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Modulation Of Estrogen Related Receptor Alpha Activity By The Kinesin Kif17, Am Pramodh Bandara Seneviratne, Zeynep Turan, Aurelie Hermant, Patrick Lecine, William O. Smith, Jean-Paul Borg, Fanny Jaulin, Geri Kreitzer
Modulation Of Estrogen Related Receptor Alpha Activity By The Kinesin Kif17, Am Pramodh Bandara Seneviratne, Zeynep Turan, Aurelie Hermant, Patrick Lecine, William O. Smith, Jean-Paul Borg, Fanny Jaulin, Geri Kreitzer
Publications and Research
Estrogen-related receptor alpha (ERR1) is an orphan nuclear receptor that can bind transcriptional co-activators constitutively. ERR1 expression correlates with poor patient outcomes in breast cancer, heightening interest in this nuclear receptor as a therapeutic target. Because ERR1 has no known regulatory ligand, a major challenge in targeting its activity is to find cellular or synthetic modulators of its function. We identified an interaction between ERR1 and KIF17, a kinesin-2 family microtubule motor, in a yeast-2-hybrid screen. We confirmed the interaction using in vitro biochemical assays and determined that binding is mediated by the ERR1 ligand-binding/AF2 domain and the KIF17 C-terminal …
Functional Studies Of Ccaat/Enhancer Binding Protein Site Located Downstream Of The Transcriptional Start Site., Yujie Liu, Michael R. Nonnemacher, Aikaterini Alexaki, Vanessa Pirrone, Anupam Banerjee, Luna Li, Evelyn Kilareski, Brian Wigdahl
Functional Studies Of Ccaat/Enhancer Binding Protein Site Located Downstream Of The Transcriptional Start Site., Yujie Liu, Michael R. Nonnemacher, Aikaterini Alexaki, Vanessa Pirrone, Anupam Banerjee, Luna Li, Evelyn Kilareski, Brian Wigdahl
Kimmel Cancer Center Papers, Presentations, and Grand Rounds
Previous studies have identified a CCAAT/enhancer binding protein (C/EBP) site located downstream of the transcriptional start site (DS3). The role of the DS3 element with respect to HIV-1 transactivation by Tat and viral replication has not been characterized. We have demonstrated that DS3 was a functional C/EBPβ binding site and mutation of this site to the C/EBP knockout DS3-9C variant showed lower HIV-1 long terminal repeat (LTR) transactivation by C/EBPβ. However, it was able to exhibit similar or even higher transcription levels by Tat compared to the parental LTR. C/EBPβ and Tat together further enhanced the transcription level of the …