Unwanted by Both the Political Left and Right: Interwar Europe’s Hungarian Migrating Artists

A little known group of Hungarian artists who were students at the Hungarian Academy of Fine Arts, Budapest in 1927-1930, joined by a few artists from outside the Academy, were modernists, explored the Soviet Russian avant-garde and abstraction, and therefore were rejected by the mainstream, official art in Hungary. However, the strictly principled left-wing Munka (Work) Circle of Lajos Kassák was not hospitable to therm, either. Members of “The Progressives” group left Hungary in 1930. The increasingly classicist Hungarian avant-garde did not tolerate bias; thus the idiosyncratic poet and artist Tamkó-Sirató had to leave Hungary, too and develop his Dimensionism in Paris

The bZIP Transcription Factor ATFx Binds Human T-Cell Leukemia Virus Type 1 (HTLV-1) Tax and Represses HTLV-1 Long Terminal Repeat-Mediated Transcription

The human T-cell leukemia virus type 1 (HTLV-1) viral protein Tax is a transactivator of transcription driven by the cognate viral long terminal repeat (LTR). Tax exerts its effect through three nonidentical copies of the Tax-responsive element (TxRE), a member of the asymmetric cyclic AMP response element (CRE) family of enhancer sequences. Transactivation is mediated via interaction of Tax with members of the CREB/ATF family bound to TxRE. We have identified a cellular repressor of transcription, activating transcription factor x (ATFx), as a novel Tax-binding protein. In addition to binding directly to Tax we show by electrophoretic mobility shift assay that ATFx binds to the TxRE enhancer element via the bZIP domain. The functional impact of this bridging interaction results in repression of both basal and Tax-induced transcription from the HTLV-1 LTR. ATFx is unique among ATF family of proteins in that it is cell cycle regulated and exerts a tight repressive control over apoptotic signaling. We propose that recruitment of ATFx to the HTLV-1 LTR serves to link viral transcription with critical events in cellular homeostasis