@inproceedings{NeumannSchaalMesserschmidtGrenzetal.2012,
  author    = {Neumann-Schaal, M. and Messerschmidt, Katrin and Grenz, N. and Micheel, Burkhard and Heilmann, K.},
  title     = {Use of antibody gene library for the isolation of specific single chain antibodies by ampicillin-antigen conjugates},
  series = {Immunology : an official journal of the British Society for Immunology},
  volume    = {137},
  booktitle = {Immunology : an official journal of the British Society for Immunology},
  number    = {3},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0019-2805},
  pages     = {661 -- 661},
  year      = {2012},
  language  = {en}
}
@article{VanderVenEhlerVakeeletal.2006,
  author    = {VanderVen, Peter F. M. and Ehler, Elisabeth and Vakeel, Padmanabhan and Eulitz, Stefan and Schenk, J{\"o}rg A. and Milting, Hendrik and Micheel, Burkhard and F{\"u}rst, Dieter Oswald},
  title     = {Unusual splicing events result in distinct Xin isoforms that associate differentially with filamin c and Mena/ VASP},
  doi       = {10.1016/j.yexcr.2006.03.015},
  year      = {2006},
  abstract  = {Filamin c is the predominantly expressed filamin isoform in striated muscles. It is localized in myofibrillar Z- discs, where it binds FATZ and myotilin, and in myotendinous junctions and intercalated discs. Here, we identify Xin, the protein encoded by the human gene 'cardiomyopathy associated 1' (CMYA1) as filamin c binding partner at these specialized structures where the ends of myofibrils are attached to the sarcolemma. Xin directly binds the EVH1 domain proteins Mena and VASP. In the adult heart, Xin and Mena/VASP colocalize with filamin c in intercalated discs. In cultured cardiomyocytes, the proteins also localize in the nonstriated part of myofibrils, where sarcomeres are assembled and an extensive reorganization of the actin cytoskeleton occurs. Unusual intraexonic splicing events result in the existence of three Xin isoforms that associate differentially with its ligands. The identification of the complex filamin c-Xin-Mena/VASP provides a first glance on the role of Xin in the molecular mechanisms involved in developmental and adaptive remodeling of the actin cytoskeleton during cardiac morphogenesis and sarcomere assembly. (c) 2006 Elsevier Inc. All rights reserved},
  language  = {en}
}
@article{BierEhrentreichFoersterSchelleretal.1996,
  author    = {Bier, Frank Fabian and Ehrentreich-F{\"o}rster, Eva and Scheller, Frieder W. and Makower, Alexander and Eremenko, A. V. and Wollenberger, Ursula and Bauer, Christian G. and Pfeiffer, Dorothea and Micheel, Burkhard},
  title     = {Ultrasensitive biosensors},
  year      = {1996},
  language  = {en}
}
@article{Micheel1998,
  author    = {Micheel, Burkhard},
  title     = {Tumorantigene und ihre Nutzung f{\"u}r eine Therapie mit Antik{\"o}rpern},
  year      = {1998},
  language  = {de}
}
@article{EngelMicheelHanack2022,
  author    = {Engel, Robert and Micheel, Burkhard and Hanack, Katja},
  title     = {Three-dimensional cell culture approach for in vitro immunization and the production of monoclonal antibodies},
  series = {Biomedical materials : materials for tissue engineering and regenerative medicine},
  volume    = {17},
  journal   = {Biomedical materials : materials for tissue engineering and regenerative medicine},
  number    = {5},
  publisher = {Inst. of Physics},
  address   = {London},
  issn      = {1748-6041},
  doi       = {10.1088/1748-605X/ac7b00},
  pages     = {11},
  year      = {2022},
  abstract  = {The generation of monoclonal antibodies using an in vitro immunization approach is a promising alternative to conventional hybridoma technology. As recently published, the in vitro approach enables an antigen-specific activation of B lymphocytes within 10-12 d followed by immortalization and subsequent selection of hybridomas. This in vitro process can be further improved by using a three-dimensional surrounding to stabilize the complex microenvironment required for a successful immune reaction. In this study, the suitability of Geltrex as a material for the generation of monoclonal antigen-specific antibodies by in vitro immunization was analyzed. We could show that dendritic cells, B cells, and T cells were able to travel through and interact inside of the matrix, leading to the antigen-specific activation of T and B cells. For cell recovery and subsequent hybridoma technique the suitability of dispase and Corning cell recovery solution (CRS) was compared. In our experiments, the use of dispase resulted in a severe alteration of cell surface receptor expression patterns and significantly higher cell death, while we could not detect an adverse effect of Corning CRS. Finally, an easy approach for high-density cell culture was established by printing an alginate ring inside a cell culture vessel. The ring was filled with Geltrex, cells, and medium to ensure a sufficient supply during cultivation. Using this approach, we were able to generate monoclonal hybridomas that produce antigen-specific antibodies against ovalbumin and the SARS-CoV-2 nucleocapsid protein.},
  language  = {en}
}
@article{SchlagOsterzielOezceliketal.2008,
  author    = {Schlag, Peter M. and Osterziel, Karl Joseph and {\"O}zcelik, Cemil and Scherneck, Siegfried and Wenzel, Katrin and Daskalow, Katjana and Herse, Florian and Seitz, Susanne and Zacharias, Ute and Schenk, J{\"o}rg A. and Schulz, Herbert and H{\"u}bner, Norbert and Micheel, Burkhard},
  title     = {The protein phosphatase 1 inhibitor KEPI is down regulated in breast cancer cell lines and tissues and involved in the regulation of the tumour suppressor EGR1 via the MEK-ERK pathway},
  year      = {2008},
  abstract  = {KEPI is a protein kinase C-potentiated inhibitory protein for type 1 Ser/Thr protein phosphatases. We found no or reduced expression of KEPI in breast cancer cell lines, breast tumors and metastases in comparison to normal breast cell lines and tissues, respectively. KEPI protein expression and ubiquitous localization was detected with a newly generated antibody. Ectopic KEPI expression in MCF7 breast cancer cells induced differential expression of 95 genes, including the up-regulation of the tumor suppressors EGR1 (early growth response 1) and PTEN (phosphatase and tensin homolog), which is regulated by EGR1. We further show that the up-regulation of EGR1 in MCF7/KEPI cells is mediated by MEK-ERK signaling. The inhibition of this pathway by the MEK inhibitor UO126 led to a strong decrease in EGR1 expression in MCF7/KEPI cells. These results reveal a novel role for KEPI in the regulation of the tumor suppressor gene EGR1 via activation of the MEK-ERK MAPK pathway.},
  language  = {en}
}
@article{HeilmannGrothBehrsingetal.2005,
  author    = {Heilmann, Katja and Groth, Thomas and Behrsing, Olaf and Wagner, Albrecht and Schossig-Tiedemann, Michael and Lendlein, Andreas and Micheel, Burkhard},
  title     = {The influence of the chemical composition of cell culture material on the growth and antibody production of hybridoma cells},
  year      = {2005},
  abstract  = {The multiplication and antibody production of murine hybridoma cells cultured on five different polymer membranes were tested and compared with conventional tissue culture polystyrene (TCPS). Membranes were prepared from polyacrylonitrile (PAN) and acrylonitrile copolymerized with N-vinylpyrrolidone (NVP20, NVP30), Na-methallylsulfonate (NaMAS) and N-(3-amino-propyl-methacrylamide-hydrochloride) (APMA). Cell number and antibody concentration were quantified as criteria for viability and productivity. Adhesion of hybridoma cells was characterized by vital and scanning electron microscopy. The results suggest that a strong adhesion of cells, observed on APMA and TCPS, increased cell growth but reduced monoclonal antibody production. In contrast membranes with lowered adhesivity such as NVP20 provided favourable conditions for monoclonal antibody production. In addition it was shown that this membrane also possessed a minor fouling as indicated by the low decrease of water flux across the membrane after protein adsorption. It was concluded that NVP20 could be a suitable material for the development of hollow fibre membranes for bioreactors.},
  language  = {en}
}
@misc{Micheel2000,
  author    = {Micheel, Burkhard},
  title     = {Stichworte zu Thema Immunologie},
  year      = {2000},
  language  = {de}
}
@misc{Micheel1999,
  author    = {Micheel, Burkhard},
  title     = {Stichworte zu Thema Immunologie},
  year      = {1999},
  language  = {de}
}
@article{JandrigSeitzHinzmannetal.2004,
  author    = {Jandrig, Burkhard and Seitz, Susanne and Hinzmann, Bernd and Arnold, Wolfgang and Micheel, Burkhard and Koelble, Konrad and Siebert, Reiner and Schwartz, Arnfried and Ruecker, Karin and Schlag, Peter M. and Scherneck, Siegfried and Rosenthal, Andra},
  title     = {ST18 is a breast cancer tumor suppressor gene at human chromosome 8q11.2},
  year      = {2004},
  abstract  = {We have identified a gene, ST18 (suppression of tumorigenicity 18, breast carcinoma, zinc-finger protein), within a frequent imbalanced region of chromosome 8q11 as a breast cancer tumor suppressor gene. The ST18 gene encodes a zinc-finger DNA-binding protein with six fingers of the C2HC type (configuration Cys-X5-Cys-X12-His-X4-Cys) and an SMC domain. ST18 has the potential to act as transcriptional regulator. ST18 is expressed in a number of normal tissues including mammary epithelial cells although the level of expression is quite low. In breast cancer cell lines and the majority of primary breast tumors, ST18 mRNA is significantly downregulated. A 160 bp region within the promoter of the ST18 gene is hypermethylated in about 80\% of the breast cancer samples and in the majority of breast cancer cell lines. The strong correlation between ST18 promoter hypermethylation and loss of ST18 expression in tumor cells suggests that this epigenetic mechanism is responsible for tumor-specific downregulation. We further show that ectopic ST18 expression in MCF-7 breast cancer cells strongly inhibits colony formation in soft agar and the formation of tumors in a xenograft mouse model},
  language  = {en}
}