Anti-BTG1 monoclonal antibody, clone FQS9385(3)

We have reported previously the physical interaction of B-cell translocation gene proteins (BTG)1 and BTG2 with the mouse protein CAF1 (CCR4-associated factor 1) and suggested that these proteins may participate, through their association with CAF1, in transcription regulation. Here we describe the in vitro and in vivo association of these proteins with hPOP2, the human paralog of hCAF1, The physical and functional relationships between the BTG proteins and their partners hCAF1 and hPOP2 were investigated to find out how these interactions affect cellular processes, and in particular transcription regulation. We defined their interaction regions and examined their expression in various human tissues. We also show functional data indicating their involvement in estrogen receptor a (ER alpha)-mediated transcription regulation. We found that BTG1 and BTG2, probably through their interaction with CAF1 via a CCR4-like complex, can play both positive or negative roles in regulating the ER alpha function. In addition, our results indicate that two LXXLL motifs, referred to as nuclear receptor boxes, present in both BTG1 and BTG2, are involved in the regulation of ER alpha -mediated activation.

Using a polymerase chain reaction-mediated cloning procedure, we have identified a novel member, termed ANA (from Abundant in Nueroepithelium Area), of Tob/BTG1 family of antiproliferative genes, Molecular cloning and analysis of cDNAs revealed that the human and mouse ANA encoded a protein of 252 amino acids, The amino-terminal half of ANA was homologous to the previously characterized antiproliferative gene products, BTG1, PC3/TIS21/BTG2, and Tob, The human, ANA gene was localized at chromosome 21q11.2-q21.1, ANA ,vas expressed in a variety of tissues and cell lines, its expression being high in the ovary, testis, prostate, thymus, and lung. Further analysis revealed that ANA expression was high in the ventricular zone of the developing central nervous system, Finally, overexpression of ANA impaired serum-induced cell cycle progression from the G(0)/G(1) to S phase. In conclusion, ANA is a fourth member of the Tob/BTG1 family that might play roles in neurogenesis in the central nervous system.