The SAS proposals for participation in FP6 projects
are listed in blocks according to the FP6 priority theme structure



FP6 priority
1.1.1   Genomics and Biotechnology for Health
1.1.2.2
Title of the proposal

Transcription factors and cancer
Institute
Slovak Academy of Sciences, Cancer Research Institute
Vlarska 7, 83391 Bratislava, Slovak Republic
www.exon.sav.sk
Contact
Name:
Juraj BIES, Ph.D.
Phone:
+421 2 59327 425
E-mail:
exonbies@savba.sk


Research subject for a potential FP6 project

It is generally accepted that neoplastic transformation of cell is a consequence of misregulated expression of genes involved in proliferation, differentiation and metastasis. Our project is aimed at the study of regulation of activity of transcription factors directly involved in the transcriptional regulation of oncogenes and tumor suppressor genes. Particularly, we are interesting in deciphering the potential role of Myb family transcription factors in human cancer.

Recently we have identified a novel post-translational modification of c-Myb by covalent attach-ment of SUMO-1 protein. It was shown that “sumolation“ of c-Myb dramatically affects its trans-activation capacity and proteolytic stability. Using a modern approaches of genomoc we would like to investigate the consequences of sumolation on the ability of c-Myb transcription factor to regulate its target genes potentially invovled in neoplastic transformation.


Recent international cooperation of the research team

Laboratory of Cellular Oncology, National Cancer Institute NIH, Bethesda, Maryland U.S.A.
Hanson Centre for Cancer Research, IMVS, Adelaide, SA 5000, Australia


Proposer´s relevant publications related to the research subject

Bies J, Markus J, Wolff L. , Covalent Attachment of the SUMO-1 Protein to the Negative Regulatory Domain of the c-Myb Transcription Factor Modifies Its Stability and Transactivation Capacity. J Biol Chem; 277(11):8999-9009, (2002)

Bies J, Feikova S, Markus J, Wolff L. Phosphorylation-dependent conformation and proteolytic stability of c-Myb. Blood Cells Mol Dis 27(2):422-428, (2001)

Bies J, Feikova S, Bottaro DP, Wolff L. Hyperphosphorylation and increased proteolytic breakdown of c-Myb induced by the inhibition of Ser/Thr protein phosphatases. Oncogene 19(24):2846-2854, (2000)