@article{ShiKuaiLeietal.2016,
  author    = {Shi, Yaoyao and Kuai, Yue and Lei, Lizhen and Weng, Yuanyuan and Berberich-Siebelt, Friederike and Zhang, Xinxia and Wang, Jinjie and Zhou, Yuan and Jiang, Xin and Ren, Guoping and Pan, Hongyang and Mao, Zhengrong and Zhou, Ren},
  title     = {The feedback loop of LITAF and BCL6 is involved in regulating apoptosis in B cell non-Hodgkin's-lymphoma},
  series = {Oncotarget},
  volume    = {7},
  journal   = {Oncotarget},
  number    = {47},
  doi       = {10.18632/oncotarget.12680},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166500},
  pages     = {77444-77456},
  year      = {2016},
  abstract  = {Dysregulation of the apoptotic pathway is widely recognized as a key step in lymphomagenesis. Notably, LITAF was initially identified as a p53-inducible gene, subsequently implicated as a tumor suppressor. Our previous study also showed LITAF to be methylated in 89.5\% B-NHL samples. Conversely, deregulated expression of BCL6 is a pathogenic event in many lymphomas. Interestingly, our study found an oppositional expression of LITAF and BCL6 in B-NHL. In addition, LITAF was recently identified as a novel target gene of BCL6. Therefore, we sought to explore the feedback loop between LITAF and BCL6 in B-NHL. Here, our data for the first time show that LITAF can repress expression of BCL6 by binding to Region A (-87 to +65) containing a putative LITAF-binding motif (CTCCC) within the BCL6 promoter. Furthermore, the regulation of BCL6 targets (PRDM1 or c-Myc) by LITAF may be associated with B-cell differentiation. Results also demonstrate that ectopic expression of LITAF induces cell apoptosis, activated by releasing cytochrome c, cleaving PARP and caspase 3 in B-NHL cells whereas knockdown of LITAF robustly protected cells from apoptosis. Interestingly, BCL6, in turn, could reverse cell apoptosis mediated by LITAF. Collectively, our findings provide a novel apoptotic regulatory pathway in which LITAF, as a transcription factor, inhibits the expression of BCL6, which leads to activation of the intrinsic mitochondrial pathway and tumor apoptosis. Our study is expected to provide a possible biomarker as well as a target for clinical therapies to promote tumor cell apoptosis.},
  language  = {en}
}
@article{ZhangWuLietal.2015,
  author    = {Zhang, Xin and Wu, Wei and Li, Gang and Wen, Lin and Sun, Qing and Ji, An-Chun},
  title     = {Phase diagram of interacting Fermi gas in spin-orbit coupled square lattices},
  series = {New Journal of Physics},
  volume    = {17},
  journal   = {New Journal of Physics},
  number    = {073036},
  doi       = {10.1088/1367-2630/17/7/073036},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151475},
  year      = {2015},
  abstract  = {The spin-orbit (SO) coupled optical lattices have attracted considerable interest. In this paper, we investigate the phase diagram of the interacting Fermi gas with Rashba-type spin-orbit coupling (SOC) on a square optical lattice. The phase diagram is investigated in a wide range of atomic interactions and SOC strength within the framework of the cluster dynamical mean-field theory (CDMFT). We show that the interplay between the atomic interactions and SOC results in a rich phase diagram. In the deep Mott insulator regime, the SOC can induce diverse spin ordered phases. Whereas near the metal-insulator transition (MIT), the SOC tends to destroy the conventional antiferromagnetic fluctuations, giving rise to distinctive features of the MIT. Furthermore, the strong fluctuations arising from SOC may destroy the magnetic orders and trigger an order to disorder transition in close proximity of the MIT.},
  language  = {en}
}
@article{KuaiGongDingetal.2018,
  author    = {Kuai, Yue and Gong, Xin and Ding, Liya and Li, Fang and Lei, Lizhen and Gong, Yuqi and Liu, Qingmeng and Tan, Huajiao and Zhang, Xinxia and Liu, Dongyu and Ren, Guoping and Pan, Hongyang and Shi, Yaoyao and Berberich-Siebelt, Friederike and Ma, Zhengrong and Zhou, Ren},
  title     = {Wilms' tumor 1-associating protein plays an aggressive role in diffuse large B-cell lymphoma and forms a complex with BCL6 via Hsp90},
  series = {Cell Communication and Signaling},
  volume    = {16},
  journal   = {Cell Communication and Signaling},
  doi       = {10.1186/s12964-018-0258-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-230168},
  year      = {2018},
  abstract  = {Background Wilms' tumor 1-associating protein (WTAP) is a nuclear protein, which is ubiquitously expressed in many tissues. Furthermore, in various types of malignancies WTAP is overexpressed and plays a role as an oncogene. The function of WTAP in diffuse large B-cell lymphoma (DLBCL), however, remains unclear. Methods Immunohistochemistry was applied to evaluate the levels of WTAP expression in DLBCL tissues and normal lymphoid tissues. Overexpression and knock-down of WTAP in DLBCL cell lines, verified on mRNA and protein level served to analyze cell proliferation and apoptosis in DLBCL cell lines by flow cytometry. Finally, co-immunoprecipitation (Co-IP), IP, and GST-pull down assessed the interaction of WTAP with Heat shock protein 90 (Hsp90) and B-cell lymphoma 6 (BCL6) as well as determined the extend of its ubiquitinylation. Results WTAP protein levels were consistently upregulated in DLBCL tissues. WTAP promoted DLBCL cell proliferation and improved the ability to confront apoptosis, while knockdown of WTAP in DLBCL cell lines allowed a significant higher apoptosis rate after treatment with Etoposide, an anti-tumor drug. The stable expression of WTAP was depended on Hsp90. In line, we demonstrated that WTAP could form a complex with BCL6 via Hsp90 in vivo and in vitro. Conclusion WTAP is highly expressed in DLBCL, promoting growth and anti-apoptosis in DLBCL cell lines. WTAP is a client protein of Hsp90 and can appear in a complex with BCL6 and Hsp90 in DLBCL. Down-regulation of WTAP could improve the chemotherapeutic treatments in DLBCL.},
  language  = {en}
}
@article{GoerlZhangStepanenkoetal.2015,
  author    = {G{\"o}rl, Daniel and Zhang, Xin and Stepanenko, Vladimir and W{\"u}rthner, Frank},
  title     = {Supramolecular block copolymers by kinetically controlled co-self-assembly of planar and core-twisted perylene bisimides},
  series = {Nature Communications},
  volume    = {6},
  journal   = {Nature Communications},
  number    = {7009},
  doi       = {10.1038/ncomms8009},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-148657},
  year      = {2015},
  abstract  = {New synthetic methodologies for the formation of block copolymers have revolutionized polymer science within the last two decades. However, the formation of supramolecular block copolymers composed of alternating sequences of larger block segments has not been realized yet. Here we show by transmission electron microscopy (TEM), 2D NMR and optical spectroscopy that two different perylene bisimide dyes bearing either a flat (A) or a twisted (B) core self-assemble in water into supramolecular block copolymers with an alternating sequence of (A\(_{m}\)BB)\(_{n}\). The highly defined ultralong nanowire structure of these supramolecular copolymers is entirely different from those formed upon self-assembly of the individual counterparts, that is, stiff nanorods (A) and irregular nanoworms (B), respectively. Our studies further reveal that the as-formed supramolecular block copolymer constitutes a kinetic self-assembly product that transforms into thermodynamically more stable self-sorted homopolymers upon heating.},
  language  = {en}
}