@article{HuangBelharazemLietal.2013,
  author    = {Huang, Bei and Belharazem, Djeda and Li, Li and Kneitz, Susanne and Schnabel, Philipp A. and Rieker, Ralf J. and K{\"o}rner, Daniel and Nix, Wilfried and Schalke, Berthold and M{\"u}ller-Hermelink, Hans Konrad and Ott, German and Rosenwald, Andreas and Str{\"o}bel, Philipp and Marx, Alexander},
  title     = {Anti-apoptotic signature in thymic squamous cell carcinomas - functional relevance of anti-apoptotic BIRC3 expression in the thymic carcinoma cell line 1889c},
  series = {Frontiers in Oncology},
  volume    = {3},
  journal   = {Frontiers in Oncology},
  number    = {316},
  doi       = {10.3389/fonc.2013.00316},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132214},
  year      = {2013},
  abstract  = {The molecular pathogenesis of thymomas and thymic arcinomas (TCs) is poorly understood and results of adjuvant therapy are unsatisfactory in case of metastatic disease and tumor recurrence. For these clinical settings, novel therapeutic strategies are urgently needed. Recently, limited sequencing efforts revealed that a broad spectrum of genes that play key roles in various common cancers are rarely affected in thymomas and TCs, suggesting that other oncogenic principles might be important.This made us re-analyze historic expression data obtained in a spectrumof thymomas and thymic squamous cell carcinomas (TSCCs) with a custom-made cDNA microarray. By cluster analysis, different anti-apoptotic signatures were detected in type B3 thymoma and TSCC, including overexpression of BIRC3 in TSCCs. This was confirmed by qRT-PCR in the original and an independent validation set of tumors. In contrast to several other cancer cell lines, the BIRC3-positive TSCC cell line, 1889c showed spontaneous apoptosis after BIRC3 knock-down. Targeting apoptosis genes is worth testing as therapeutic principle in TSCC.},
  language  = {en}
}
@article{SchlerethHeylKrampitzetal.2013,
  author    = {Schlereth, Katharina and Heyl, Charlotte and Krampitz, Anna-Maria and Mernberger, Marco and Finkernagel, Florian and Scharfe, Maren and Jarek, Michael and Leich, Ellen and Rosenwald, Andreas and Stiewe, Thorsten},
  title     = {Characterization of the p53 Cistrome - DNA Binding Cooperativity Dissects p53's Tumor Suppressor Functions},
  series = {PLOS Genetics},
  volume    = {9},
  journal   = {PLOS Genetics},
  number    = {8},
  issn      = {1553-7404},
  doi       = {10.1371/journal.pgen.1003726},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-127579},
  pages     = {e1003726},
  year      = {2013},
  abstract  = {p53 protects us from cancer by transcriptionally regulating tumor suppressive programs designed to either prevent the development or clonal expansion of malignant cells. How p53 selects target genes in the genome in a context-and tissue-specific manner remains largely obscure. There is growing evidence that the ability of p53 to bind DNA in a cooperative manner prominently influences target gene selection with activation of the apoptosis program being completely dependent on DNA binding cooperativity. Here, we used ChIP-seq to comprehensively profile the cistrome of p53 mutants with reduced or increased cooperativity. The analysis highlighted a particular relevance of cooperativity for extending the p53 cistrome to non-canonical binding sequences characterized by deletions, spacer insertions and base mismatches. Furthermore, it revealed a striking functional separation of the cistrome on the basis of cooperativity; with low cooperativity genes being significantly enriched for cell cycle and high cooperativity genes for apoptotic functions. Importantly, expression of high but not low cooperativity genes was correlated with superior survival in breast cancer patients. Interestingly, in contrast to most p53-activated genes, p53-repressed genes did not commonly contain p53 binding elements. Nevertheless, both the degree of gene activation and repression were cooperativity-dependent, suggesting that p53-mediated gene repression is largely indirect and mediated by cooperativity-dependently transactivated gene products such as CDKN1A, E2F7 and non-coding RNAs. Since both activation of apoptosis genes with non-canonical response elements and repression of pro-survival genes are crucial for p53's apoptotic activity, the cistrome analysis comprehensively explains why p53-induced apoptosis, but not cell cycle arrest, strongly depends on the intermolecular cooperation of p53 molecules as a possible safeguard mechanism protecting from accidental cell killing.},
  language  = {en}
}
@article{MuellerQuandtMarienfeldetal.2013,
  author    = {Mueller, Kerstin and Quandt, Jasmin and Marienfeld, Ralf B. and Weihrich, Petra and Fiedler, Katja and Claussnitzer, Melina and Laumen, Helmut and Vaeth, Martin and Berberich-Siebelt, Frederike and Serfling, Edgar and Wirth, Thomas and Brunner, Cornelia},
  title     = {Octamer-dependent transcription in T cells is mediated by NFAT and \(NF-\kappa B\)},
  series = {Nucleic Acids Research},
  volume    = {41},
  journal   = {Nucleic Acids Research},
  number    = {4},
  issn      = {1362-4962},
  doi       = {10.1093/nar/gks1349},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123280},
  pages     = {2138-2154},
  year      = {2013},
  abstract  = {The transcriptional co-activator BOB.1/OBF.1 was originally identified in B cells and is constitutively expressed throughout B cell development. BOB.1/OBF.1 associates with the transcription factors Oct1 and Oct2, thereby enhancing octamer-dependent transcription. In contrast, in T cells, BOB.1/OBF.1 expression is inducible by treatment of cells with PMA/Ionomycin or by antigen receptor engagement, indicating a marked difference in the regulation of BOB.1/OBF.1 expression in B versus T cells. The molecular mechanisms underlying the differential expression of BOB.1/OBF.1 in T and B cells remain largely unknown. Therefore, the present study focuses on mechanisms controlling the transcriptional regulation of BOB.1/OBF.1 and Oct2 in T cells. We show that both calcineurin- and \(NF-\kappa B\)-inhibitors efficiently attenuate the expression of BOB.1/OBF.1 and Oct2 in T cells. In silico analyses of the BOB.1/OBF.1 promoter revealed the presence of previously unappreciated combined NFAT/\(NF-\kappa B\) sites. An array of genetic and biochemical analyses illustrates the involvement of the \(Ca^{2+}\)/calmodulin-dependent phosphatase calcineurin as well as NFAT and \(NF-\kappa B\) transcription factors in the transcriptional regulation of octamer-dependent transcription in T cells. Conclusively, impaired expression of BOB.1/OBF.1 and Oct2 and therefore a hampered octamer-dependent transcription may participate in T cell-mediated immunodeficiency caused by the deletion of NFAT or \(NF-\kappa B\) transcription factors.},
  language  = {en}
}