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Role of ASCIZ in the DNA damage response and cancer development

Role of ASCIZ in the DNA damage response and cancer development

PhD/Honours project

DNA damage responses play a critical role in the natural prevention of cancer and in the cellular response to the majority of clinically used cancer chemotherapeutics.  We have recently identified ASCIZ as a novel factor in the response to DNA base damage, and ASCIZ also has DNA damage-independent functions as a transcription factor.  The aim of this project is to elucidate the molecular mechanisms by which ASCIZ affects repair of DNA base damage, using both biochemical and cell-based in vitro studies, as well as innovative in vivo mouse models of tumorigenesis and chemotherapeutic responses.

Related publications:
McNees et al, ASCIZ regulates lesion-specific Rad51 focus formation and apoptosis after methylating DNA damage, EMBO Journal 24, 2447-57 (2005); Jurado et al, Dual Functions of ASCIZ in the DNA base damage response and pulmonary organogenesis, PLoS Genetics 6, e1001170 (2010); Jurado et al, ATM substrate Chk2-ineracting Zn2+-finger (ASCIZ) is a bi-functional transcriptional activator and feedback sensor of dynein light chain (DYNLL1) expression, Journal of Biological Chemistry 287, 3156-64; Jurado et al, The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim. Journal of Experimental Medicine 209, advance-online-publication 13/08/2012.

Supervised by:

  • A/Prof Jörg Heierhorst
  • Disease Focus:

  • Cancer
  • Research Unit:

  • Molecular genetics