Gary L Johnson

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. pmc Sequence patches on MAPK surfaces define protein-protein interactions
    Gary L Johnson
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7365, USA
    Genome Biol 10:222. 2009
  2. doi request reprint Defining MAPK interactomes
    Gary L Johnson
    Department of Pharmacology, University of North Carolina, Chapel Hill, 27599, United States
    ACS Chem Biol 6:18-20. 2011
  3. pmc Trophoblast stem cell maintenance by fibroblast growth factor 4 requires MEKK4 activation of Jun N-terminal kinase
    Amy N Abell
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    Mol Cell Biol 29:2748-61. 2009
  4. ncbi request reprint MEKK4 stimulation of p38 and JNK activity is negatively regulated by GSK3beta
    Amy N Abell
    Department of Pharmacology and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 282:30476-84. 2007
  5. ncbi request reprint Rac-MEKK3-MKK3 scaffolding for p38 MAPK activation during hyperosmotic shock
    Mark T Uhlik
    Department of Pharmacology and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine Chapel Hill, NC 27599 7365, USA
    Nat Cell Biol 5:1104-10. 2003
  6. pmc Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype
    Asya L Borikova
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, School of Dentistry, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    J Biol Chem 285:11760-4. 2010
  7. pmc SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c controls epithelial-mesenchymal transition by inducing Wnt5a signaling
    Nicole Vincent Jordan
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA
    Mol Cell Biol 33:3011-25. 2013
  8. pmc Tracking the intermediate stages of epithelial-mesenchymal transition in epithelial stem cells and cancer
    Nicole Vincent Jordan
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA
    Cell Cycle 10:2865-73. 2011
  9. pmc PB1 domain interaction of p62/sequestosome 1 and MEKK3 regulates NF-kappaB activation
    Kazuhiro Nakamura
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 285:2077-89. 2010
  10. pmc Ablation of MEKK4 kinase activity causes neurulation and skeletal patterning defects in the mouse embryo
    Amy N Abell
    Department of Pharmacology, University of North Carolina, Chapel Hill, 27599 7365, USA
    Mol Cell Biol 25:8948-59. 2005

Collaborators

Detail Information

Publications46

  1. pmc Sequence patches on MAPK surfaces define protein-protein interactions
    Gary L Johnson
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7365, USA
    Genome Biol 10:222. 2009
    ..Recent studies on the modularity of mitogen-activated protein kinases show how redesigning 'surface patches' on a protein can change the topology of a signaling network...
  2. doi request reprint Defining MAPK interactomes
    Gary L Johnson
    Department of Pharmacology, University of North Carolina, Chapel Hill, 27599, United States
    ACS Chem Biol 6:18-20. 2011
    ..This discovery process provides a rich data and reagent resource for defining complexities of protein networks involving MAPKs and control of cellular physiology...
  3. pmc Trophoblast stem cell maintenance by fibroblast growth factor 4 requires MEKK4 activation of Jun N-terminal kinase
    Amy N Abell
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    Mol Cell Biol 29:2748-61. 2009
    ..Our results define MEKK4 as a signaling hub for FGF4 activation of JNK that is required for maintenance of TS cells in an undifferentiated state...
  4. ncbi request reprint MEKK4 stimulation of p38 and JNK activity is negatively regulated by GSK3beta
    Amy N Abell
    Department of Pharmacology and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 282:30476-84. 2007
    ..Thus, control of MEKK4 dimerization is regulated both positively and negatively by its interaction with specific proteins...
  5. ncbi request reprint Rac-MEKK3-MKK3 scaffolding for p38 MAPK activation during hyperosmotic shock
    Mark T Uhlik
    Department of Pharmacology and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine Chapel Hill, NC 27599 7365, USA
    Nat Cell Biol 5:1104-10. 2003
    ..The Rac-OSM-MEKK3-MKK3 complex is the mammalian counterpart of the CDC42-STE50-STE11-Pbs2 complex in Saccharomyces cerevisiae that is required for the regulation of p38 activity...
  6. pmc Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype
    Asya L Borikova
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, School of Dentistry, University of North Carolina, Chapel Hill, North Carolina 27599, USA
    J Biol Chem 285:11760-4. 2010
    ..The results define Rho kinase as a therapeutic target to rescue endothelial cells from loss of CCM protein function...
  7. pmc SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c controls epithelial-mesenchymal transition by inducing Wnt5a signaling
    Nicole Vincent Jordan
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA
    Mol Cell Biol 33:3011-25. 2013
    ..Inhibition of Wnt5a by either RNAi knockdown or blocking antibody reversed Smarcd3/Baf60c-induced EMT. Thus, Smarcd3/Baf60c epigenetically regulates EMT by activating WNT signaling pathways...
  8. pmc Tracking the intermediate stages of epithelial-mesenchymal transition in epithelial stem cells and cancer
    Nicole Vincent Jordan
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA
    Cell Cycle 10:2865-73. 2011
    ..This intersection between EMT and stemness in TS cells and claudin-low metastatic breast cancer demonstrates the usefulness of developmental EMT systems to understand EMT in cancer...
  9. pmc PB1 domain interaction of p62/sequestosome 1 and MEKK3 regulates NF-kappaB activation
    Kazuhiro Nakamura
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 285:2077-89. 2010
    ..The rear end acidic cluster of the p62 PB1 domain is used to organize cytosolic aggregates or speckles-associated TRAF6-p62-MEKK3 complex for control of NF-kappaB activation...
  10. pmc Ablation of MEKK4 kinase activity causes neurulation and skeletal patterning defects in the mouse embryo
    Amy N Abell
    Department of Pharmacology, University of North Carolina, Chapel Hill, 27599 7365, USA
    Mol Cell Biol 25:8948-59. 2005
    ..Together, these data demonstrate MEKK4 regulation of p38 and that substrates downstream of p38 control cellular homeostasis. The findings are the first demonstration that MEKK4-regulated p38 activity is critical for neurulation...
  11. ncbi request reprint MEKK4 is an effector of the embryonic TRAF4 for JNK activation
    Amy N Abell
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 280:35793-6. 2005
    ..The findings identify MEKK4 as the MAPK kinase kinase for TRAF4 regulation of the JNK pathway...
  12. pmc Noncanonical function of MEKK2 and MEK5 PB1 domains for coordinated extracellular signal-regulated kinase 5 and c-Jun N-terminal kinase signaling
    Kazuhiro Nakamura
    Department of Pharmacology, 1108 Mary Ellen Jones Building, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7365, USA
    Mol Cell Biol 27:4566-77. 2007
    ..The findings define how the MEKK2 and MEK5 PB1 domains are uniquely used for differential binding of two mitogen-activated protein kinase kinases, MEK5 and MKK7, for the coordinated control of ERK5 and c-Jun N-terminal kinase activation...
  13. ncbi request reprint MEKK1 regulates the AP-1 dimer repertoire via control of JunB transcription and Fra-2 protein stability
    Bruce D Cuevas
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7365, USA
    Oncogene 24:801-9. 2005
    ..Controlling the repertoire of a transcription factor complex is a newly defined function for an MAPK kinase kinase...
  14. pmc Defining the functional domain of programmed cell death 10 through its interactions with phosphatidylinositol-3,4,5-trisphosphate
    Christopher F Dibble
    Department of Pharmacology, School of Medicine, and the Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, United States of America
    PLoS ONE 5:e11740. 2010
    ..Combining computational modeling and biological data, we propose that the CCM protein complex functions in the PI3K signaling pathway through the interaction between PDCD10 and PtdIns(3,4,5)P3...
  15. ncbi request reprint Proteomic identification of the cerebral cavernous malformation signaling complex
    Thomas L Hilder
    Department of Pharmacology and the Lineberger Comprehensive Cancer Center, School of Dentistry, University of North Carolina, Chapel Hill, CB 7365, Chapel Hill, North Carolina 27599 7365, USA
    J Proteome Res 6:4343-55. 2007
    ..The findings define the targeting of the CCM complex to membranes and to proteins regulating trafficking and the cytoskeleton...
  16. pmc PB1 domain-dependent signaling complex is required for extracellular signal-regulated kinase 5 activation
    Kazuhiro Nakamura
    Department of Pharmacology, CB 7365, 1108 Mary Ellen Jones Building, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7365, USA
    Mol Cell Biol 26:2065-79. 2006
    ..The MEK5 PB1 domain confers stringent MAP3K regulation of ERK5 relative to more promiscuous MAP3K control of ERK1/2, JNK, and p38...
  17. ncbi request reprint Rac2D57N, a dominant inhibitory Rac2 mutant that inhibits p38 kinase signaling and prevents surface ruffling in bone-marrow-derived macrophages
    Amy N Abell
    Department of Pharmacology, University of Colorado Health Sciences Center, 4200 East Ninth Ave, Denver, CO 80262, USA
    J Cell Sci 117:243-55. 2004
    ..Enhanced binding of Rac2D57N to its upstream regulators would inhibit Rac-dependent effects on actin cytoskeletal dynamics and p38 kinase signaling...
  18. pmc Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple-negative breast cancer
    James S Duncan
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Cell 149:307-21. 2012
    ..This approach defines mechanisms of drug resistance, allowing rational design of combination therapies for cancer...
  19. ncbi request reprint Wiring diagrams of MAPK regulation by MEKK1, 2, and 3
    Mark T Uhlik
    Department of Pharmacology, University of North Carolina School of Medicine, 1108 Mary Ellen Jones Building, CB 7365, Chapel Hill, NC 27599, USA
    Biochem Cell Biol 82:658-63. 2004
    ..We propose that signal transduction network wiring diagrams are valuable tools for hypothesis building and filtering physiologically relevant phenotypic responses from less connected protein relations in the regulation of MAPK pathways...
  20. ncbi request reprint Hyperosmotic induction of mitogen-activated protein kinase scaffolding
    Thomas L Hilder
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
    Methods Enzymol 428:297-312. 2007
    ....
  21. pmc MAP3K4/CBP-regulated H2B acetylation controls epithelial-mesenchymal transition in trophoblast stem cells
    Amy N Abell
    Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7365, USA
    Cell Stem Cell 8:525-37. 2011
    ..Taken together, our data define an epigenetic switch that maintains the epithelial phenotype in TS cells and reveals previously unrecognized genes potentially contributing to breast cancer...
  22. pmc MEKK1 regulates calpain-dependent proteolysis of focal adhesion proteins for rear-end detachment of migrating fibroblasts
    Bruce D Cuevas
    Department of Pharmacology, Craniofacial Biology, University of Colorado Health Sciences Center, Denver, CO 80262, USA
    EMBO J 22:3346-55. 2003
    ..Inhibition of ERK1/2 or calpain, but not of JNK, mimics MEKK1 deficiency. Therefore, MEKK1 regulates calpain-mediated substratum release of migrating fibroblasts...
  23. pmc MicroRNA 9-3p targets β1 integrin to sensitize claudin-low breast cancer cells to MEK inhibition
    Jon S Zawistowski
    Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill, NC, USA
    Mol Cell Biol 33:2260-74. 2013
    ..The miRNA screen led to identification of a druggable protein, ITGB1, whose functional inhibition synergizes with MEK inhibitor...
  24. pmc The dynamic nature of the kinome
    Lee M Graves
    The Department of Pharmacology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Biochem J 450:1-8. 2013
    ..The development of technologies to study the kinome, as well as examples of kinome resilience and reprogramming, will be discussed in the present review...
  25. pmc Cerebral cavernous malformation 2 protein promotes smad ubiquitin regulatory factor 1-mediated RhoA degradation in endothelial cells
    Lisa E S Crose
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 284:13301-5. 2009
    ....
  26. doi request reprint Activity assays for extracellular signal-regulated kinase 5
    Kazuhiro Nakamura
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, School of Medicine, University of North Carolina, Chapel Hill, NC, USA
    Methods Mol Biol 661:91-106. 2010
    ..ERK5 is also critical for maintenance of vascular integrity and endothelial cell survival. In this chapter, we define methods used to measure the activation of ERK5 using different biochemical and cell-based assays...
  27. ncbi request reprint PB1 domains of MEKK2 and MEKK3 interact with the MEK5 PB1 domain for activation of the ERK5 pathway
    Kazuhiro Nakamura
    Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biol Chem 278:36989-92. 2003
    ..The free PB1 domain of MEKK2 or MEKK3 functions effectively to inhibit the ERK5 pathway but not the p38 or JNK pathways, demonstrating the specific and unique requirement of the MEKK2 and MEKK3 PB1 domain in regulating ERK5 activation...
  28. doi request reprint Homogeneous time-resolved fluorescence resonance energy transfer assay for measurement of Phox/Bem1p (PB1) domain heterodimerization
    Kazuhiro Nakamura
    Department of Pharmacology and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Biomol Screen 13:396-405. 2008
    ..Disruption of PB1 domain interactions represents a novel approach for selectively regulating the ERK5 signaling pathway independent of kinase active site-directed adenosine triphosphate competitive inhibitors...
  29. doi request reprint In vivo profiling endogenous interactions with knock-out in mammalian cells
    Ling Xie
    Department of Biochemistry and Biophysics, School of Medicine, University of North Carolina, 120 Mason Farm Road, Genetic Medicine, Ste 3010, Campus Box No 7260, Chapel Hill, North Carolina 27599 7260, USA
    Anal Chem 81:1411-7. 2009
    ..Because of the availability of a large library of knockout mice models with various target proteins of biological interests our method is generally applicable to screen any endogenous target-specific PPIs of physiological relevance...
  30. pmc Combined PI3K/mTOR and MEK inhibition provides broad antitumor activity in faithful murine cancer models
    Patrick J Roberts
    Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA
    Clin Cancer Res 18:5290-303. 2012
    ..Anticancer drug development is inefficient, but genetically engineered murine models (GEMM) and orthotopic, syngeneic transplants (OST) of cancer may offer advantages to in vitro and xenograft systems...
  31. pmc MEK kinase 2 and the adaptor protein Lad regulate extracellular signal-regulated kinase 5 activation by epidermal growth factor via Src
    Weiyong Sun
    Department of Pharmacology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    Mol Cell Biol 23:2298-308. 2003
    ....
  32. pmc The c-jun kinase/stress-activated pathway: regulation, function and role in human disease
    Gary L Johnson
    University of North Carolina at Chapel Hill, Department of Pharmacology, and Lineberger Comprehensive Cancer Center, 31 331 LCC Chapel Hill, NC 27599, USA
    Biochim Biophys Acta 1773:1341-8. 2007
    ..In this review, we present our current understanding of JNK regulation and their involvement in homeostasis and dysregulation in human disease...
  33. ncbi request reprint Ubiquitylation of MEKK1 inhibits its phosphorylation of MKK1 and MKK4 and activation of the ERK1/2 and JNK pathways
    James A Witowsky
    Department of Pharmacology, University of Colorado Health Sciences Center and University of Colorado Cancer Center, Denver, Colorado 80262, USA
    J Biol Chem 278:1403-6. 2003
    ..MEKK1 ubiquitylation represents a mechanism for inhibiting the ability of a protein kinase to phosphorylate substrates and regulate downstream signaling pathways...
  34. pmc Tousled-like kinases modulate reactivation of gammaherpesviruses from latency
    Patrick J Dillon
    Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Cell Host Microbe 13:204-14. 2013
    ..TLKs were also found to play a role in regulating reactivation from latency of another related oncogenic gammaherpesvirus, Epstein-Barr virus. Our results establish the TLKs as cellular repressors of gammaherpesvirus reactivation...
  35. ncbi request reprint Integrated activation of MAP3Ks balances cell fate in response to stress
    Ann M Winter-Vann
    Department of Pharmacology, 1108 Mary Ellen Jones Bldg, Campus Box 7365, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599 7365, USA
    J Cell Biochem 102:848-58. 2007
    ..The interrelationships among different stressors are discussed, with an emphasis on how the balance of signaling through MAP3Ks controls the MAPK response to determine cell fate...
  36. pmc Laser-scanning velocimetry: a confocal microscopy method for quantitative measurement of cardiovascular performance in zebrafish embryos and larvae
    Michael H Malone
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    BMC Biotechnol 7:40. 2007
    ..A laser scan line placed parallel to the path of blood in the dorsal aorta measures blood cell velocity, from which cardiac output and indices of vascular resistance and contractility are calculated...
  37. ncbi request reprint MEKK1-induced apoptosis requires TRAIL death receptor activation and is inhibited by AKT/PKB through inhibition of MEKK1 cleavage
    Andrea H Bild
    Department of Pharmacology, University of Colorado, 2400 East Ninth Street, Denver, Colorado, CO 80262, USA
    Oncogene 21:6649-56. 2002
    ..Thus, MEKK1-induced apoptosis requires TRAIL death receptor activation and is blocked by AKT through inhibition of MEKK1 cleavage...
  38. pmc Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling
    Bryan T Richardson
    Department of Pharmacology and Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
    Biol Chem 394:35-42. 2013
    ..Inhibition of the ROCK rescues CCM endothelial cell dysfunction, suggesting that the inhibition of RhoA-ROCK signaling may be a therapeutic strategy to prevent or arrest the progression of the CCM lesions...
  39. ncbi request reprint Structural and evolutionary division of phosphotyrosine binding (PTB) domains
    Mark T Uhlik
    Department of Pharmacology and University of North Carolina School of Medicine, 1108 Mary Ellen Jones Building, Campus Box 7365, Chapel Hill, NC 27599 7365, USA
    J Mol Biol 345:1-20. 2005
    ..The signaling complexes organized by PTB domain encoded proteins are largely unknown and represents an important challenge in systems biology for the future...
  40. ncbi request reprint MEKK1 is required for inducible urokinase-type plasminogen activator expression
    James Witowsky
    Department of Pharmacology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    J Biol Chem 278:5941-6. 2003
    ..Importantly, disrupted expression of MEKK2, a related MAPK kinase kinase, had no effect on uPA activity. Therefore, we conclude that MEKK1 expression is required for PMA- or FGF-2-induced signals to control uPA expression and function...
  41. ncbi request reprint MAPK kinase kinases (MKKKs) as a target class for small-molecule inhibition to modulate signaling networks and gene expression
    Gary L Johnson
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, NC 27599 7365, USA
    Curr Opin Chem Biol 9:325-31. 2005
    ....
  42. pmc Efficiently identifying genome-wide changes with next-generation sequencing data
    Weichun Huang
    Biostatistics Branch, National Institute of Environmental Health Sciences, RTP, NC 27709, USA
    Nucleic Acids Res 39:e130. 2011
    ..In particular, we show that our novel and robust 'parsimony' normalization method is superior to the widely-used 'tagRatio' method. Our software EpiCenter is freely available to the public...
  43. pmc Application of multiplexed kinase inhibitor beads to study kinome adaptations in drug-resistant leukemia
    Matthew J Cooper
    Department of Pharmacology, School of Medicine, University of North Carolina, Chapel Hill, North Carolina, United States of America
    PLoS ONE 8:e66755. 2013
    ..These results demonstrate the utility of MIB/MS as a tool to identify dysregulated kinases and to interrogate kinome dynamics as cells respond to targeted kinase inhibition. ..
  44. ncbi request reprint Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases
    Gary L Johnson
    Department of Pharmacology, University of Colorado Health Sciences Center, Denver, CO 80262, USA
    Science 298:1911-2. 2002
    ..The p38 MAPKs are activated by inflammatory cytokines and environmental stresses and may contribute to diseases like asthma and autoimmunity...
  45. pmc Data-driven modeling of cellular stimulation, signaling and output response in RAW 264.7 cells
    Yang Wu
    Joint Department of Biomedical Engineering, University of North Carolina School of Medicine, Chapel Hill, North Carolina, USA
    J Mol Signal 3:11. 2008
    ..Of particular interest is the establishment of methods for the analysis of cellular-level input-output signaling relationships that have been characterized over time...
  46. ncbi request reprint TRAIL and inhibitors of apoptosis are opposing determinants for NF-kappaB-dependent, genotoxin-induced apoptosis of cancer cells
    Aaron C Spalding
    Department of Pharmacology, University of Colorado Cancer Center, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, Colorado, CO 80262, USA
    Oncogene 21:260-71. 2002
    ..These findings demonstrate that TRAIL signaling via its death receptors is a significant contributor to genotoxin-induced apoptosis in human epithelial carcinomas...