Title
vMyb proteins and their oncogenic potential: A study on how two point mutations affect the interaction of vMyb with other prot,Used
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Product Description The oncogene vmyb of the retroviruses AMV (avian myeloblastosis virus) and E26 (avian leukaemia virus) encodes a transcription factor (vMyb) which is a truncated homolog of its cellular progenitor cMyb. cMyb plays an essential role in the development of haematopoietic cells and is known to be a regulator for many target genes. vMyb AMV is responsible for the transformation of myelomonocytic cells and for arresting them in an immature stage, presumably because of a deregulation of the expression of specific target genes. In addition to the truncation of the coding region, a number of amino acid substitutions are responsible for the high oncogenicity of vMyb AMV. Due to the amino acid substitutions, vMyb AMV and vMyb E26 differ in their target gene spectrum. The chicken mim1 gene is activated by vMyb E26 and cMyb but not by vMyb AMV. The gene consists of two cisregulatory regions, a Myb responsive promoter and a cellspecific Mybinducible enhancer. Recently, it has been proven that two amino acid substitutions in a hydrophobic patch in the transactivation domain of vMyb AMV are sufficient to disrupt its ability to stimulate the enhancer. This work focuses on the consequences of these amino acid substitutions by investigating proteinprotein interactions of the hydrophobic region of vMyb AMV in comparison to v Myb E26. Previous experiments identified GRP78 as an interaction partner of v Myb. In this study, a cytosolic variant of GRP78, GRP78va, was confirmed to interact with both vMyb proteins. It was shown that its interaction site is limited to a very small region of vMyb preceding the hydrophobic patch. Additionally, it was shown that GRP78va associated with all other members of the Mybfamily and also with C/EBP and HIPK2, suggesting a nonsequencespecific binding of GRP78va. Furthermore, reporter gene experiments demonstrated a repressing effect of GRP78va on the transactivation potential of vMyb E26. In addition, GST pull down assays and coi About the Author Beeke Eienert, M.Sc., was born in Bremen in 1985. After finishing a Bachelor's degree in Biology and Chemistry at the CarlvonOssietzky Universitt Oldenburg, she completed her Master's degree in Biowissenschaften in 2011. During a research stay in Australia, the author focused on researching transcription factors. She continued to focus on these in her Master's thesis and plans to further work within this research area in her doctoral dissertation at the UNSW, Sydney.
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