http://hdl.handle.net/2451/29920 Search the Channel search http://archive.nyu.edu/simple-search http://hdl.handle.net/2451/29921 Title: Supplements to article: A novel transcription complex that selectivelymodulates apoptosis of breast cancer cells through regulation of FASTKD2<br/><br/>Yeung, Kay T.; Das, Sharmistha; Lomniczi, Alejandro; Ojeda, Sergio R.; Xu, Chong-Feng; Neubert, Thomas A.; Samuels, Herbert H.<br/><br/>Abstract: (This refers to the article.) We previously reported that expression ofNRIF3 (Nuclear Receptor Interacting Factor-3) rapidly and selectivelyleads to apoptosis of breast cancer cells. DIF-1 (a.k.a IRF-2BP2), thecellular target of NRIF3, was identified as a transcriptional repressorand DIF-1 knockdown leads to apoptosis of breast cancer cells but notother cell types. Here, we identify IRF2BP1 (Interferon RegulatoryFactor-2 Binding Protein 1) and EAP1 (Enhanced At Puberty 1) asimportant components of the DIF-1 complex mediating both complexstability and transcriptional repression. This interaction of DIF-1,IRF2BP1, and EAP1 occurs through the conserved C4 zinc-fingers of theseproteins. Microarray studies were carried out in breast cancer celllines engineered to conditionally and rapidly increase the levels of theDeath Domain region of NRIF3 (DD1). The DIF-1 complex was found torepress FASTKD2, a putative pro-apoptotic gene, in breast cancer cellsand to bind to the FASTKD2 gene by chromatin immunoprecipitation.FASTKD2 knockdown prevents apoptosis of breast cancer cells from NRIF3expression or DIF-1 knockdown while expression of FASTKD2 leads toapoptosis of both breast and non-breast cancer cells. Thus, regulationof FASTKD2 by NRIF3 and the DIF-1 complex acts as a novel death switchthat selectively modulates apoptosis in breast cancer.<br/><br/>Description: The materials provided here are supplemental tables and figures to anarticle to be published in 'Molecular and Cellular Biology.' Wed, 23 Mar 2011 21:04:57 GMT