443-50. 2008
    ..Thus, tumor cell-derived TNFalpha plays a profound role in malignancy of PDAC, and inhibition of TNFalpha represents a promising therapeutic option particularly in adjuvant therapy after subtotal pancreatectomy...
  45. doi request reprint Superior activity of fusion protein scFvRit:sFasL over cotreatment with rituximab and Fas agonists
    Edwin Bremer
    Groningen University Institute for Drug Exploration, Department of Pathology and Laboratory Medicine, University Medical Center Groningen, Groningen, The Netherlands
    Cancer Res 68:597-604. 2008
    ..In conclusion, scFvRit:sFasL efficiently activates CD20 and Fas-apoptotic signaling and may be useful for the elimination of malignant B cells...
  46. ncbi request reprint The CD95 receptor: apoptosis revisited
    Marcus E Peter
    Ben May Department for Cancer Research, University of Chicago, Chicago, IL 60637, USA
    Cell 129:447-50. 2007
    ..Recent evidence suggests, however, that CD95 mediates not only apoptosis but also diverse nonapoptotic functions depending on the tissue and the conditions...
  47. ncbi request reprint Generation of a FasL-based proapoptotic fusion protein devoid of systemic toxicity due to cell-surface antigen-restricted Activation
    Dierk Samel
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany
    J Biol Chem 278:32077-82. 2003
    ..The principle described here for the first time, in which cell-surface antigen-mediated activation of Fas permits local activation of Fas in vivo, opens novel avenues for the use of Fas signaling in cancer therapy...
  48. ncbi request reprint Death receptors
    Harald Wajant
    Department of Molecular Internal Medicine, Medical Polyclinic, University of Wuerzburg, Roentgenring 11, 97 070 Wuerzburg, Germany
    Essays Biochem 39:53-71. 2003
    ..This review is focused on the molecular mechanisms of apoptotic and non-apoptotic death receptor signalling in light of the phenotype of mice deficient in the various death receptors...
  49. ncbi request reprint A CD40-CD95L fusion protein interferes with CD40L-induced prosurvival signaling and allows membrane CD40L-restricted activation of CD95
    Constance Assohou-Luty
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany
    J Mol Med (Berl) 84:785-97. 2006
    ....
  50. ncbi request reprint Target-selective activation of a TNF prodrug by urokinase-type plasminogen activator (uPA) mediated proteolytic processing at the cell surface
    Jeannette Gerspach
    Institute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, Stuttgart, 70569, Germany
    Cancer Immunol Immunother 55:1590-600. 2006
    ..Processing optimised TNF prodrugs should increase the proportion of active therapeutic within the targeted tissue and thus potentially enhance tumor response rate...
  51. ncbi request reprint Interferons induce proteolytic degradation of TRAILR4
    Andreas Wicovsky
    Department of Molecular Internal Medicine, Medical Polyclinic, University of Wurzburg, Rontgenring 11, 97070 Wurzburg, Germany
    Biochem Biophys Res Commun 337:184-90. 2005
    ..Thus, the apoptosis-inducing action of interferons may not only rely on the well-established induction of TRAIL in effector cells but also on concomitant down-regulation of its antagonizing decoy receptor TRAILR4 in target cells...