E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis

Kamil Wolyniec; Jake Shortt; Elisa de Stanchina; Yaara Levav-Cohen; Osnat Alsheich-Bartok; Igal Louria-Hayon; Vincent Corneille; Beena Kumar; Simone J Woods; Stephen Opat; Ricky W Johnstone; Clare L Scott; David Segal; Pier Paolo Pandolfi; Stephen Fox; Andreas Strasser; Yong-Hui Jiang; Scott W Lowe; Sue Haupt; Ygal Haupt

Journal article

E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis

Kamil Wolyniec, Jake Shortt, Elisa de Stanchina, Yaara Levav-Cohen, Osnat Alsheich-Bartok, Igal Louria-Hayon, Vincent Corneille, Beena Kumar, Simone J Woods, Stephen Opat, Ricky W Johnstone, Clare L Scott, David Segal, Pier Paolo Pandolfi, Stephen Fox, Andreas Strasser, Yong-Hui Jiang, Scott W Lowe, Sue Haupt, Ygal Haupt

Blood | AMER SOC HEMATOLOGY | Published : 2012

DOI: 10.1182/blood-2011-10-387647

University of Melbourne Researchers

Jake Shortt Author The Sir Peter MacCallum Department of Oncology

Clare Scott Author Obstetrics and Gynaecology Royal Women's Hospital/Mercy

Susan Haupt Author Clinical Pathology

Ricky Johnstone Author The Sir Peter MacCallum Department of Oncology

Stephen Fox Author The Sir Peter MacCallum Department of Oncology

Related Projects (3)

How The Tumor Suppressor Protein Pml Is Regulated And The Consequences For Cancer.

PML is a vital tumour suppressor, but little is known about its regulation. We established that PML levels are affected by another cellular ..

Treatment Of B-Lymphoma By Targeting Protein Degradation

B-cell lymphoma is the most common type blood cancer diagnosed in Australia, and Australia's fifth most common cancer. Despite remarkable ad..

Regulation Of Cellular Senescence

Cancer is constantly being suppressed in our bodies by a process that stops damaged cells from growing: 'senescence'. The mechanism that tra..

Grants

Awarded by National Health and Medical Research Council (NHMRC) of Australia

Awarded by Leukemia and Lymphoma Society (SCOR)

Funding Acknowledgements

This work was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia to Y.H. (NHMRC 509196, 509197, 1026990, and 1026988) and A.S. (Program Grant 461221); by a grant from the Cancer Council Victoria; the Leukemia and Lymphoma Society (SCOR grant 7413 to A.S.); and by the VESKI award. Y.H. is an NHMRC Senior Research Fellow and A.S. an NHMRC Australia Fellow. This work was made possible by operational infrastructure grants through the Australian Government IRISS and the Victorian State Government OIS.