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@article{Jiang2004,  abstract = {All nuclear transcription is interrupted during mitosis. We examined the role of human TTF2, an RNA polymerase (Pol) I and II termination factor, in mitotic repression of transcription elongation. We find that TTF2 levels rise in the cytoplasm in S and G2 and at the onset of mitosis TTF2 translocates into the nucleus. Consistent with a role in termination of all transcription, TTF2 is the only ATP-dependent termination activity associated with Pol II transcription elongation complexes, is largely unaffected by template position, and is impervious to the phosphorylation state of the polymerase. Cells in which TTF2 levels are knocked down showed dramatic retention of Ser2 phosphorylated Pol II on mitotic chromosomes and an increase in chromosome segregation defects.},  author = {Jiang, Yan and Liu, Mingyi and Spencer, Charlotte A. and Price, David H.},  doi = {10.1016/S1097-2765(04)00234-5},  file = {::},  issn = {10972765},  journal = {Molecular Cell},  month = may,  number = {3},  pages = {375--386},  title = {{Involvement of Transcription Termination Factor 2 in Mitotic Repression of Transcription Elongation}},  url = {http://www.sciencedirect.com/science/article/pii/S1097276504002345},  volume = {14},  year = {2004}  }  @article{Gottesfeld1997,  abstract = {Nuclear RNA transcription is silenced when eukaryotic cells enter mitosis. Until recently, this repression was thought to derive solely from the condensation of interphase chromatin into mitotic chromosomes. Recent studies, however, have shown that changes in chromatin structure and occupancy of promoter elements by both general and gene-specific transcription factors also play a role in transcriptional silencing. In addition, studies with simplified systems reveal that reversible phosphorylation of the basal transcriptional machinery represses transcription at mitosis.},  author = {Gottesfeld, J},