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|Title: ||Supplements to article: A novel transcription complex that selectively
modulates apoptosis of breast cancer cells through regulation of FASTKD2|
|Authors: ||Yeung, Kay T.|
Ojeda, Sergio R.
Neubert, Thomas A.
Samuels, Herbert H.
|Issue Date: ||23-Mar-2011 |
|Abstract: ||(This refers to the article.) We previously reported that expression of
NRIF3 (Nuclear Receptor Interacting Factor-3) rapidly and selectively
leads to apoptosis of breast cancer cells. DIF-1 (a.k.a IRF-2BP2), the
cellular target of NRIF3, was identified as a transcriptional repressor
and DIF-1 knockdown leads to apoptosis of breast cancer cells but not
other cell types. Here, we identify IRF2BP1 (Interferon Regulatory
Factor-2 Binding Protein 1) and EAP1 (Enhanced At Puberty 1) as
important components of the DIF-1 complex mediating both complex
stability and transcriptional repression. This interaction of DIF-1,
IRF2BP1, and EAP1 occurs through the conserved C4 zinc-fingers of these
proteins. Microarray studies were carried out in breast cancer cell
lines engineered to conditionally and rapidly increase the levels of the
Death Domain region of NRIF3 (DD1). The DIF-1 complex was found to
repress FASTKD2, a putative pro-apoptotic gene, in breast cancer cells
and to bind to the FASTKD2 gene by chromatin immunoprecipitation.
FASTKD2 knockdown prevents apoptosis of breast cancer cells from NRIF3
expression or DIF-1 knockdown while expression of FASTKD2 leads to
apoptosis of both breast and non-breast cancer cells. Thus, regulation
of FASTKD2 by NRIF3 and the DIF-1 complex acts as a novel death switch
that selectively modulates apoptosis in breast cancer.|
|Description: ||The materials provided here are supplemental tables and figures to an
article to be published in 'Molecular and Cellular Biology.'|
|Appears in Collections:||Herbert Samuels Collection|
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