Zbtb7
IntroductionIntroduction
Zbtb7 which was originally named as Pokemon (POK erythroid myeloid ontogenic factor) is a gene which plays a critical role in development, cellular differentiation and oncogenesis and has a crucial role in interacting with other POK family proteins.The gene was discovered in 2005 by the team of scientists from Memorial Sloan-Kettering Cancer Center, New York and Institute of Cancer Research, London. Scientists have reported the transcriptional repressor Pokemon as a critical factor in oncogenesis.[1]
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FunctionFunction
Pokemon functions as a transcription regulator with active roles in cell growth, differentiation and oncogenesis. Pokemon interferes with GC box recognition by Sp1 via interacting with the zinc finger DNA binding domain, resulting in the repression of ADH5/FDH transcription. Pokemon also affects the transcription of nuclear factor (NF)-κB-responsive genes by associating with the p65 subunit and inducing its nuclear import and stabilization. The target genes of Pokemon include extracellular matrix collagen types I, II, IX, X and XI; aggrecan; fibronectin; elastin; cartilage oligomeric matrix protein (COMP); alcohol dehydrogenase ADH5/FDH, ARF and Rb tumor suppressors; and c-fos and c-myc oncoproteins [2]
DiseaseDisease
Expression of Pokemon is proved to be required for normal growth, development and differentiation of cells although overexpression of this transcriptional factor has been found to be oncogenic as tested in mice both in vitro and in vivo.According to the research published in 2011 it was reported that Pokemon promotes breast cancer progression by upregulating survivin expression.[1,3]
Structural highlightsStructural highlights
Members of the POK family of proteins contain an amino-terminal POZ domain and a carboxy-terminal DNA-binding domain made of Kru¨ppel-type zinc fingers and can act as potent transcriptional repressors through the recruitment of histone deacetylases (HDACs) and subsequent chromatin remodelling.[1]
ReferencesReferences
[1] Takahiro Maeda1,2, Robin M. Hobbs1,2, Taha Merghoub1,2, Ilhem Guernah1,2, Arthur Zelent3, Carlos Cordon-Cardo2, Julie Teruya-Feldstein & Pier Paolo Pandolfi1,2. 1Cancer Biology and Genetics Program, 2Department of Pathology, Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York,New York 10021, USA Leukemia Research Fund Center at the Institute of Cancer Research, Chester Beatty Laboratories, Fulham Road, London SW3 6JB, UK
[2]Xuyu Zu, Jun Ma, Hongxia Liu, Feng Liu, Chunyan Tan, Lingling Yu, Jue Wang, Zhenhua Xie, Deliang Cao and Yuyang JiangEmail author Breast Cancer Research201113:R26 DOI: 10.1186/bcr2843© Zu et al.; licensee BioMed Central Ltd. 2011