@article{SinghSinghDanietal.2005,
  author    = {Singh, Jasbir and Singh, S. and Dani, H. M. and Sharma, Reeta and Steinberg, Pablo},
  title     = {Interactions of aflatoxin B-1 with SRP components can disrupt protein targeting},
  issn      = {0263-6484},
  year      = {2005},
  abstract  = {Spectrofluorimetric studies have revealed that aflatoxin B-1 (AFB(1)) interacts with signal recognition particle (SRP), which acts as an escort for polyribosomes with signal peptides to be transported and bound to the cytoplasmic face of the endoplasmic reticulum (ER). We further report that the binding of AFB(1) to SRP is selective as it only binds to two (SRP9 and 14) out of its three constituent polypeptides studied. Binding of AFB(1) to proteins is known to alter their conformations. Interactions of AFB(1) with SRP polypeptides may generate structural and functional alterations in this particle and hinder secretory protein synthesis. Copyright (C) 2004 John Wiley Sons, Ltd},
  language  = {en}
}
@article{ThierbachSchulzIskenetal.2005,
  author    = {Thierbach, Ren{\`e} and Schulz, Tim Julius and Isken, Frank and Voigt, Aanja and Mietzner, Brun and Drewes, Gunnar and von Kleist-Retzow, J{\"u}rgen-Christoph and Wiesner, Rudolf J. and Magnuson, Mark A. and Puccio, Helene and Pfeiffer, Andreas F. H. and Steinberg, Pablo and Ristow, Michael},
  title     = {Targeted disruption of hepatic frataxin expression causes impaired mitochondrial function, decreased life span and tumor growth in mice},
  year      = {2005},
  abstract  = {We have disrupted expression of the mitochondrial Friedreich ataxia protein frataxin specifically in murine hepatocytes to generate mice with impaired mitochondrial function and decreased oxidative phosphorylation. These animals have a reduced life span and develop multiple hepatic tumors. Livers also show increased oxidative stress, impaired respiration and reduced ATP levels paralleled by reduced activity of iron-sulfur cluster (Fe/S) containing proteins (ISP), which all leads to increased hepatocyte turnover by promoting both apoptosis and proliferation. Accordingly, phosphorylation of the stress-inducible p38 MAP kinase was found to be specifically impaired following disruption of frataxin. Taken together, these findings indicate that frataxin may act as a mitochondrial tumor suppressor protein in mammals},
  language  = {en}
}
@article{FuchsTeubnerSteinberg2004,
  author    = {Fuchs, J. and Teubner, Wera and Steinberg, Pablo},
  title     = {The resistance of intestinal epithelial cells towards the transforming activity of 2-hydroxyamino-1-methyl-6- phenylimidazo[4,5-B]pyridine is accompanied by glutathione S-transferase induction},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{TeubnerLangheinrichSeideletal.2004,
  author    = {Teubner, Wera and Langheinrich, C. and Seidel, Albrecht and Steinberg, Pablo},
  title     = {Inhibition of p53 transactivation activity does not promote mutagen-induced transformation of IEC-18},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{KuehnelSteinbergScholtka2004,
  author    = {K{\"u}hnel, Dana and Steinberg, Pablo and Scholtka, Bettina},
  title     = {A human-relevant dose of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PHIP) can induce precancerous lesions in rat intestine after 6 months of exposure},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{ThierbachSchulzVoigtetal.2004,
  author    = {Thierbach, Rene and Schulz, Tim Julius and Voigt, Aanja and Drewes, Gunnar and Isken, F. and Pfeiffer, Andreas F. H. and Ristow, Michael and Steinberg, Pablo},
  title     = {Targeted disruption of frataxin in hepatocytes causes spontaneous neoplasia accompanied by increased ROS formation},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{HerbstFuchsTeubneretal.2004,
  author    = {Herbst, Uta and Fuchs, Iris Judith and Teubner, Wera and Seidel, Albrecht and Frank, Heinz and Steinberg, Pablo},
  title     = {Malignant transformation of human colon epithelial cells by polycyclic aromatic hydrocarbons and heterocyclic aromatic amines},
  issn      = {0028-1298},
  year      = {2004},
  language  = {en}
}
@article{StarkPoratVolohonskyetal.2003,
  author    = {Stark, Avishay abraham and Porat, Noga and Volohonsky, Gloria and Konlosh, A. and Bluvshtein, Evgenia and Tubi, C. and Steinberg, Pablo},
  title     = {The role of gamma-glutamyl transpeptidase in the biosynthesis of glutathione},
  year      = {2003},
  language  = {en}
}
@article{OkanoShiotaMatsumotoetal.2003,
  author    = {Okano, J. and Shiota, G. and Matsumoto, K. and Yasui, S. and Kurimasa, A. and Hisatome, I. and Steinberg, Pablo and Murawaki, Y.},
  title     = {Hepatocyte growth factor exerts a proliferative effect on oval cells through the PI3K/AKT signaling pathway},
  year      = {2003},
  language  = {en}
}
@article{BartschZschalerHaseloffetal.2003,
  author    = {Bartsch, Ingrid and Zschaler, Ingrid and Haseloff, Monika and Steinberg, Pablo},
  title     = {Establishment of a long-term culture system for rat colon epithelial cells},
  issn      = {1071-2690},
  doi       = {10.1290/0404035.1},
  year      = {2003},
  abstract  = {The aim of this study was to establish a long-term culture. system for rat colon epithelia isolaled by incubating a 4-cm-long rat colon segment cut longitudinally with all ethylenediaminetetraacetic acid [disodium salt]- containing buffer, taken up in conditioned medium from the normal rat kidney fibroblast cell line NRK (i.e., the supernatant Of pure NRK cultures), directly plated on mitomycin C-treated NRK cells and subcultured with conditioned medium from NRK cells. Cells started to migrate out of the crypts shortly after plating them on NRK feeder layers. Some of the crypts fell apart during the isolation procedure. whereas the vast majority of them did it within I to 2 Ill after plating. The cells proliferated extremely slowly but continuously over a period of 4 mo and were epithelial because they expressed cytokeratin 19 and were stained by crystal violet at pH 2.8. In conclusion, the experimental system described ill this study allows to maintain rat colon epithelial cells for up to 4 mo in culture and can be used to Study the effects of a variety of tumor-modulating factors on growth and gene expression of normal colon epithelial cells in vitro},
  language  = {en}
}