Peer-reviewed Artikel
Gene Ther. 2000; 7:1317-1325.
Improved safety through tamoxifen-regulated induction of cytotoxic genes delivered by Ad vectors for cancer gene therapy.
Pützer BM, Stiewe T, Crespo F, Esche H.Cell Death Differ. 2000; 7:177-188.
E1A is sufficient by itself to induce apoptosis independent of p53 and other adenoviral gene products.
Pützer BM, Stiewe T, Parssanedjad K, Rega S, Esche H.Tumor Diag Ther. 2000; 21:1-7.
The Role of Tumor Suppressor Gene Therapy for Anticancer Treatment.
Pützer BM.2000
AbstractCancer Res. 2000; 60:3957-3964.
E1A overcomes the apoptosis block in BCR/ABL-positive leukemia cells and renders cells susceptible to induction of apoptosis by chemotherapeutic agents
Stiewe T, Parssanedjad K, Esche H, Opalka B, Pützer BM.Gene Expression. 1999; 8:1-18.
A multi-protein complex consisting of the cellular coactivator p300, AP-1/ATF as well as NF-kB is responsible for the activation of the mouse major histocompatibility class I (H-2Kb) enhancer A.
Brockmann, Pützer BM, Lipinski KL, Schmücker U, Esche HProc Natl Acad Sci USA. 1997; 94:10889-10894.
Combination therapy with Interleukin-2 and wild-type p53 expressed by adenoviral vectors potentiates tumor regression in a murine model of breast cancer.
Pützer BM, Bramson J, Addison CL, Hitt M, Siegel P, Muller WJ, Graham FL.Proc Natl Acad Sci USA. 1997; 94:10889-10894.
Interleukin-12 and B7-1 costimulatory molecule expressed by an adenovirus vector act synergistically to facilitate tumor regression.
Pützer BM, Hitt M, Muller WJ, Emtage P, Gauldie J, Graham FL. J Virol. 1997; 71:9538-9548.
E1A 12S and 13S of the transformation-defective adenovirus type 12 strain CS-1 inactivate proteins of the RB family, permitting transactivation of the E2F-dependent promoter.
Pützer BM, Rumpf H, Rega S, Brockmann D, Esche H.J Gen Virol. 1997; 78:879-891
A cis-acting element 7 bp upstream of the ESF-1-binding motif is involved in E1A 13S autoregulation of the adenovirus 12 TS2 promoter.
Pützer BM, Gnauck J, Kirch HC, Brockmann D, Esche H.Eur J Biochem. 1997; 246:736-744