Vishva M Dixit

Summary

Affiliation: Genentech Inc
Country: USA

Publications

  1. pmc Glyburide inhibits the Cryopyrin/Nalp3 inflammasome
    Mohamed Lamkanfi
    Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA
    J Cell Biol 187:61-70. 2009
  2. ncbi request reprint ATM engages autodegradation of the E3 ubiquitin ligase COP1 after DNA damage
    David Dornan
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 313:1122-6. 2006
  3. ncbi request reprint Cryopyrin activates the inflammasome in response to toxins and ATP
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 440:228-32. 2006
  4. doi request reprint Non-canonical inflammasome activation targets caspase-11
    Nobuhiko Kayagaki
    Department of Physiological Chemistry, Genentech Inc, South San Francisco, California 94080, USA
    Nature 479:117-21. 2011
  5. ncbi request reprint Rip2 participates in Bcl10 signaling and T-cell receptor-mediated NF-kappaB activation
    Astrid A Ruefli-Brasse
    Department of Molecular Oncology, Genentech, Inc, South San Francisco, California 94080, USA
    J Biol Chem 279:1570-4. 2004
  6. doi request reprint COP1 is a tumour suppressor that causes degradation of ETS transcription factors
    Alberto C Vitari
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 474:403-6. 2011
  7. doi request reprint Deubiquitinase USP9X stabilizes MCL1 and promotes tumour cell survival
    Martin Schwickart
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 463:103-7. 2010
  8. doi request reprint Phosphorylation of NLRC4 is critical for inflammasome activation
    Yan Qu
    Department of Physiological Chemistry, Genentech Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 490:539-42. 2012
  9. ncbi request reprint Loss of the tumor suppressor BAP1 causes myeloid transformation
    Anwesha Dey
    Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 337:1541-6. 2012
  10. pmc Improved quantitative mass spectrometry methods for characterizing complex ubiquitin signals
    Lilian Phu
    Departments of Protein Chemistry, Genentech, Inc, South San Francisco, California 94080, USA
    Mol Cell Proteomics 10:M110.003756. 2011

Collaborators

Detail Information

Publications58

  1. pmc Glyburide inhibits the Cryopyrin/Nalp3 inflammasome
    Mohamed Lamkanfi
    Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA
    J Cell Biol 187:61-70. 2009
    ..Therefore, glyburide is the first identified compound to prevent Cryopyrin activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion...
  2. ncbi request reprint ATM engages autodegradation of the E3 ubiquitin ligase COP1 after DNA damage
    David Dornan
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 313:1122-6. 2006
    ..Furthermore, phosphorylation of COP1 on Ser(387) was required to permit p53 to become stabilized and to exert its tumor suppressor properties in response to DNA damage...
  3. ncbi request reprint Cryopyrin activates the inflammasome in response to toxins and ATP
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 440:228-32. 2006
    ..Therefore, cryopyrin is essential for inflammasome activation in response to signalling pathways triggered specifically by ATP, nigericin, maitotoxin, S. aureus or L. monocytogenes...
  4. doi request reprint Non-canonical inflammasome activation targets caspase-11
    Nobuhiko Kayagaki
    Department of Physiological Chemistry, Genentech Inc, South San Francisco, California 94080, USA
    Nature 479:117-21. 2011
    ..These data highlight a unique pro-inflammatory role for caspase-11 in the innate immune response to clinically significant bacterial infections...
  5. ncbi request reprint Rip2 participates in Bcl10 signaling and T-cell receptor-mediated NF-kappaB activation
    Astrid A Ruefli-Brasse
    Department of Molecular Oncology, Genentech, Inc, South San Francisco, California 94080, USA
    J Biol Chem 279:1570-4. 2004
    ..Together these data define an important role for Rip2 in TCR-induced NF-kappaB activation and T-cell function and highlight the significance of post-translational modification of Bcl10 by Rip2 in T-cell signaling...
  6. doi request reprint COP1 is a tumour suppressor that causes degradation of ETS transcription factors
    Alberto C Vitari
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 474:403-6. 2011
    ..These findings identify COP1 as a tumour suppressor whose downregulation promotes prostatic epithelial cell proliferation and tumorigenesis...
  7. doi request reprint Deubiquitinase USP9X stabilizes MCL1 and promotes tumour cell survival
    Martin Schwickart
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 463:103-7. 2010
    ..These results identify USP9X as a prognostic and therapeutic target, and they show that deubiquitinases may stabilize labile oncoproteins in human malignancies...
  8. doi request reprint Phosphorylation of NLRC4 is critical for inflammasome activation
    Yan Qu
    Department of Physiological Chemistry, Genentech Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 490:539-42. 2012
    ..typhimurium infection, so phosphorylation of NLRC4 S533 probably drives conformational changes necessary for NLRC4 inflammasome activity and host innate immunity...
  9. ncbi request reprint Loss of the tumor suppressor BAP1 causes myeloid transformation
    Anwesha Dey
    Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 337:1541-6. 2012
    ..A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans...
  10. pmc Improved quantitative mass spectrometry methods for characterizing complex ubiquitin signals
    Lilian Phu
    Departments of Protein Chemistry, Genentech, Inc, South San Francisco, California 94080, USA
    Mol Cell Proteomics 10:M110.003756. 2011
    ..By combining these two powerful tools, we show that polyubiquitinated substrates purified from cells can be modified by mixtures of K48, K63, and K11 linkages...
  11. ncbi request reprint Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 430:213-8. 2004
    ..Notably, cell death triggered by stimuli that engage caspase-1 was ablated in macrophages lacking either ASC or Ipaf, suggesting a coupling between the inflammatory and cell death pathways...
  12. pmc Inflammasome-dependent release of the alarmin HMGB1 in endotoxemia
    Mohamed Lamkanfi
    Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA
    J Immunol 185:4385-92. 2010
    ..Thus, HMGB1 secretion, which is critical for endotoxemia, occurs downstream of inflammasome assembly and caspase 1 activation...
  13. ncbi request reprint The ubiquitin ligase COP1 is a critical negative regulator of p53
    David Dornan
    Department of Molecular Oncology, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 429:86-92. 2004
    ..Overall, these results indicate that COP1 is a critical negative regulator of p53 and represents a new pathway for maintaining p53 at low levels in unstressed cells...
  14. doi request reprint Ubiquitin binding to A20 ZnF4 is required for modulation of NF-κB signaling
    Ivan Bosanac
    Department of Structural Biology, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Mol Cell 40:548-57. 2010
    ....
  15. ncbi request reprint Constitutive NF-kappaB activation by the t(11;18)(q21;q21) product in MALT lymphoma is linked to deregulated ubiquitin ligase activity
    Honglin Zhou
    Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA
    Cancer Cell 7:425-31. 2005
    ..Thus, t(11;18)(q21;q21) deregulates MALT1/paracaspase ubiquitin ligase activity, causing constitutive NF-kappaB activation and promoting tumorigenesis...
  16. ncbi request reprint The inhibitor of apoptosis protein fusion c-IAP2.MALT1 stimulates NF-kappaB activation independently of TRAF1 AND TRAF2
    Eugene Varfolomeev
    Departments of Protein Engineering and Physiological Chemistry, Genentech, Inc, South San Francisco, California 94110, USA
    J Biol Chem 281:29022-9. 2006
    ..Therefore, the t(11, 18)(q21;q21) translocation creating the c-IAP2.MALT1 fusion protein activates NF-kappaB and contributes to human malignancy in the absence of signaling adaptors that might otherwise regulate its activity...
  17. doi request reprint Ubiquitin hydrolase Dub3 promotes oncogenic transformation by stabilizing Cdc25A
    Yaron Pereg
    Department of Physiological Chemistry, 1 DNA Way, South San Francisco, California, 94080, USA
    Nat Cell Biol 12:400-6. 2010
    ..As a major regulator of Cdc25A, Dub3 is an example of a transforming ubiquitin hydrolase that subverts a key component of the cell cycle machinery...
  18. ncbi request reprint Regulation of NF-kappaB-dependent lymphocyte activation and development by paracaspase
    Astrid A Ruefli-Brasse
    Molecular Oncology Department, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 302:1581-4. 2003
    ..Paracaspase acts downstream of Bcl10 to induce NF-kappaB activation and is required for the normal development of B cells, indicating that paracaspase provides the missing link between Bcl10 and activation of the IkappaB kinase complex...
  19. pmc Innate immunity against Francisella tularensis is dependent on the ASC/caspase-1 axis
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech Inc, South San Francisco, CA 94080, USA
    J Exp Med 202:1043-9. 2005
    ....
  20. doi request reprint Engineering and structural characterization of a linear polyubiquitin-specific antibody
    Marissa L Matsumoto
    Department of Antibody Engineering, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    J Mol Biol 418:134-44. 2012
    ..This antibody provides an essential tool for further investigation of the function of linear chains...
  21. doi request reprint Phosphorylation-dependent activity of the deubiquitinase DUBA
    Oscar W Huang
    Department of Early Discovery Biochemistry, Genentech, South San Francisco, California, USA
    Nat Struct Mol Biol 19:171-5. 2012
    ..Phosphoactivation of DUBA represents an unprecedented mode of protease regulation and a clear link between two major cellular signal transduction systems: phosphorylation and ubiquitin modification...
  22. ncbi request reprint IAP antagonists induce autoubiquitination of c-IAPs, NF-kappaB activation, and TNFalpha-dependent apoptosis
    Eugene Varfolomeev
    Department of Protein Engineering, Genentech, Inc, South San Francisco, CA 94080, USA
    Cell 131:669-81. 2007
    ..Through their ubiquitin E3 ligase activities c-IAP1 and c-IAP2 promote proteasomal degradation of NIK, the central ser/thr kinase in the noncanonical NF-kappaB pathway...
  23. pmc Phosphorylation of Dishevelled by protein kinase RIPK4 regulates Wnt signaling
    Xiaodong Huang
    Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 339:1441-5. 2013
    ..Wnt-dependent growth of xenografted human tumor cells was suppressed by RIPK4 knockdown, suggesting that RIPK4 overexpression may contribute to the growth of certain tumor types...
  24. ncbi request reprint BAFF/BLyS receptor 3 comprises a minimal TNF receptor-like module that encodes a highly focused ligand-binding site
    Nathaniel C Gordon
    Department of Protein Engineering, Genentech, Inc, One DNA Way, South San Francisco, California 94080, USA
    Biochemistry 42:5977-83. 2003
    ..Thus, BR3 binds BAFF through a highly focused interaction site, unprecedented in the TNFR family...
  25. ncbi request reprint The crystal structures of EDA-A1 and EDA-A2: splice variants with distinct receptor specificity
    Sarah G Hymowitz
    Department of Protein Engineering, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Structure 11:1513-20. 2003
    ..While the backbone conformation around the splice difference is similar in both isoforms, the conformation of the following loop, the surface charge, and the shape of the expected receptor binding site differ significantly...
  26. pmc Polyclonal hyper-IgE mouse model reveals mechanistic insights into antibody class switch recombination
    Shahram Misaghi
    Genentech, Inc, South San Francisco, CA 94080
    Proc Natl Acad Sci U S A 110:15770-5. 2013
    ..sequential switching, and reduces intraswitch recombination events at native Sμ. These results suggest that the sufficiency of Sμ to mediate IgH rearrangements may be influenced by context-dependent cues. ..
  27. doi request reprint Deubiquitinase USP37 is activated by CDK2 to antagonize APC(CDH1) and promote S phase entry
    Xiaodong Huang
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Mol Cell 42:511-23. 2011
    ..USP37 was inactive in mitosis because it was no longer phosphorylated by CDK2. Indeed, it switched from an antagonist to a substrate of APC(CDH1) and was modified with degradative K11-linked polyubiquitin...
  28. doi request reprint Inflammasomes: guardians of cytosolic sanctity
    Mohamed Lamkanfi
    Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA
    Immunol Rev 227:95-105. 2009
    ..Further understanding of inflammasomes and their role in innate immunity should provide new insights into the mechanisms of host defense and the pathogenesis of autoimmune diseases...
  29. ncbi request reprint Loss of TACI causes fatal lymphoproliferation and autoimmunity, establishing TACI as an inhibitory BLyS receptor
    Dhaya Seshasayee
    Department of Immunology, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Immunity 18:279-88. 2003
    ..These results demonstrate the critical requirement for TACI in regulating B cell homeostasis...
  30. doi request reprint Pannexin-1 is required for ATP release during apoptosis but not for inflammasome activation
    Yan Qu
    Physiological Chemistry Department, Genentech, Inc, South San Francisco, CA 94080, USA
    J Immunol 186:6553-61. 2011
    ..These data are consistent with pannexin-1 liberating ATP and other yet to be defined "find me" signals necessary for macrophage recruitment to apoptotic cells...
  31. doi request reprint Modulation of K11-linkage formation by variable loop residues within UbcH5A
    Ivan Bosanac
    Department of Structural Biology, Genentech Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    J Mol Biol 408:420-31. 2011
    ..This study provides direct evidence that the linkage specificity of E2 enzymes may be altered through active-site mutagenesis...
  32. ncbi request reprint DUBA: a deubiquitinase that regulates type I interferon production
    Nobuhiko Kayagaki
    Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA
    Science 318:1628-32. 2007
    ..A discrete ubiquitin interaction motif within DUBA was required for efficient deubiquitination of TRAF3 and optimal suppression of IFN-I. Our data identify DUBA as a negative regulator of innate immune responses...
  33. pmc Kinase RIP3 is dispensable for normal NF-kappa Bs, signaling by the B-cell and T-cell receptors, tumor necrosis factor receptor 1, and Toll-like receptors 2 and 4
    Kim Newton
    Molecular Oncology Department, Genentech, Inc, South San Francisco, California 94080, USA
    Mol Cell Biol 24:1464-9. 2004
    ..Thus, we can exclude RIP3 as an essential modulator of NF-kappa B signaling downstream of several receptor systems...
  34. pmc Association of C-terminal ubiquitin hydrolase BRCA1-associated protein 1 with cell cycle regulator host cell factor 1
    Shahram Misaghi
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Mol Cell Biol 29:2181-92. 2009
    ....
  35. doi request reprint Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis
    Kim Newton
    Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Science 343:1357-60. 2014
    ..Our data indicate that the kinase activity of RIPK3 is essential for necroptosis but also governs whether a cell activates caspase-8 and dies by apoptosis. ..
  36. doi request reprint Noncanonical inflammasome activation by intracellular LPS independent of TLR4
    Nobuhiko Kayagaki
    Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA
    Science 341:1246-9. 2013
    ..coli LPS. These data unveil a TLR4-independent mechanism for innate immune recognition of LPS. ..
  37. ncbi request reprint Bcl10 activates the NF-kappaB pathway through ubiquitination of NEMO
    Honglin Zhou
    Department of Molecular Oncology, Genentech Inc 1 DNA Way, South San Francisco, California 94080, USA
    Nature 427:167-71. 2004
    ..Thus, the adaptor protein Bcl10 promotes activation of NF-kappaB transcription factors through paracaspase- and UBC13-dependent ubiquitination of NEMO...
  38. pmc Myodegeneration in EDA-A2 transgenic mice is prevented by XEDAR deficiency
    Kim Newton
    Molecular Oncology Department, Genentech, Inc, South San Francisco, California 94080, USA
    Mol Cell Biol 24:1608-13. 2004
    ..These data indicate that XEDAR-transduced signals are dispensable for development of ectoderm-derived organs but might play a role in skeletal muscle homeostasis...
  39. ncbi request reprint COP1, the negative regulator of p53, is overexpressed in breast and ovarian adenocarcinomas
    David Dornan
    Department of Molecular Oncology, Genentech, Inc, South San Francisco, California, USA
    Cancer Res 64:7226-30. 2004
    ..Overall, these results suggest that overexpression of COP1 contributes to the accelerated degradation of p53 protein in cancers and attenuates the tumor suppressor function of p53...
  40. doi request reprint Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7
    Ingrid E Wertz
    Department of Early Discovery Biochemistry, Genentech, South San Francisco, California 94080, USA
    Nature 471:110-4. 2011
    ..Our findings suggest that profiling the FBW7 and MCL1 status of tumours, in terms of protein levels, messenger RNA levels and genetic status, could be useful to predict the response of patients to antitubulin chemotherapeutics...
  41. doi request reprint K11-linked polyubiquitination in cell cycle control revealed by a K11 linkage-specific antibody
    Marissa L Matsumoto
    Department of Antibody Engineering, Genentech, Inc, South San Francisco, CA 94080, USA
    Mol Cell 39:477-84. 2010
    ..Our results underscore the importance of K11-linked ubiquitin chains as critical regulators of mitotic protein degradation...
  42. pmc Signaling to NF-kappaB: regulation by ubiquitination
    Ingrid E Wertz
    Department of Protein Engineering, Genentech, Inc, South San Francisco, California 94080, USA
    Cold Spring Harb Perspect Biol 2:a003350. 2010
    ....
  43. doi request reprint Using linkage-specific monoclonal antibodies to analyze cellular ubiquitylation
    Kim Newton
    Physiological Chemistry Department, Genentech, Inc, South San Francisco, CA, USA
    Methods Mol Biol 832:185-96. 2012
    ..Here, we describe protocols for revealing K11-, K48-, and K63-linked polyubiquitin chains by western blotting, immunoprecipitation, or immunostaining...
  44. ncbi request reprint BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete surface loop and promotes processing of NF-kappaB2
    Nobuhiko Kayagaki
    Department of Molecular Oncology, Genentech, Inc, South San Francisco, CA 94080, USA
    Immunity 17:515-24. 2002
    ..When stabilized within a structured beta-hairpin peptide, six of these residues were sufficient to confer binding to BAFF...
  45. ncbi request reprint Human De-etiolated-1 regulates c-Jun by assembling a CUL4A ubiquitin ligase
    Ingrid E Wertz
    Department of Molecular Oncology, Genentech, Inc, South San Francisco, CA 94080, USA
    Science 303:1371-4. 2004
    ..Ablation of any subunit by RNA interference stabilized c-Jun and increased c-Jun-activated transcription. These findings characterize a c-Jun ubiquitin ligase and define a specific function for hDET1 in mammalian cells...
  46. ncbi request reprint Ubiquitin chain editing revealed by polyubiquitin linkage-specific antibodies
    Kim Newton
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Cell 134:668-78. 2008
    ..Polyubiquitin editing may therefore be a general mechanism for attenuating innate immune signaling...
  47. pmc Yersinia virulence factor YopJ acts as a deubiquitinase to inhibit NF-kappa B activation
    Honglin Zhou
    Molecular Oncology Department, Genentech, Inc, San Francisco, CA 94080, USA
    J Exp Med 202:1327-32. 2005
    ..Moreover, an in vitro assay was established to demonstrate directly the deubiquitinating activity of purified YopJ...
  48. ncbi request reprint Identification of a novel death domain-containing adaptor molecule for ectodysplasin-A receptor that is mutated in crinkled mice
    Minhong Yan
    Department of Molecular Oncology, Genentech Inc, South San Francisco, CA 94080, USA
    Curr Biol 12:409-13. 2002
    ..This is an unprecedented example of naturally occurring mutations in ligand, receptor, or adaptor giving rise to the same phenotypic disease characterized by a defect in the proper development of epidermal appendages...
  49. ncbi request reprint Increased targeting of donor switch region and IgE in Sgamma1-deficient B cells
    Shahram Misaghi
    Department of Physiological Chemistry, Genentech, San Francisco, CA 94080, USA
    J Immunol 185:166-73. 2010
    ..Thus, prominently transcribed S regions, such as Sgamma1, might provide a sufficient sink for AID protein to titrate away AID from other accessible sites within or outside the Ig locus...
  50. doi request reprint IL-33 raises alarm
    Mohamed Lamkanfi
    Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Immunity 31:5-7. 2009
    ..In this issue of Immunity, Lüthi et al. (2009) show that IL-33 is not a caspase-1 substrate. IL-33 is inactivated by caspase-3 and -7 to prevent an inappropriate immune response during apoptosis, but not in necrosis...
  51. ncbi request reprint Mice lacking the CARD of CARMA1 exhibit defective B lymphocyte development and impaired proliferation of their B and T lymphocytes
    Kim Newton
    Molecular Oncology Department, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA
    Curr Biol 13:1247-51. 2003
    ..Thus, CARMA1 has an essential role in mediating B and T lymphocyte proliferation and requires its CARD to engage downstream signaling components...
  52. doi request reprint USP1 deubiquitinates ID proteins to preserve a mesenchymal stem cell program in osteosarcoma
    Samuel A Williams
    Department of Physiological Chemistry, Genentech, Inc, 1 DNA Way, South San Francisco, CA 94080, USA
    Cell 146:918-30. 2011
    ..Our observations implicate USP1 in preservation of the stem cell state that characterizes osteosarcoma and identify USP1 as a target for differentiation therapy...
  53. doi request reprint Ubiquitylation in apoptosis: a post-translational modification at the edge of life and death
    Domagoj Vucic
    Department of Early Discovery Biochemistry, Genentech Inc, South San Francisco, California 94080, USA
    Nat Rev Mol Cell Biol 12:439-52. 2011
    ..Therapeutic agents that target apoptotic regulatory proteins, including those that are part of the ubiquitin-proteasome system, might afford clinical benefits...
  54. ncbi request reprint Ubiquitin-mediated regulation of TNFR1 signaling
    Ingrid E Wertz
    Department of Protein Engineering, Genentech, Inc, 1 DNA Way, M S 40, South San Francisco, CA 94080, United States
    Cytokine Growth Factor Rev 19:313-24. 2008
    ..In this review, we will summarize the ubiquitin/proteasome system and discuss the ubiquitin-mediated regulation of TNFR1 signaling...
  55. pmc Masking MALT1: the paracaspase's potential for cancer therapy
    Domagoj Vucic
    Department of Protein Engineering, Genentech, Inc, South San Francisco, CA 94080, USA
    J Exp Med 206:2309-12. 2009
    ..New data shows that targeting MALT1 protease activity may be a promising therapeutic strategy for treating aggressive B cell lymphomas...
  56. pmc Mitochondrial reactive oxygen species drive proinflammatory cytokine production
    Edwina Naik
    Genentech, Inc, South San Francisco, CA 94080, USA
    J Exp Med 208:417-20. 2011
    ..New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways...
  57. ncbi request reprint SMAC negatively regulates the anti-apoptotic activity of melanoma inhibitor of apoptosis (ML-IAP)
    Domagoj Vucic
    Department of Molecular Oncology, Genentech, Inc, South San Francisco, California 94080, USA
    J Biol Chem 277:12275-9. 2002
    ..These results demonstrate the feasibility of using SMAC peptides as a way to sensitize IAP-expressing cells to pro-apoptotic stimuli such as chemotherapeutic agents...
  58. pmc Modulation of inflammasome activity for the treatment of auto-inflammatory disorders
    Edwina Naik
    Genentech, Inc, South San Francisco, CA, USA
    J Clin Immunol 30:485-90. 2010
    ..As much is now known about how inflammasomes are regulated, it is hoped that this can be channeled into the development of novel therapeutics, for example, those that may block the upstream activation and assembly of inflammasomes...