Brian Gabrielli

Summary

Affiliation: University of Queensland
Country: Australia

Publications

  1. doi request reprint Histone deacetylase inhibitors disrupt the mitotic spindle assembly checkpoint by targeting histone and nonhistone proteins
    Brian Gabrielli
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Adv Cancer Res 116:1-37. 2012
  2. pmc The miR-17-5p microRNA is a key regulator of the G1/S phase cell cycle transition
    Nicole Cloonan
    Institute for Molecular Bioscience, The University of Queensland, Carmody Road, St Lucia, 4072, Australia
    Genome Biol 9:R127. 2008
  3. ncbi request reprint Finally, how histone deacetylase inhibitors disrupt mitosis!
    Brian Gabrielli
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Cell Cycle 10:2658-61. 2011
  4. pmc MAPK pathway activation delays G2/M progression by destabilizing Cdc25B
    Puji Astuti
    Diamantina Institute for Cancer Immunology and Metabolic Medicine, University of Queensland, Brisbane 4102, Queensland, Australia
    J Biol Chem 284:33781-8. 2009
  5. pmc CDC25B overexpression stabilises centrin 2 and promotes the formation of excess centriolar foci
    Rose Boutros
    Princess Alexandra Hospital, The University of Queensland Diamantina Institute, Brisbane, Queensland, Australia
    PLoS ONE 8:e67822. 2013
  6. pmc Generation of a genome scale lentiviral vector library for EF1α promoter-driven expression of human ORFs and identification of human genes affecting viral titer
    Dubravka Skalamera
    University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    PLoS ONE 7:e51733. 2012
  7. pmc CDC25B associates with a centrin 2-containing complex and is involved in maintaining centrosome integrity
    Rose Boutros
    Diamantina Institute, Princess Alexandra Hospital, The University of Queensland, Brisbane, Australia
    Biol Cell 103:55-68. 2011
  8. ncbi request reprint Inhibition of S/G2 phase CDK4 reduces mitotic fidelity
    Andrew Burgess
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia
    J Biol Chem 281:9987-95. 2006
  9. ncbi request reprint The EBNA-3 gene family proteins disrupt the G2/M checkpoint
    Kenia G Krauer
    Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Brisbane, Australia
    Oncogene 23:1342-53. 2004
  10. doi request reprint Truncated MEK1 is required for transient activation of MAPK signalling in G2 phase cells
    Tanya Pike
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Cell Signal 25:1423-8. 2013

Collaborators

Detail Information

Publications27

  1. doi request reprint Histone deacetylase inhibitors disrupt the mitotic spindle assembly checkpoint by targeting histone and nonhistone proteins
    Brian Gabrielli
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Adv Cancer Res 116:1-37. 2012
    ..The overall mitotic phenotype of drug treatment appears to be the sum of these disrupted mechanisms...
  2. pmc The miR-17-5p microRNA is a key regulator of the G1/S phase cell cycle transition
    Nicole Cloonan
    Institute for Molecular Bioscience, The University of Queensland, Carmody Road, St Lucia, 4072, Australia
    Genome Biol 9:R127. 2008
    ....
  3. ncbi request reprint Finally, how histone deacetylase inhibitors disrupt mitosis!
    Brian Gabrielli
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Cell Cycle 10:2658-61. 2011
    ..However, the mechanism by which these drugs affect mitosis is poorly understood. A number of recent papers have now thrown considerable light onto how these drugs elicit this very distinctive cell cycle disruption...
  4. pmc MAPK pathway activation delays G2/M progression by destabilizing Cdc25B
    Puji Astuti
    Diamantina Institute for Cancer Immunology and Metabolic Medicine, University of Queensland, Brisbane 4102, Queensland, Australia
    J Biol Chem 284:33781-8. 2009
    ..This represents a novel mechanism by which factors that activate MAPK signaling can influence the timing of entry into mitosis, particularly exit from a G(2) phase checkpoint arrest...
  5. pmc CDC25B overexpression stabilises centrin 2 and promotes the formation of excess centriolar foci
    Rose Boutros
    Princess Alexandra Hospital, The University of Queensland Diamantina Institute, Brisbane, Queensland, Australia
    PLoS ONE 8:e67822. 2013
    ....
  6. pmc Generation of a genome scale lentiviral vector library for EF1α promoter-driven expression of human ORFs and identification of human genes affecting viral titer
    Dubravka Skalamera
    University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    PLoS ONE 7:e51733. 2012
    ..Identification of human genes that affect lentivirus production may lead to improved technology for gene expression using lentiviral vectors...
  7. pmc CDC25B associates with a centrin 2-containing complex and is involved in maintaining centrosome integrity
    Rose Boutros
    Diamantina Institute, Princess Alexandra Hospital, The University of Queensland, Brisbane, Australia
    Biol Cell 103:55-68. 2011
    ..We have recently identified a pool of CDC25B at the centrosome of interphase cells that plays a role in regulating centrosome numbers...
  8. ncbi request reprint Inhibition of S/G2 phase CDK4 reduces mitotic fidelity
    Andrew Burgess
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia
    J Biol Chem 281:9987-95. 2006
    ..These data provide evidence for a novel function for CDK4-cyclin D3 activity in S and G(2) phase that is critical for G(2)/M progression and the fidelity of mitosis...
  9. ncbi request reprint The EBNA-3 gene family proteins disrupt the G2/M checkpoint
    Kenia G Krauer
    Queensland Institute of Medical Research and Joint Oncology Program, University of Queensland, Brisbane, Australia
    Oncogene 23:1342-53. 2004
    ..The function of EBNA-3, -4 and -6 proteins appears to be more complex than anticipated and these data suggest a role for these proteins in disrupting the host cell cycle machinery...
  10. doi request reprint Truncated MEK1 is required for transient activation of MAPK signalling in G2 phase cells
    Tanya Pike
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Cell Signal 25:1423-8. 2013
    ....
  11. ncbi request reprint Tumor cell-selective cytotoxicity by targeting cell cycle checkpoints
    Robyn Warrener
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Brisbane, Queensland 4102, Australia
    FASEB J 17:1550-2. 2003
    ..This study of histone deacetylase inhibitors demonstrates that drugs targeting cell cycle checkpoints can provide the selectivity and cytotoxicity desired in effective chemotherapeutic agents...
  12. doi request reprint Inhibition of histone deacetylase 3 produces mitotic defects independent of alterations in histone H3 lysine 9 acetylation and methylation
    Robyn Warrener
    Diamantina Institute, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Mol Pharmacol 78:384-93. 2010
    ..These data demonstrate that H3K9 methylation and HP1 binding are not the targets responsible for HDACi-induced aberrant mitosis, but it is a consequence of selective inhibition of HDAC3...
  13. doi request reprint A UVR-induced G2-phase checkpoint response to ssDNA gaps produced by replication fork bypass of unrepaired lesions is defective in melanoma
    Matthew Wigan
    University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    J Invest Dermatol 132:1681-8. 2012
    ..We propose that defects in the UVR-induced G2-phase checkpoint and repair mechanism are likely to contribute to melanoma development...
  14. pmc Cyclin A/cdk2 regulates adenomatous polyposis coli-dependent mitotic spindle anchoring
    Heather Beamish
    University of Queensland Diamantina Institute for Cancer Immunology and Metabolic Medicine, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia
    J Biol Chem 284:29015-23. 2009
    ..Mutation of APC Ser-1360 to Ala results in identical off-centered mitotic spindles. Thus, this cyclin A/cdk2-dependent phosphorylation of APC affects astral microtubule attachment to the cortical surface in mitosis...
  15. ncbi request reprint Phosphorylation of Cdc25B3 Ser169 regulates 14-3-3 binding to Ser151 and Cdc25B activity
    Puji Astuti
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Cell Cycle 10:1960-7. 2011
    ..This indicates that Ser169 phosphorylation can disrupt 14-3-3 binding to Ser151 activating Cdc25B3, providing a mechanism for regulating Cdc25B3 activation without dephosphorylation of the 14-3-3 binding sites...
  16. ncbi request reprint Caffeine promotes apoptosis in mitotic spindle checkpoint-arrested cells
    Brian Gabrielli
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Brisbane, Queensland 4102, Australia
    J Biol Chem 282:6954-64. 2007
    ..Knockdown of PAK1 also increased apoptosis in spindle checkpoint-arrested cells. This study demonstrates that the spindle checkpoint not only regulates mitotic exit but apoptosis in mitosis through the activity of PAK1...
  17. ncbi request reprint Defining the chemotherapeutic targets of histone deacetylase inhibitors
    Brian Gabrielli
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4120, Australia
    Ann N Y Acad Sci 1030:627-35. 2004
    ....
  18. pmc Mitotic phosphorylation of Cdc25B Ser321 disrupts 14-3-3 binding to the high affinity Ser323 site
    Puji Astuti
    University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia
    J Biol Chem 285:34364-70. 2010
    ..The mitotic phosphorylation of Ser(321) acts to maintain full activation of Cdc25B by disrupting 14-3-3 binding to Ser(323) and enhancing the dephosphorylation of Ser(323) to block 14-3-3 binding to this site...
  19. doi request reprint The histone deacetylase inhibitor MGCD0103 has both deacetylase and microtubule inhibitory activity
    Keeming Chia
    University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    Mol Pharmacol 78:436-43. 2010
    ..This is the first example of an HDACi with microtubule destabilizing activity, and the combined effects of this drug have advantages for its therapeutic use...
  20. ncbi request reprint Histone deacetylase inhibitors specifically kill nonproliferating tumour cells
    Andrew Burgess
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia
    Oncogene 23:6693-701. 2004
    ..These drugs have enormous potential for the treatment of not only rapidly proliferating tumours, but tumours with a low mitotic index...
  21. doi request reprint Defective decatenation checkpoint function is a common feature of melanoma
    Kelly Brooks
    The University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Queensland, Australia
    J Invest Dermatol 134:150-8. 2014
    ..We also demonstrate that decatenation is dependent on both TopoIIα and β isoforms. The high incidence of decatenation checkpoint defect is likely to be a major contributor to the high level of genomic instability found in melanomas. ..
  22. doi request reprint Histone deacetylase inhibitors in the generation of the anti-tumour immune response
    Graham R Leggatt
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital, The University of Queensland, Brisbane, Queensland, Australia
    Immunol Cell Biol 90:33-8. 2012
    ..This review will examine the evidence for the generation of anti-tumour immunity after treatment of cancers with HDAC inhibitors...
  23. pmc A high-throughput platform for lentiviral overexpression screening of the human ORFeome
    Dubravka Skalamera
    University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Queensland, Australia
    PLoS ONE 6:e20057. 2011
    ..The screen demonstrates the reliability, versatility and utility of our screening platform, and identifies novel cell cycle/proliferative activities for a number of genes...
  24. doi request reprint DNA repair and cell cycle checkpoint defects as drivers and therapeutic targets in melanoma
    Sandra Pavey
    The University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, QLD, Australia
    Pigment Cell Melanoma Res 26:805-16. 2013
    ..Loss of the checkpoint responses may also provide an opportunity to target melanomas using a synthetic lethal approach to identify and inhibit mechanisms that compensate for the defective checkpoints. ..
  25. pmc Defective cell cycle checkpoints as targets for anti-cancer therapies
    Brian Gabrielli
    The University of Queensland Diamantina Institute, Princess Alexandra Hospital Brisbane, QLD, Australia
    Front Pharmacol 3:9. 2012
    ..Here we will discuss the utility of targeting checkpoint defects as novel anti-cancer therapies...
  26. ncbi request reprint 14-3-3 acts as an intramolecular bridge to regulate cdc25B localization and activity
    Nichole Giles
    Cancer Biology Program, Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia
    J Biol Chem 278:28580-7. 2003
    ..Mutation of the Ser-323 site was functionally equivalent to the mutation of all three sites, resulting in the complete loss of 14-3-3 binding, increased access of the catalytic site, and access to nuclear localization sequence...
  27. ncbi request reprint A histone deacetylase inhibitor, azelaic bishydroxamic acid, shows cytotoxicity on Epstein-Barr virus transformed B-cell lines: a potential therapy for posttransplant lymphoproliferative disease
    Tom B Sculley
    Queensland Institute of Medical Research and University of Queensland Joint Oncology Program, Herston 4029, Brisbane, Australia
    Transplantation 73:271-9. 2002
    ..The prognosis for many patients with PTLD is poor, and the optimal treatment strategy is not well defined...