Research Topics
Genomes and GenesSpecies | Helen RizosSummaryAffiliation: University of Sydney Country: Australia Publications
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Publications
Association of p14ARF with the p120E4F transcriptional repressor enhances cell cycle inhibitionHelen Rizos
Westmead Institute for Cancer Research, University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia
J Biol Chem 278:4981-9. 2003....- p14ARF regulates E2F-1 ubiquitination and degradation via a p53-dependent mechanismHelen Rizos
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, Australia
Cell Cycle 6:1741-7. 2007..Importantly, these data establish that the ARF-E2F-1 pathway is an extension of the p53-mdm2-ARF tumor suppressor network and is unlikely to constitute a p53-independent pathway for ARF function... - p14ARF interacts with the SUMO-conjugating enzyme Ubc9 and promotes the sumoylation of its binding partnersHelen Rizos
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, Australia
Cell Cycle 4:597-603. 2005..Furthermore, p14ARF-induced sumoylation is abrogated by a subset of melanoma-associated p14ARF mutations. These results provide a mechanism for p14ARF action through a common modification of diverse binding partners... - A melanoma-associated germline mutation in exon 1beta inactivates p14ARFH Rizos
Westmead Institute for Cancer Research, University of Sydney, Westmead Hospital, Westmead NSW 2145, Australia
Oncogene 20:5543-7. 2001..This is the first example of an exon 1beta mutation that inactivates p14ARF, and thus implicates a role for this tumour suppressor in melanoma predisposition... - Mutations in the INK4a/ARF melanoma susceptibility locus functionally impair p14ARFH Rizos
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, New South Wales 2145, Australia
J Biol Chem 276:41424-34. 2001..This work establishes the importance of p14(ARF) in melanoma predisposition... - Physical and functional interaction of the p14ARF tumor suppressor with ribosomesHelen Rizos
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, New South Wales 2145, Australia
J Biol Chem 281:38080-8. 2006..These results suggest a ribosome-dependent p14(ARF) pathway that regulates cell growth and thus complements p53-dependent p14(ARF) functions... 
Predicting functional significance of cancer-associated p16(INK4a) mutations in CDKN2AHeather A McKenzie
Westmead Institute for Cancer Research and Melanoma Institute of Australia, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead NSW 2145, Australia
Hum Mutat 31:692-701. 2010..The ability to determine variant functional activity accurately would identify disease-associated mutations and facilitate effective genetic counselling of individuals at high risk of melanoma...- Absence of distinguishing senescence traits in human melanocytic neviSieu L Tran
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, New South Wales, Australia
J Invest Dermatol 132:2226-34. 2012..We conclude that on the basis of current evidence it cannot be reasonably inferred that nevi are permanently growth arrested via senescence... 
The chromatin remodelling factor BRG1 is a novel binding partner of the tumor suppressor p16INK4aTherese M Becker
Westmead Institute for Cancer Research, University of Sydney, Westmead Millennium Institute and Westmead Hospital, Australia
Mol Cancer 8:4. 2009..To identify such functions we conducted a yeast-two-hybrid screen for novel p16INK4a binding partners...- IGFBP7 is not required for B-RAF-induced melanocyte senescenceLyndee L Scurr
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, New South Wales 2145, Australia
Cell 141:717-27. 2010..Therefore, we conclude that the secreted protein IGFBP7 is dispensable for B-RAF(V600E)-induced senescence in human melanocytes... - The relative contributions of the p53 and pRb pathways in oncogene-induced melanocyte senescenceSebastian Haferkamp
Westmead Institute for Cancer Research and Melanoma Institute of Australia, University of Sydney at Westmead, Westmead NSW 2145, Australia
Aging (Albany NY) 1:542-56. 2009..Thus, in melanocytes with oncogenic signalling only p16(INK4a) can fully engage the pRb pathway to alter chromatin structure and silence the genes that are required for proliferation... - p16INK4a expression and absence of activated B-RAF are independent predictors of chemosensitivity in melanoma tumorsStuart J Gallagher
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead NSW 2145, Australia
Neoplasia 10:1231-9. 2008..This study shows that high expression of p16(INK4a) or the absence of activated B-RAF correlates with in vivo response of melanoma to cytotoxic drugs... - Oncogene-induced senescence does not require the p16(INK4a) or p14ARF melanoma tumor suppressorsSebastian Haferkamp
Westmead Institute for Cancer Research, Westmead Hospital, University of Sydney at Westmead Millennium Institute, Westmead, New South Wales, Australia
J Invest Dermatol 129:1983-91. 2009..Our data are consistent with observations showing that senescent nevus cells do not always express p16(INK4a), and highlight the need to thoroughly explore INK4a/ARF-independent molecular pathways of senescence in human melanocytes... - Amino terminal hydrophobic import signals target the p14(ARF) tumor suppressor to the mitochondriaMal Irvine
Westmead Institute for Cancer Research and Melanoma Institute of Australia, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, NSW, Australia
Cell Cycle 9:829-39. 2010..This allows the interaction of p14(ARF) with mitochondrial proteins, including p32 and enables p53-independent cell death... - The melanoma-associated 24 base pair duplication in p16INK4a is functionally impairedTherese M Becker
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, New South Wales, Australia
Int J Cancer 117:569-73. 2005..We also show that the cell cycle-regulatory defect of the p16INK4a duplication mutant was associated with decreased inhibition of pRb phosphorylation even though it retained significant binding to CDK4... - p16INK4a-induced senescence is disabled by melanoma-associated mutationsSebastian Haferkamp
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, NSW, Australia
Aging Cell 7:733-45. 2008..Our data provide the first evidence that p16(INK4a) can initiate a CDK4/6-dependent autonomous senescence programme that is disabled by inherited melanoma-associated mutations... - A parallel genome-wide mRNA and microRNA profiling of the frontal cortex of HIV patients with and without HIV-associated dementia shows the role of axon guidance and downstream pathways in HIV-mediated neurodegenerationLi Zhou
Retroviral Genetics Division, Center for Virus Research, Westmead Millennium Institute, Westmead Hospital, The University of Sydney, Westmead, NSW 2145, Sydney, Australia
BMC Genomics 13:677. 2012..abstract:.. - Enforced expression of p14ARF induces p53-dependent cell cycle arrest but not apoptosisStuart Gallagher
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, Australia
Cell Cycle 4:465-72. 2005..Thus, loss of p14ARF would be an important step in the selection of apoptotic resistant tumour cells... - Acquired resistance to BRAF inhibition can confer cross-resistance to combined BRAF/MEK inhibitionKavitha Gowrishankar
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute and Melanoma Institute Australia, Westmead Hospital, Westmead, New South Wales, Australia
J Invest Dermatol 132:1850-9. 2012..These data indicate that melanoma tumors are likely to develop heterogeneous mechanisms of resistance, many of which will confer resistance to multiple MAPK inhibitory therapies... - Ankyrin repeat domain 1, ANKRD1, a novel determinant of cisplatin sensitivity expressed in ovarian cancerLyndee L Scurr
Westmead Institute for Cancer Research, University of Sydney at the Westmead Millennium Institute, Westmead Hospital, Westmead, NSW, Australia
Clin Cancer Res 14:6924-32. 2008.... - Impaired inhibition of NF-kappaB activity by melanoma-associated p16INK4a mutationsT M Becker
Westmead Institute for Cancer Research, University of Sydney, Westmead Millennium Institute, Westmead, NSW 2145, Australia
Biochem Biophys Res Commun 332:873-9. 2005..p16INK4a does not affect NF-kappaB nuclear translocation or DNA binding, suggesting a mechanism that reduces NF-kappaB transactivation activity... - Functional impairment of melanoma-associated p16(INK4a) mutants in melanoma cells despite retention of cyclin-dependent kinase 4 bindingT M Becker
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, NSW 2145, Australia
Clin Cancer Res 7:3282-8. 2001..We examined the relationship between loss of CDK binding by mutant proteins and various measures of cellular growth in melanoma cells... - Two arginine rich domains in the p14ARF tumour suppressor mediate nucleolar localizationH Rizos
Westmead Institute for Cancer Research, University of Sydney, Westmead Hospital, Westmead NSW 2145, Australia
Oncogene 19:2978-85. 2000..The INK4a/ARF exon2-mutations could affect the function of both the p16INK4a and p14ARF tumour suppressors. Oncogene (2000)... - Multiple abnormalities of the p16INK4a-pRb regulatory pathway in cultured melanoma cellsH Rizos
Westmead Institute for Cancer Research, University of Sydney Westmead Hospital, NSW, Australia
Melanoma Res 9:10-9. 1999..This suggests that the selective growth advantages afforded by CDKN2A inactivation and CDK4 insensitivity are distinct and may involve the mediation of other CDK inhibitors or CDKs... - First evidence of overlaps between HIV-Associated Dementia (HAD) and non-viral neurodegenerative diseases: proteomic analysis of the frontal cortex from HIV+ patients with and without dementiaLi Zhou
Center for Virus Research, Westmead Millennium Institute, Westmead Hospital, The University of Sydney, Westmead, NSW 2145, Sydney, Australia
Mol Neurodegener 5:27. 2010..The pathogenesis of HIV-associated dementia (HAD) is poorly understood. To date, detailed proteomic fingerprinting directly from autopsied brain tissues of HAD and HIV non-dementia patients has not been performed... - The ARF tumour suppressorStuart J Gallagher
Westmead Institute for Cancer Research, University of Sydney at Westmead Millennium Institute, Westmead Hospital, Westmead, NSW 2145, Australia
Int J Biochem Cell Biol 38:1637-41. 2006..The biological functions of ARF interactions with other binding partners remain uncertain, but ARF-mediated sumoylation may represent a unifying effector pathway... - Gene expression profiling in melanoma identifies novel downstream effectors of p14ARFLeisl M Packer
Oncogenomics Laboratory, Queensland Institute of Medical Research, Brisbane, Australia
Int J Cancer 121:784-90. 2007..We propose that regulation of these genes may contribute to melanoma development when p14ARF function is lost...