J C Reed

Summary

Affiliation: The Burnham Institute
Country: USA

Publications

  1. pmc Bcl-2 interacting protein, BAG-1, binds to and activates the kinase Raf-1
    H G Wang
    The Burnham Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 93:7063-8. 1996
  2. ncbi request reprint Interaction of BAG-1 with retinoic acid receptor and its inhibition of retinoic acid-induced apoptosis in cancer cells
    R Liu
    The Burnham Institute, Cancer Research Center, La Jolla, California 92037, USA
    J Biol Chem 273:16985-92. 1998
  3. ncbi request reprint Bcl-2 family proteins and mitochondria
    J C Reed
    The Burnham Institute, Program on Apoptosis and Cell Death Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Biochim Biophys Acta 1366:127-37. 1998
  4. ncbi request reprint A method for functional evaluation of caspase activation pathways in intact lymphoid cells using electroporation-mediated protein delivery and flow cytometric analysis
    Emel Eksioglu-Demiralp
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    J Immunol Methods 275:41-56. 2003
  5. ncbi request reprint The domains of apoptosis: a genomics perspective
    John C Reed
    The Burnham Institute, La Jolla, CA 92037, USA
    Sci STKE 2004:re9. 2004
  6. ncbi request reprint Apoptosis-based therapies
    John C Reed
    Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Rev Drug Discov 1:111-21. 2002
  7. pmc Comparative analysis of apoptosis and inflammation genes of mice and humans
    John C Reed
    The Burnham Institute, La Jolla, California 92037, USA
    Genome Res 13:1376-88. 2003
  8. ncbi request reprint Apoptosis-regulating proteins as targets for drug discovery
    J C Reed
    The Burnham Institute, La Jolla, CA 92037, USA
    Trends Mol Med 7:314-9. 2001
  9. ncbi request reprint Apoptosis-targeted therapies for cancer
    John C Reed
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Cancer Cell 3:17-22. 2003
  10. ncbi request reprint Bifunctional apoptosis inhibitor (BAR) protects neurons from diverse cell death pathways
    W Roth
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 10:1178-87. 2003

Collaborators

Detail Information

Publications136 found, 100 shown here

  1. pmc Bcl-2 interacting protein, BAG-1, binds to and activates the kinase Raf-1
    H G Wang
    The Burnham Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 93:7063-8. 1996
    ..BAG-1 also activates this mammalian kinase in yeast. These observations suggest that the Bcl-2 binding protein BAG-1 joins Ras and 14-3-3 proteins as potential activators of the kinase Raf-1...
  2. ncbi request reprint Interaction of BAG-1 with retinoic acid receptor and its inhibition of retinoic acid-induced apoptosis in cancer cells
    R Liu
    The Burnham Institute, Cancer Research Center, La Jolla, California 92037, USA
    J Biol Chem 273:16985-92. 1998
    ..These results demonstrate that BAG-1 can regulate retinoid activities through its interaction with RAR and suggest that elevated levels of BAG-1 protein could potentially contribute to retinoid resistance in cancer cells...
  3. ncbi request reprint Bcl-2 family proteins and mitochondria
    J C Reed
    The Burnham Institute, Program on Apoptosis and Cell Death Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Biochim Biophys Acta 1366:127-37. 1998
    ....
  4. ncbi request reprint A method for functional evaluation of caspase activation pathways in intact lymphoid cells using electroporation-mediated protein delivery and flow cytometric analysis
    Emel Eksioglu-Demiralp
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    J Immunol Methods 275:41-56. 2003
    ....
  5. ncbi request reprint The domains of apoptosis: a genomics perspective
    John C Reed
    The Burnham Institute, La Jolla, CA 92037, USA
    Sci STKE 2004:re9. 2004
    ....
  6. ncbi request reprint Apoptosis-based therapies
    John C Reed
    Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Rev Drug Discov 1:111-21. 2002
    ....
  7. pmc Comparative analysis of apoptosis and inflammation genes of mice and humans
    John C Reed
    The Burnham Institute, La Jolla, California 92037, USA
    Genome Res 13:1376-88. 2003
    ..With this caveat, we discuss similarities and differences in human and murine genes from these domain families...
  8. ncbi request reprint Apoptosis-regulating proteins as targets for drug discovery
    J C Reed
    The Burnham Institute, La Jolla, CA 92037, USA
    Trends Mol Med 7:314-9. 2001
    ....
  9. ncbi request reprint Apoptosis-targeted therapies for cancer
    John C Reed
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Cancer Cell 3:17-22. 2003
  10. ncbi request reprint Bifunctional apoptosis inhibitor (BAR) protects neurons from diverse cell death pathways
    W Roth
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 10:1178-87. 2003
    ..Taken together, the expression pattern and functional data suggest that the BAR protein is involved in the regulation of neuronal survival...
  11. ncbi request reprint Regulation of Nur77 nuclear export by c-Jun N-terminal kinase and Akt
    Y H Han
    Burnham Institute for Medical Research, Cancer Center, La Jolla, CA 92037, USA
    Oncogene 25:2974-86. 2006
    ..Together, our results demonstrate that both activation of JNK and inhibition of Akt play a role in translocation of Nur77 from the nucleus to the cytoplasm...
  12. ncbi request reprint A diverse family of proteins containing tumor necrosis factor receptor-associated factor domains
    J M Zapata
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:24242-52. 2001
    ..We propose the moniker TEFs (TD-encompassing factors) for this large family of proteins...
  13. pmc BAR: An apoptosis regulator at the intersection of caspases and Bcl-2 family proteins
    H Zhang
    Program on Apoptosis and Cell Death Regulation, The Burnham Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 97:2597-602. 2000
    ..The BAR protein is anchored in intracellular membranes where Bcl-2 resides. BAR therefore may represent a scaffold protein capable of bridging two major apoptosis pathways...
  14. pmc Microtubule-targeting drugs induce bcl-2 phosphorylation and association with Pin1
    N Pathan
    The Burnham Institute, 10901 N Torrey Pines Rd, La Jolla, CA 92037, USA
    Neoplasia 3:550-9. 2001
    ....
  15. ncbi request reprint TRAF1 is a substrate of caspases activated during tumor necrosis factor receptor-alpha-induced apoptosis
    E Leo
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:8087-93. 2001
    ..These data identify TRAF1 as a specific target of caspases activated during TNF- and Fas-induced apoptosis and illustrate differences in the repertoire of protease substrates cleaved during activation of different apoptotic pathways...
  16. ncbi request reprint Bcl-B, a novel Bcl-2 family member that differentially binds and regulates Bax and Bak
    N Ke
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:12481-4. 2001
    ..Bcl-B thus displays a unique pattern of selectivity for binding and regulating the function of other members of the Bcl-2 family...
  17. ncbi request reprint CLAN, a novel human CED-4-like gene
    J S Damiano
    The Burnham Institute, La Jolla, California 92037, USA
    Genomics 75:77-83. 2001
    ..The CARD of the CLAN proteins binds a number of other CARD-containing proteins including caspase-1, BCL10, NOD2, and NAC. Once their physiologic functions are uncovered, CLAN proteins may prove to be valuable therapeutic targets...
  18. ncbi request reprint TUCAN, an antiapoptotic caspase-associated recruitment domain family protein overexpressed in cancer
    N Pathan
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:32220-9. 2001
    ..Thus, TUCAN represents a new member of the CARD family that selectively suppresses apoptosis induced via the mitochondrial pathway for caspase activation...
  19. ncbi request reprint Structure-function analysis of Bag1 proteins. Effects on androgen receptor transcriptional activity
    D A Knee
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:12718-24. 2001
    ..Thus, both the unique NH(2)-terminal domain and the COOH-terminal Hsc70-binding domain of Bag1L are simultaneously required for its function as an AR regulator, whereas the conserved ubiquitin-like domain is expendable...
  20. ncbi request reprint Siah-1, SIP, and Ebi collaborate in a novel pathway for beta-catenin degradation linked to p53 responses
    S I Matsuzawa
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Cell 7:915-26. 2001
    ..Expression of Siah is induced by p53, revealing a way of linking genotoxic injury to destruction of beta-catenin, thus reducing activity of Tcf/LEF transcription factors and contributing to cell cycle arrest...
  21. ncbi request reprint Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis
    S Matsuyama
    Programme on Apoptosis and Cell Death Regulation, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Cell Biol 2:318-25. 2000
    ..These findings indicate that mitochondria-mediated alteration of intracellular pH may be an early event that regulates caspase activation in the mitochondrial pathway for apoptosis...
  22. ncbi request reprint Bax inhibitor-1, a mammalian apoptosis suppressor identified by functional screening in yeast
    Q Xu
    Burnham Institute Program on Apoptosis and Cell Death Research La Jolla, California 92037, USA
    Mol Cell 1:337-46. 1998
    ..Conversely, BI-1 antisense induced apoptosis. BI-1 thus represents a new type of regulator of cell death pathways controlled by Bcl-2 and Bax...
  23. ncbi request reprint Expression and location of Hsp70/Hsc-binding anti-apoptotic protein BAG-1 and its variants in normal tissues and tumor cell lines
    S Takayama
    The Burnham Institute, La Jolla, California 92037, USA
    Cancer Res 58:3116-31. 1998
    ....
  24. pmc IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases
    Q L Deveraux
    The Burnham Institute, Program on Apoptosis and Cell Death Research, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    EMBO J 17:2215-23. 1998
    ..These findings demonstrate that IAPs can suppress different apoptotic pathways by inhibiting distinct caspases and identify pro-caspase-9 as a new target for IAP-mediated inhibition of apoptosis...
  25. ncbi request reprint Dynamics of expression of apoptosis-regulatory proteins Bid, Bcl-2, Bcl-X, Bax and Bak during development of murine nervous system
    M Krajewska
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 9:145-57. 2002
    ..Among the Bcl-2 family proteins only Bid and Bcl-XL continue to be expressed at high levels in the adult brain...
  26. pmc The c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspases
    N Roy
    The Burnham Institute, Program on Apoptosis and Cell Death Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    EMBO J 16:6914-25. 1997
    ..Taken together, these findings suggest that c-IAP-1 and c-IAP-2 function similarly to XIAP by inhibiting the distal cell death proteases, caspases-3 and -7, whereas NAIP presumably inhibits apoptosis via other targets...
  27. ncbi request reprint Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD
    H G Wang
    The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Science 284:339-43. 1999
    ..Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells...
  28. ncbi request reprint Immunohistochemical analysis of in vivo patterns of expression of CPP32 (Caspase-3), a cell death protease
    M Krajewska
    Apoptosis and Cell Death Research Program, The Burnham Institute, La Jolla, California 92037, USA
    Cancer Res 57:1605-13. 1997
    ..These findings establish for the first time the cell type- and differentiation-specific patterns of expression of an interleukin-1beta converting enzyme/CED-3 (Caspase) family protease...
  29. pmc Release of caspase-9 from mitochondria during neuronal apoptosis and cerebral ischemia
    S Krajewski
    The Burnham Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 96:5752-7. 1999
    ..Loss of mitochondrial barrier function during neuronal damage from ischemia or other insults therefore may play an important role in making certain caspases available to participate in apoptosis...
  30. ncbi request reprint Structural analysis of BAG1 cochaperone and its interactions with Hsc70 heat shock protein
    K Briknarová
    The Burnham Institute, La Jolla, California 92037, USA
    Nat Struct Biol 8:349-52. 2001
    ..The results provide a structural basis for understanding the mechanism by which BAG proteins link molecular chaperones and cell signaling pathways...
  31. ncbi request reprint The carboxyl-terminal lobe of Hsc70 ATPase domain is sufficient for binding to BAG1
    L Brive
    The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, California 92037, USA
    Biochem Biophys Res Commun 289:1099-105. 2001
    ..This result suggests that the stabilizing contacts for docking of BAG1 to Hsc70 are located in the C-terminal lobe of the ATPase domain. These findings provide new insights into the role of co-chaperones as nucleotide exchange factors...
  32. ncbi request reprint IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs
    I Tamm
    The Burnham Institute, La Jolla, California 92037, USA
    Cancer Res 58:5315-20. 1998
    ..Although quantitative differences may exist, these observations suggest commonality in the mechanisms used by IAP-family proteins to suppress apoptosis...
  33. doi request reprint TRAF2-binding BIR1 domain of c-IAP2/MALT1 fusion protein is essential for activation of NF-kappaB
    J B Garrison
    Program on Apoptosis and Cell Death Research, Cancer Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Oncogene 28:1584-93. 2009
    ....
  34. pmc BAG-1 modulates the chaperone activity of Hsp70/Hsc70
    S Takayama
    The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, CA 92037, USA
    EMBO J 16:4887-96. 1997
    ..The inhibitory effects of BAG-1 on Hsp/Hsc70 chaperone activity suggest that BAG-1 represents a novel type of chaperone regulatory proteins and thus suggest a link between cell signaling, cell death and the stress response...
  35. ncbi request reprint A GTP-binding adapter protein couples TRAIL receptors to apoptosis-inducing proteins
    T Miyazaki
    The Burnham Institute, 10901 N Torrey Pines Rd, La Jolla, CA 92037, USA
    Nat Immunol 2:493-500. 2001
    ..Elucidation of this mechanism suggests GTP-binding proteins as potential targets for pharmacological intervention in TRAIL-induced apoptosis...
  36. ncbi request reprint Regulation of cell death protease caspase-9 by phosphorylation
    M H Cardone
    Program on Apoptosis and Cell Death Research, The Burnham Institute, La Jolla, CA 92037, USA
    Science 282:1318-21. 1998
    ..Mutant pro-Casp9(Ser196Ala) was resistant to Akt-mediated phosphorylation and inhibition in vitro and in cells, resulting in Akt-resistant induction of apoptosis. Thus, caspases can be directly regulated by protein phosphorylation...
  37. ncbi request reprint BIRinging chromosomes through cell division--and survivin' the experience
    J C Reed
    The Burnham Institute, La Jolla, California 92037, USA
    Cell 102:545-8. 2000
  38. ncbi request reprint TNFR-associated factor family protein expression in normal tissues and lymphoid malignancies
    J M Zapata
    The Burnham Institute, Program on Apoptosis and Cell Death Regulation, La Jolla, California 92037, USA
    J Immunol 165:5084-96. 2000
    ..01), as determined by immunoblotting. These findings contribute to an improved understanding of the cell-specific roles of TRAFs in normal tissues and provide evidence of altered TRAF1 expression in lymphoid malignancies...
  39. pmc Microtubule-targeting drugs induce Bcl-2 phosphorylation and association with Pin1
    N Pathan
    The Burnham Institute, 10901 N Torrey Pines, La Jolla, CA 92037, USA
    Neoplasia 3:70-9. 2001
    ....
  40. ncbi request reprint A novel enhancer of the Apaf1 apoptosome involved in cytochrome c-dependent caspase activation and apoptosis
    Z L Chu
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:9239-45. 2001
    ..NAC expression in vivo is associated with terminal differentiation of short lived cells in epithelia and some other tissues. The ability of NAC to enhance Apaf1-apoptosome function reveals a novel paradigm for apoptosis regulation...
  41. ncbi request reprint Bcl-2 targets the protein kinase Raf-1 to mitochondria
    H G Wang
    The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA
    Cell 87:629-38. 1996
    ..Bcl-2 can therefore target Raf-1 to mitochondrial membranes, allowing this kinase to phosphorylate BAD or possibly other protein substrates involved in apoptosis regulation...
  42. ncbi request reprint An evolutionarily conserved family of Hsp70/Hsc70 molecular chaperone regulators
    S Takayama
    The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 274:781-6. 1999
    ..The findings suggest opportunities for specification and diversification of Hsp70/Hsc70 chaperone functions through interactions with various BAG-family proteins...
  43. pmc Bax directly induces release of cytochrome c from isolated mitochondria
    J M Jurgensmeier
    Program on Apoptosis and Cell Death Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 95:4997-5002. 1998
    ....
  44. ncbi request reprint Bag1 is a regulator and marker of neuronal differentiation
    P Kermer
    The Burnham Institute, Program on Apoptosis and Cell Death Research, 10901 N Torrey Pines Road, La Jolla, California, CA 92037, USA
    Cell Death Differ 9:405-13. 2002
    ..Taken together, these findings raise the possibility that the Bag1 protein is expressed early in neurogenesis in vivo and is capable of modulating neuronal cell survival and differentiation at least in part from a nuclear location...
  45. pmc p53-inducible human homologue of Drosophila seven in absentia (Siah) inhibits cell growth: suppression by BAG-1
    S Matsuzawa
    Burnham Institute, La Jolla, CA 92037, USA
    EMBO J 17:2736-47. 1998
    ..We suggest that Siah-1A may be an important mediator of p53-dependent cell-cycle arrest and demonstrate that Siah-1A is directly inhibited by BAG-1...
  46. ncbi request reprint Caspase-9 can be activated without proteolytic processing
    H R Stennicke
    The Program for Apoptosis and Cell Death Research, The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 274:8359-62. 1999
    ..Thus caspase-9 has an unusually active zymogen that does not require proteolytic processing, but instead is dependent on cytosolic factors for expression of its activity...
  47. ncbi request reprint Drosophila pro-apoptotic Bcl-2/Bax homologue reveals evolutionary conservation of cell death mechanisms
    H Zhang
    Program on Apoptosis and Cell Death Regulation, Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 275:27303-6. 2000
    ..Moreover, DBok targets mitochondria and triggers cytochrome c release through a caspase-independent mechanism. These characteristics of DBok reveal evolutionary conservation of cell death mechanisms in flies and humans...
  48. ncbi request reprint The Drosophila tumor necrosis factor receptor-associated factor-1 (DTRAF1) interacts with Pelle and regulates NFkappaB activity
    J M Zapata
    The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 275:12102-7. 2000
    ..Interactions of DTRAF1 with human TRAF-, TNF receptor-, and IAP-family proteins imply strong evolutionary conservation of TRAF protein structure and function throughout Metazoan evolution...
  49. ncbi request reprint Thymidine-phosphorothioate oligonucleotides induce activation and apoptosis of CLL cells independently of CpG motifs or BCL-2 gene interference
    J E Castro
    John and Rebecca Moores Cancer Center, University of California San Diego, La Jolla, CA, USA
    Leukemia 20:680-8. 2006
    ..We conclude that thymidine-containing PS-ODN can activate CLL cells and induce apoptosis via a mechanism that is independent of BCL-2 gene interference or CpG motifs...
  50. ncbi request reprint Characterization of interactions between the anti-apoptotic protein BAG-1 and Hsc70 molecular chaperones
    J K Stuart
    Burnham Institute, Cancer Research Center, La Jolla, California 92037, USA
    J Biol Chem 273:22506-14. 1998
    ..Molecular modeling permitted a comparison of structural features between the functionally homologous BAG-1 and GrpE proteins. These data were used to propose a mechanism for BAG-1 in the regulation of Hsp70/Hsc70 chaperone activity...
  51. ncbi request reprint Bcl-G, a novel pro-apoptotic member of the Bcl-2 family
    B Guo
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:2780-5. 2001
    ..A mutant of Bcl-G(L) in which the BH2 domain was deleted displayed increased apoptotic activity and coimmunoprecipitated with Bcl-X(L), suggesting that the BH2 domain autorepresses Bcl-G(L)...
  52. ncbi request reprint BAG1L enhances trans-activation function of the vitamin D receptor
    M Guzey
    Burnham Institute, La Jolla, California 92037 and RIGEB, MAM TUBITAK, P K 21 Gebze 41 470, Kocaeli, Turkey
    J Biol Chem 275:40749-56. 2000
    ..Thus, BAG1L is a direct regulator of VDR, which enhances its trans-activation function and improves tumor cell responses to growth-suppressive VDR ligands...
  53. ncbi request reprint Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3
    H Li
    The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Science 289:1159-64. 2000
    ..Our results reveal a mechanism by which a nuclear transcription factor translocates to mitochondria to initiate apoptosis...
  54. ncbi request reprint X-linked IAP is a direct inhibitor of cell-death proteases
    Q L Deveraux
    The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA
    Nature 388:300-4. 1997
    ....
  55. ncbi request reprint A single BIR domain of XIAP sufficient for inhibiting caspases
    R Takahashi
    Burnham Institute, Program on Apoptosis and Cell Death Regulation, La Jolla, California 92037, USA
    J Biol Chem 273:7787-90. 1998
    ..These findings identify BIR2 as the minimal caspase-inhibitory domain of XIAP and indicate that a single BIR domain can be sufficient for binding and inhibiting caspases...
  56. ncbi request reprint BAG-1L protein enhances androgen receptor function
    B A Froesch
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 273:11660-6. 1998
    ..These findings implicate BAG-1L in the regulation of AR function and may have relevance to mechanisms of prostate cancer resistance to hormone-ablative and anti-androgen therapy...
  57. ncbi request reprint Cloning of cDNAs encoding the human BAG1 protein and localization of the human BAG1 gene to chromosome 9p12
    S Takayama
    Bumham Institute, La Jolla, California 92037, USA
    Genomics 35:494-8. 1996
    ....
  58. ncbi request reprint TRAF family proteins interact with the common neurotrophin receptor and modulate apoptosis induction
    X Ye
    The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 274:30202-8. 1999
    ..These results demonstrate that TRAF family proteins interact with p75(NTR) and differentially modulate its NF-kappaB activation and cell death induction...
  59. ncbi request reprint PAAD - a new protein domain associated with apoptosis, cancer and autoimmune diseases
    K Pawłowski
    Program in Bioinformatics and Biological Complexity, The Burnham Institute, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Trends Biochem Sci 26:85-7. 2001
    ..Its location within these proteins and predicted fold suggests that it functions as a protein-protein interaction domain, possibly uniting different signaling pathways...
  60. pmc Mechanisms of apoptosis
    J C Reed
    Burnham Institute, La Jolla, California 92037, USA
    Am J Pathol 157:1415-30. 2000
    ..Knowledge of the molecular mechanisms of apoptosis is providing insights into the causes of multiple pathologies where aberrant cell death regulation occurs and is beginning to provide new approaches to the treatment of human diseases...
  61. pmc Expression and potential role of Fas-associated phosphatase-1 in ovarian cancer
    I Meinhold-Heerlein
    Program on Apoptosis and Cell Death Research, The Burnham Institute, 10901 North Torrey Pines Rd, La Jolla, CA 92037, USA
    Am J Pathol 158:1335-44. 2001
    ..We conclude that FAP-1 correlates significantly with Fas resistance in ovarian cancer cell lines and is commonly expressed in ovarian cancers...
  62. ncbi request reprint Bcl-2 family proteins
    J C Reed
    The Burnham Institute, La Jolla, California 92037, USA
    Oncogene 17:3225-36. 1998
    ....
  63. ncbi request reprint Developmental expression patterns of Bcl-2, Bcl-x, Bax, and Bak in teeth
    S Krajewski
    The Burnham Institute formerly La Jolla Cancer Research Foundation, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 5:408-15. 1998
    ....
  64. pmc Molecular basis for CD40 signaling mediated by TRAF3
    C Z Ni
    Cancer Center, The Burnham Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 97:10395-9. 2000
    ..TRAF2 suggests that CD40 may assume different conformations when bound to different TRAF family members. This molecular adaptation may influence binding affinity and specific cellular triggers...
  65. ncbi request reprint Synthetic triterpenoids activate a pathway for apoptosis in AML cells involving downregulation of FLIP and sensitization to TRAIL
    W S Suh
    The Burnham Institute, La Jolla, CA 92037, USA
    Leukemia 17:2122-9. 2003
    ..The findings suggest that synthetic triterpenoids warrant further investigation in the treatment of AML, alone or in combination with TRAIL or other immune-based therapies...
  66. ncbi request reprint Proapoptotic multidomain Bcl-2/Bax-family proteins: mechanisms, physiological roles, and therapeutic opportunities
    J C Reed
    Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Cell Death Differ 13:1378-86. 2006
    ....
  67. ncbi request reprint Drug discovery opportunities from apoptosis research
    J C Reed
    The Burnham Institute, La Jolla, CA 92037, USA
    Curr Opin Biotechnol 11:586-92. 2000
    ....
  68. ncbi request reprint Bc1-2, Raf-1 and mitochondrial regulation of apoptosis
    H G Wang
    Burnham Institute, La Jolla, CA 92037, USA
    Biofactors 8:13-6. 1998
    ..The findings suggest that Bcl-2 targets Raf-1 to mitochondria, allowing this kinase to contribute to cellular survival by phosphorylating BAD or possibly other protein substrates in the vicinity of Bcl-2...
  69. ncbi request reprint Antiapoptotic proteins. The bcl-2 and inhibitor of apoptosis protein families
    Q L Deveraux
    The Burnham Institute Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA
    Cardiol Clin 19:57-74. 2001
    ..Although much has been learned about these families of proteins, future studies of the Bcl-2 and IAP families are sure to hold more exciting discoveries and will continue to reveal new strategies for combating human diseases...
  70. ncbi request reprint IAP family proteins--suppressors of apoptosis
    Q L Deveraux
    The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037 USA
    Genes Dev 13:239-52. 1999
  71. ncbi request reprint Lysosomal protease pathways to apoptosis. Cleavage of bid, not pro-caspases, is the most likely route
    V Stoka
    Programs in Apoptosis and Cell Death Research and Glycobiology, Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 276:3149-57. 2001
    ..Together these data suggest that Bid represents a sensor that allows cells to initiate apoptosis in response to widespread adventitious proteolysis...
  72. ncbi request reprint Structure-function analysis of Bcl-2 family proteins. Regulators of programmed cell death
    J C Reed
    La Jolla Cancer Research Foundation, California 92037, USA
    Adv Exp Med Biol 406:99-112. 1996
    ..Further studies however are required to delineate the full significance of Bcl-2/Bcl-2, Bcl-2/Bax, and Bax/Bax dimers and the biochemical mechanisms by which Bcl-2 family proteins ultimately control cell life and death...
  73. ncbi request reprint Immunohistochemical analysis of in vivo patterns of TRAF-3 expression, a member of the TNF receptor-associated factor family
    S Krajewski
    The Burnham Institute, La Jolla, CA 92037, USA
    J Immunol 159:5841-52. 1997
    ..The findings establish for the first time the cell type- and differentiation-specific patterns of expression of a member of the TRAF family of proteins...
  74. ncbi request reprint Double identity for proteins of the Bcl-2 family
    J C Reed
    Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037, USA
    Nature 387:773-6. 1997
    ..The mechanisms used by this and related anti-apoptotic proteins to protect cells from cytotoxic stimuli are now emerging, with the discovery that Bcl-2 can function both as an ion channel and as an adaptor or docking protein...
  75. ncbi request reprint The apoptosis database
    K S Doctor
    The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cell Death Differ 10:621-33. 2003
    ..The resource is available at http://www.apoptosis-db.org and is updated on a regular basis...
  76. ncbi request reprint Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype
    N Rampino
    The Burnham Institute, La Jolla Cancer Research Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Science 275:967-9. 1997
    ..These results suggest that inactivating BAX mutations are selected for during the progression of colorectal MMP+ tumors and that the wild-type BAX gene plays a suppressor role in a p53-independent pathway for colorectal carcinogenesis...
  77. ncbi request reprint Proapoptotic protein Bax heterodimerizes with Bcl-2 and homodimerizes with Bax via a novel domain (BH3) distinct from BH1 and BH2
    H Zha
    La Jolla Cancer Research Foundation, California 92037, USA
    J Biol Chem 271:7440-4. 1996
    ..The findings suggest that the structural features of Bax and Bcl-2 that allow them to participate in homo-and heterodimerization phenomena are markedly different, despite their amino-acid sequence similarity...
  78. pmc TRAF-4 expression in epithelial progenitor cells. Analysis in normal adult, fetal, and tumor tissues
    M Krajewska
    Burnham Institute, La Jolla, CA 92037, USA
    Am J Pathol 152:1549-61. 1998
    ..Although also expressed in some types of mesenchymal cells, these findings suggest that TRAF-4 is a marker of normal epithelial stem cells, the expression of which often ceases on differentiation and malignant transformation...
  79. doi request reprint Bcl-2 family proteins and cancer
    K W Yip
    Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Oncogene 27:6398-406. 2008
    ..Experimental therapies targeting Bcl-2-family mRNAs or proteins are currently in clinical testing, raising hopes that a new class of anticancer drugs may soon be available...
  80. pmc TNF receptor-associated factor (TRAF) domain and Bcl-2 cooperate to induce small B cell lymphoma/chronic lymphocytic leukemia in transgenic mice
    Juan M Zapata
    The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 101:16600-5. 2004
    ..Given that many human chronic lymphocytic leukemias overexpress TRAF1 and Bcl-2, our findings suggest that cooperation between Bcl-2 and TRAF pathways contributes to the development of this type of leukemia...
  81. pmc Quinone biogenesis: Structure and mechanism of PqqC, the final catalyst in the production of pyrroloquinoline quinone
    Olafur Th Magnusson
    Departments of Chemistry and of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA
    Proc Natl Acad Sci U S A 101:7913-8. 2004
    ..We propose a reaction sequence that involves base-catalyzed cyclization and a series of quinone-quinol tautomerizations that are followed by cycles of O2/H2O2-mediated oxidations...
  82. ncbi request reprint Direct binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADD
    Lance R Thomas
    Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Medical Center Blvd Winston Salem, North Carolina 27157, USA
    J Biol Chem 279:32780-5. 2004
    ..We conclude that in contrast to current models where the death domain of FADD functions independently of the death effector domain, the death effector domain of FADD comes into direct contact with both TRAIL and Fas/CD95 receptors...
  83. ncbi request reprint Humanin binds and nullifies Bid activity by blocking its activation of Bax and Bak
    Dayong Zhai
    Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 280:15815-24. 2005
    ..We conclude that Bid represents an additional cellular target of HN, and we propose that HN-mediated suppression of Bid contributes to the antiapoptotic activity of this endogenous peptide...
  84. ncbi request reprint An IAP-IAP complex inhibits apoptosis
    Takehiko Dohi
    Department of Cancer Biology and the Cancer Center, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
    J Biol Chem 279:34087-90. 2004
    ..Therefore, orchestration of an IAP-IAP complex regulates apoptosis...
  85. ncbi request reprint Functional role of death-associated protein 3 (DAP3) in anoikis
    Tadaaki Miyazaki
    The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 279:44667-72. 2004
    ..Involvement of DAP3 in anoikis signaling demonstrates a novel role for this GTP-binding protein in apoptosis induction caused by cell detachment...
  86. ncbi request reprint Cytoprotective peptide humanin binds and inhibits proapoptotic Bcl-2/Bax family protein BimEL
    Frederic Luciano
    The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 280:15825-35. 2005
    ..Taken together, our results indicate that the inhibition of BimEL may contribute to the antiapoptotic properties of the HN peptide...
  87. ncbi request reprint Cellular, biochemical, and genetic analysis of mechanism of small molecule IAP inhibitors
    Zhiliang Wang
    The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 279:48168-76. 2004
    ....
  88. ncbi request reprint The C-terminal tails of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas receptors have opposing functions in Fas-associated death domain (FADD) recruitment and can regulate agonist-specific mechanisms of receptor activation
    Lance R Thomas
    Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston Salem, North Carolina 27157, USA
    J Biol Chem 279:52479-86. 2004
    ....
  89. ncbi request reprint Key molecular contacts promote recognition of the BAFF receptor by TNF receptor-associated factor 3: implications for intracellular signaling regulation
    Chao Zhou Ni
    Cancer Research Center, The Burnham Institute, La Jolla, CA 92037, USA
    J Immunol 173:7394-400. 2004
    ..The structure of the complex provides a molecular explanation for binding affinities and selective protein interactions in TNFR-TRAF interactions...
  90. ncbi request reprint cIAP1 Localizes to the nuclear compartment and modulates the cell cycle
    Temesgen Samuel
    Burnham Institute, La Jolla, CA 92037, USA
    Cancer Res 65:210-8. 2005
    ..Our findings demonstrate a role for overexpressed cIAP1 in genetic instability, possibly by interfering with mitotic functions of Survivin. These findings may have important implications for cancers in which cIAP1 overexpression occurs...
  91. ncbi request reprint Apoptosis-based therapies for hematologic malignancies
    John C Reed
    Burnham Institute, 10901 N Torrey Pines Rd, La Jolla, CA 92037, USA
    Blood 106:408-18. 2005
    ....
  92. pmc A short Nur77-derived peptide converts Bcl-2 from a protector to a killer
    Siva Kumar Kolluri
    Cancer Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Cancer Cell 14:285-98. 2008
    ..NuBCP-9s act as molecular switches to dislodge the Bcl-2 BH4 domain, exposing its BH3 domain, which in turn blocks the activity of antiapoptotic Bcl-X(L)...
  93. pmc Bax Inhibitor-1 Is a pH-dependent regulator of Ca2+ channel activity in the endoplasmic reticulum
    Hyung Ryong Kim
    Department of Dental Pharmacology and Wonkwang Biomaterial Implant Research Institute, School of Dentistry, Wonkwang University, Iksan, Chonbuk 570 749, Republic of Korea
    J Biol Chem 283:15946-55. 2008
    ..The findings also reveal a cell death-promoting phenotype for BI-1 that is manifested under low pH conditions...
  94. pmc Bcl-2 antagonist apogossypol (NSC736630) displays single-agent activity in Bcl-2-transgenic mice and has superior efficacy with less toxicity compared with gossypol (NSC19048)
    Shinichi Kitada
    Burnham Institute for Medical Research, Cancer Research Center, La Jolla, CA 92037, USA
    Blood 111:3211-9. 2008
    ..Taken together, these studies indicate that apogossypol is superior to parent compound gossypol with respect to toxicology and efficacy, suggesting that further development of this compound for cancer therapy is warranted...
  95. doi request reprint BLOC1S2 interacts with the HIPPI protein and sensitizes NCH89 glioblastoma cells to apoptosis
    Georg Gdynia
    Molecular Neuro Oncology, German Cancer Research Center DKFZ, Im Neuenheimer Feld 280, 69120, Heidelberg, Germany
    Apoptosis 13:437-47. 2008
    ..Given its interaction with HIPPI and its pro-apoptotic activity, BLOC1S2 might play an important functional role in cancer and neurodegenerative diseases...
  96. ncbi request reprint Targeting TRAfs for therapeutic intervention
    Juan M Zapata
    Burnham Institute for Medical Research, La Jolla, California 92037, USA
    Adv Exp Med Biol 597:188-201. 2007
    ....
  97. pmc Cellular pyrin domain-only protein 2 is a candidate regulator of inflammasome activation
    Andrea Dorfleutner
    Mary Babb Randolph Cancer Center and Department of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, 2826 MBRCC, 1 Medical Center Drive, Morgantown, WV 26506 9300, USA
    Infect Immun 75:1484-92. 2007
    ..Existence of a second cPOP provides additional insights into inflammasome formation and suggests that POPs might be a common regulatory mechanism to "fine-tune" the activity of specific PYD-NLR family protein-containing inflammasomes...
  98. ncbi request reprint Protective role of Cop in Rip2/caspase-1/caspase-4-mediated HeLa cell death
    Xin Wang
    Neuroapoptosis Laboratory, Department of Neurosurgery, Brigham and Women s Hospital, Harvard Medical School, LMRC 123, Boston, MA 02115, USA
    Biochim Biophys Acta 1762:742-54. 2006
    ..Cop, as an inhibitor of an important apical caspase cell death axis, may provide a tool for modulating pathological cell death...
  99. pmc Differential regulation of Bax and Bak by anti-apoptotic Bcl-2 family proteins Bcl-B and Mcl-1
    Dayong Zhai
    Burnham Institute for Medical Research, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    J Biol Chem 283:9580-6. 2008
    ..Altogether, the findings reveal striking distinctions in the behaviors of Bcl-B and Mcl-1 relative to the other anti-apoptotic Bcl-2 family members, where Bcl-B and Mcl-1 display reciprocal abilities to bind and neutralize Bax and Bak...
  100. ncbi request reprint Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors
    Aaron D Schimmer
    Burnham Institute for Medical Research, La Jolla, California 92037, USA
    Cancer Res 66:2367-75. 2006
    ....
  101. ncbi request reprint Dysregulation of receptor interacting protein-2 and caspase recruitment domain only protein mediates aberrant caspase-1 activation in Huntington's disease
    Xin Wang
    Department of Neurosurgery, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 25:11645-54. 2005
    ....