@article{HofmannSandigJenningsetal.1995,
  author    = {Hofmann, Ch. and Sandig, V. and Jennings, G. and Rudolph, Michael and Schlag, Peter M. and Strauss, M.},
  title     = {Efficient gene transfer into human hepatocytes by baculovirus vectors},
  year      = {1995},
  language  = {en}
}
@article{HofmannSandigKirillovaetal.1995,
  author    = {Hofmann, Ch. and Sandig, V. and Kirillova, I. and Jennings, G. and Rudolph, Michael and Schlag, Peter M. and Strauss, M.},
  title     = {Hepatocyte- specific binding of L/S-HBV protein particles expressed in insect cells},
  year      = {1995},
  language  = {en}
}
@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}
}
@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}
}