R W Johnstone

Summary

Affiliation: University of Melbourne
Country: Australia

Publications

  1. ncbi request reprint Functional interaction between p53 and the interferon-inducible nucleoprotein IFI 16
    R W Johnstone
    The Peter MacCallum Cancer Institute, Cancer Immunology Division, East Melbourne, Victoria, Australia
    Oncogene 19:6033-42. 2000
  2. ncbi request reprint P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Heidelberg, Victoria, Australia
    Blood 93:1075-85. 1999
  3. ncbi request reprint Structural organization, tissue expression, and chromosomal localization of Ciao 1, a functional modulator of the Wilms' tumor suppressor, WT1
    R W Johnstone
    Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA
    Immunogenetics 49:900-5. 1999
  4. ncbi request reprint Isotypic variants of the interferon-inducible transcriptional repressor IFI 16 arise through differential mRNA splicing
    R W Johnstone
    The John Connell Laboratory, The Austin Research Institute, Heidelberg, Australia
    Biochemistry 37:11924-31. 1998
  5. ncbi request reprint The human interferon-inducible protein, IFI 16, is a repressor of transcription
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Studley Road, Heidelberg 3084, Victoria, Australia
    J Biol Chem 273:17172-7. 1998
  6. ncbi request reprint Multiple physiological functions for multidrug transporter P-glycoprotein?
    R W Johnstone
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Austin Hospital, Studley Road, Heidelberg 3084, Victoria, Australia
    Trends Biochem Sci 25:1-6. 2000
  7. ncbi request reprint A role for P-glycoprotein in regulating cell death
    R W Johnstone
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Australia, Victoria
    Leuk Lymphoma 38:1-11. 2000
  8. ncbi request reprint Ciao 1 is a novel WD40 protein that interacts with the tumor suppressor protein WT1
    R W Johnstone
    Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 273:10880-7. 1998
  9. ncbi request reprint P-glycoprotein does not protect cells against cytolysis induced by pore-forming proteins
    R W Johnstone
    Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, St Andrews Place, East Melbourne 3002, Victoria, Australia
    J Biol Chem 276:16667-73. 2001
  10. ncbi request reprint Mutational analysis of P-glycoprotein: suppression of caspase activation in the absence of ATP-dependent drug efflux
    K M Tainton
    Cancer Immunology Program, The Peter MacCallum Cancer Centre, Trescowthick Research Laboratories, East Melbourne, Victoria, Australia
    Cell Death Differ 11:1028-37. 2004

Collaborators

Detail Information

Publications32

  1. ncbi request reprint Functional interaction between p53 and the interferon-inducible nucleoprotein IFI 16
    R W Johnstone
    The Peter MacCallum Cancer Institute, Cancer Immunology Division, East Melbourne, Victoria, Australia
    Oncogene 19:6033-42. 2000
    ..These findings demonstrate a possible link between gene induction following interferon stimulation and p53-mediated cellular events...
  2. ncbi request reprint P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Heidelberg, Victoria, Australia
    Blood 93:1075-85. 1999
    ..This study has confirmed a potential novel physiological function for P-glycoprotein and it now remains to dissect the molecular mechanisms involved in the inhibition of capsase-dependent cell death by P-glycoprotein...
  3. ncbi request reprint Structural organization, tissue expression, and chromosomal localization of Ciao 1, a functional modulator of the Wilms' tumor suppressor, WT1
    R W Johnstone
    Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA
    Immunogenetics 49:900-5. 1999
  4. ncbi request reprint Isotypic variants of the interferon-inducible transcriptional repressor IFI 16 arise through differential mRNA splicing
    R W Johnstone
    The John Connell Laboratory, The Austin Research Institute, Heidelberg, Australia
    Biochemistry 37:11924-31. 1998
    ..Finally, IFI 16 isoforms can homo- and heterodimerize, and we have mapped the dimerization domain to the amino terminus which contains an imperfect leucine zipper domain...
  5. ncbi request reprint The human interferon-inducible protein, IFI 16, is a repressor of transcription
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Studley Road, Heidelberg 3084, Victoria, Australia
    J Biol Chem 273:17172-7. 1998
    ..Thus, IFI 16 is a transcriptional repressor, with a modular structure typical of many known transcription regulators...
  6. ncbi request reprint Multiple physiological functions for multidrug transporter P-glycoprotein?
    R W Johnstone
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Austin Hospital, Studley Road, Heidelberg 3084, Victoria, Australia
    Trends Biochem Sci 25:1-6. 2000
    ....
  7. ncbi request reprint A role for P-glycoprotein in regulating cell death
    R W Johnstone
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Australia, Victoria
    Leuk Lymphoma 38:1-11. 2000
    ..There is now a lively debate regarding the possible role of P-gp in regulating cell differentiation, proliferation and survival...
  8. ncbi request reprint Ciao 1 is a novel WD40 protein that interacts with the tumor suppressor protein WT1
    R W Johnstone
    Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 273:10880-7. 1998
    ..Thus, Ciao 1 appears to specifically modulate the transactivation activity of WT1 and may function to regulate the physiological functions of WT1 in cell growth and differentiation...
  9. ncbi request reprint P-glycoprotein does not protect cells against cytolysis induced by pore-forming proteins
    R W Johnstone
    Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, St Andrews Place, East Melbourne 3002, Victoria, Australia
    J Biol Chem 276:16667-73. 2001
    ..Based on these results, we conclude that P-gp does not affect cell lysis induced by pore-forming proteins...
  10. ncbi request reprint Mutational analysis of P-glycoprotein: suppression of caspase activation in the absence of ATP-dependent drug efflux
    K M Tainton
    Cancer Immunology Program, The Peter MacCallum Cancer Centre, Trescowthick Research Laboratories, East Melbourne, Victoria, Australia
    Cell Death Differ 11:1028-37. 2004
    ..The structure-function analyses described herein provide novel insight into the mechanisms of action of P-gp in mediating MDR...
  11. ncbi request reprint Mapping of the human PAWR (par-4) gene to chromosome 12q21
    R W Johnstone
    Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, Massachusetts, 02115, USA
    Genomics 53:241-3. 1998
  12. ncbi request reprint P-glycoprotein inhibits caspase-8 activation but not formation of the death inducing signal complex (disc) following Fas ligation
    A A Ruefli
    Peter MacCallum Cancer Institute, St Andrew s Place, East Melbourne, Victoria, Australia
    Cell Death Differ 9:1266-72. 2002
    ..These studies demonstrate that P-gp inhibits Fas-induced caspase-8 activation but not formation of the DISC and that this activity of P-gp is dependent on ATP hydrolysis...
  13. pmc A novel repressor, par-4, modulates transcription and growth suppression functions of the Wilms' tumor suppressor WT1
    R W Johnstone
    Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Mol Cell Biol 16:6945-56. 1996
    ..Significantly, par-4, but not a mutant unable to interact with WT1, rescued growth suppression caused by WT1. Thus, we identified a novel repressor that modulates transcription as well as growth suppression functions of WT1...
  14. pmc Fas ligand-mediated lysis of self bystander targets by human papillomavirus-specific CD8+ cytotoxic T lymphocytes
    M J Smyth
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg 3084, Victoria, Australia
    J Virol 72:5948-54. 1998
    ....
  15. pmc The drug efflux protein, P-glycoprotein, additionally protects drug-resistant tumor cells from multiple forms of caspase-dependent apoptosis
    M J Smyth
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Studley Road, Heidelberg, 3084, Victoria, Australia
    Proc Natl Acad Sci U S A 95:7024-9. 1998
    ..These observations suggest that, in addition to effluxing drugs, P-gp may play a specific role in regulating some caspase-dependent apoptotic pathways...
  16. ncbi request reprint The IFN-inducible nucleoprotein IFI 16 is expressed in cells of the monocyte lineage, but is rapidly and markedly down-regulated in other myeloid precursor populations
    M J Dawson
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg, Australia
    J Leukoc Biol 64:546-54. 1998
    ..This differential expression of IFI 16 in myeloid precursor subpopulations and its perceived molecular properties are consistent with a possible role in regulating myelopoiesis...
  17. pmc HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses
    J E Bolden
    Cancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne 3002, Victoria, Australia
    Cell Death Dis 4:e519. 2013
    ..This study provides new insight into the transcriptional effects of HDACi in human donor-matched normal and transformed cells, and implicates specific molecules and pathways in the tumor-selective cytotoxic activity of these compounds...
  18. pmc Preclinical screening of histone deacetylase inhibitors combined with ABT-737, rhTRAIL/MD5-1 or 5-azacytidine using syngeneic Vk*MYC multiple myeloma
    G M Matthews
    Gene Regulation Laboratory, Cancer Therapeutics, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia
    Cell Death Dis 4:e798. 2013
    ..Taken together, our studies provide evidence that the transplanted Vk*MYC model of MM is a useful screening tool for anti-MM drugs and should aid in the prioritization of novel drug testing in the clinic...
  19. doi request reprint Efficacy of CHK inhibitors as single agents in MYC-driven lymphoma cells
    P T Ferrao
    Molecular Oncology Laboratory and Cancer Therapeutics Program, Research Division, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia
    Oncogene 31:1661-72. 2012
    ..We propose that inhibitors of CHK can act in a synthetically lethal manner in cancers with replication stress as a result of these cancers being reliant on CHK proteins for an effective DDR and cell survival...
  20. ncbi request reprint Multiple deficiencies underlie NK cell inactivity in lymphotoxin-alpha gene-targeted mice
    M J Smyth
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg, Victoria, Australia
    J Immunol 163:1350-3. 1999
    ..5- to 3-fold in LT-alpha-deficient mice, as compared with wild-type mice. Combined defects in NK cell development and effector function contribute to compromised NK cell antitumor function in LT-alpha-deficient mice...
  21. doi request reprint Thalidomide-analogue biology: immunological, molecular and epigenetic targets in cancer therapy
    J Shortt
    Gene Regulation Laboratory, Cancer Therapeutics Program, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett St, Melbourne, Victoria, Australia
    Oncogene 32:4191-202. 2013
    ..It is anticipated that elucidation of important IMiD targets will allow the rational development of new-generation therapeutics with the potential to separate thalidomide-analogue efficacy from clinical toxicity...
  22. pmc Translation inhibitors induce cell death by multiple mechanisms and Mcl-1 reduction is only a minor contributor
    L M Lindqvist
    The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia
    Cell Death Dis 3:e409. 2012
    ..Indeed, loss of clonogenic survival proved to be independent of the Bax/Bak-mediated apoptosis altogether. Our findings warn of potential toxicity as these translation inhibitors are cytotoxic to many differentiated non-cycling cells...
  23. pmc Novel properties of the protein kinase CK2-site-regulated nuclear- localization sequence of the interferon-induced nuclear factor IFI 16
    L J Briggs
    Nuclear Signalling Laboratory, Division for Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, P O Box 334, Canberra City, A C T 2601, Australia
    Biochem J 353:69-77. 2001
    ....
  24. ncbi request reprint Critical role of the transcription factor AP-1 for the constitutive and interferon-induced expression of IFI 16
    C J P Clarke
    Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria 3002, Australia
    J Cell Biochem 89:80-93. 2003
    ..These experiments define the transcriptional mechanisms of IFI 16 gene regulation and provide evidence suggesting that AP-1 activation may be an important event in IFN signaling...
  25. ncbi request reprint Identification, cloning, expression, and biochemical characterization of the testis-specific RNA polymerase II elongation factor ELL3
    T Miller
    Edward A Doisy Department of Biochemistry, St Louis University School of Medicine, St Louis, Missouri 63104, USA
    J Biol Chem 275:32052-6. 2000
    ..ELL3 was localized by immunofluorescence to the nucleus of cells, and Northern analysis indicated that ELL3 is a testis-specific RNA polymerase II elongation factor...
  26. pmc The histone deacetylase inhibitor and chemotherapeutic agent suberoylanilide hydroxamic acid (SAHA) induces a cell-death pathway characterized by cleavage of Bid and production of reactive oxygen species
    A A Ruefli
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Saint Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 98:10833-8. 2001
    ..These data provide evidence of a mechanism of cell death mediated by transcriptional events that result in the cleavage of Bid, disruption of the mitochondrial membrane, and production of reactive oxygen species to induce cell death...
  27. pmc Functional analysis of the leukemia protein ELL: evidence for a role in the regulation of cell growth and survival
    R W Johnstone
    The Peter MacCallum Cancer Institute, Gene Regulation Laboratory, Cancer Immunology Division, East Melbourne, 3002 Victoria, Australia
    Mol Cell Biol 21:1672-81. 2001
    ..These novel results indicate that ELL can regulate cell growth and survival and may explain how ELL translocations result in the development of human malignancies...
  28. pmc Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma
    R K Lindemann
    Cancer Immunology Program, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, St Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 104:8071-6. 2007
    ..Our studies provide important information regarding the mechanisms of action of HDACi that have broad implications regarding stratification of patients receiving HDACi therapy alone or in combination with other anticancer agents...
  29. doi request reprint Blocking granule-mediated death by primary human NK cells requires both protection of mitochondria and inhibition of caspase activity
    K A Sedelies
    Cancer Cell Death Laboratory, Cancer Immunology Program, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett Street, Melbourne, Victoria 8006, Australia
    Cell Death Differ 15:708-17. 2008
    ....
  30. ncbi request reprint Filamin (280-kDa actin-binding protein) is a caspase substrate and is also cleaved directly by the cytotoxic T lymphocyte protease granzyme B during apoptosis
    K A Browne
    Cancer Immunology Laboratory, Peter MacCallum Cancer Institute, Locked Bag 1, A Beckett Street, Melbourne 8006, Australia
    J Biol Chem 275:39262-6. 2000
    ..Thus, filamin is a functionally important substrate for granzyme B, as its cleavage may account at least partly for caspase-independent cell death mediated by the granzyme...
  31. ncbi request reprint Cloning a novel member of the human interferon-inducible gene family associated with control of tumorigenicity in a model of human melanoma
    K L DeYoung
    Laboratory of Cancer Genetics, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Oncogene 15:453-7. 1997
    ..We have also demonstrated that, like IFI16 and MNDA, AIM2 is induced in HL60 cells by interferon gamma. Our findings support the existence of a family of genes in this region similar to the well-characterized mouse Ifi200 gene family...
  32. pmc Initiation of apoptosis by granzyme B requires direct cleavage of bid, but not direct granzyme B-mediated caspase activation
    V R Sutton
    Cancer Immunology Laboratory, Peter MacCallum Cancer Institute, Melbourne 8006, Australia
    J Exp Med 192:1403-14. 2000
    ..Overall, our results indicate that mitochondrial perturbation by Bid is necessary to achieve a lethal threshold of caspase activity and cell death due to granzyme B...