Hubert J. Stoppler, PhD

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
stoppler_hubert

Manager, Tissue Core Facility, UCSF Helen Diller Family Comprehensive Cancer Center

hubert.stoppler@ucsf.edu

Phone: (415) 476-0435 (voice)
Box 0875, UCSF
San Francisco, CA 94143-0875


Education

University of Giessen, Germany, 1981-1984, Biology
University of Heidelberg, Germany, M.S., 1984-1988, Molecular Biology
University of Heidelberg, Germany, Ph.D., 1988-1992, Molecular Biology / Virology
Georgetown University School of Medicine, postdoc, 1992-1994, Tumor Biology

Professional Experience

  • 1994-1997
    Research Associate, Department of Pathology, Georgetown University Medical Center
  • 1997-2003
    Faculty position (Group Leader), Institute for Pharmacology and Toxicology, Philipps-University of Marburg, Germany
  • 2003-2007
    Associate Professor at the Medical College of Georgia, joint appointment in OB/GYN and Institute of Molecular Medicine and Genetics
  • 2007-present
    Tissue Core Manager at the Helen Diller Family Comprehensive Cancer Center, University of California San Francisco

Honors & Awards

  • 1992-1994
    Member of the "Scientist Exchange Program", Office of International Affairs, National Cancer Institute
  • April 2000
    Habilitation (award of Professorship qualification) School of Medicine, University of Marburg, Germany

Selected Publications

  • Rittner K, Stoppler H, Pawlita M, and Sczakiel G. Versatile eukaryotic vectors for strong and constitutive transient and stable gene expression. Methods in Molecular and Cellular Biology 1991 (2) 176-181.
  • Steuer B, Stoppler H, Breuer B, and Alonso A. Transcription of BPV-1 genes in transfected F9 cells. Oncogene 1992 (7) 1875-1878.
  • Steinmann KE, Pei XF, Stoppler H, Schlegel R, and Schlegel R. Elevated expression and activity of mitotic regulatory proteins in human papillomavirus-immortalized human keratinocytes. Oncogene 1994 (9) 387-394.
  • Stoppler H, Conrad Stoppler M, Adduci A, Koval D, and Schlegel R. The serine protease inhibitors TLCK and TPCK react with the Rb-binding core of the HPV-18 E7 protein and abolish its Rb-binding capability. Virology, 1996 (217), 542-553.
  • Stoppler H, Kirchhoff T, Alonso A, and Gissmann L. Influence of the Human Papillomavirus type 16 (HPV-16) gene expression on the in vitro differentiation of the Human Teratocarcinoma cell line 2102 Ep. Molecular Carcinogenesis, 1996 (16), 109-114.
  • Conrad Stoppler M, Ching K, Stoppler H, Clancy K, Schlegel R, and Icenogle J. Natural variants of the Human Papillomavirus type 16 (HPV-16) E6 protein differ in their ability to alter keratinocyte differentiation and to induce p53 degradation. Journal of Virology, 1996 (70), 6987-6993.
  • Stoppler H, Koval D, and Schlegel R. The serine protease inhibitors TLCK and TPCK inhibit the in vitro immortalization of primary human keratinocytes by HPV-18 DNA. Oncogene, 1996 (13), 1545-1548.
  • Araujo JC, Doniger J, Stoppler H, Sadaie RM, and Rosenthal LJ. Cell lines containing and expressing the human herpesvirus 6A ts gene are protected from both H-ras and BPV-1 transformation. Oncogene, 1997 (14), 937-943.
  • Stoppler H, Hartmann DP, Sherman L, and Schlegel R. The human papillomavirus type 16 E6 and E7 oncoproteins dissociate cellular telomerase activity from the maintenance of telomere length. Journal of Biological Chemistry, 1997 (20), 13332-13337.
  • Stoppler H, Conrad Stoppler M, Johnson E, Simbulan-Rosenthal CM, Smulson ME, Iyer S, Rosenthal D, and Schlegel R. The E7 protein of human papillomavirus type 16 sensitizes primary human keratinocytes to apoptosis. Oncogene, 1998 (17), 1207-1214.
  • Stoppler H, Conrad Stoppler M, Kisiela M, Holzbach A, Moll I, Houdek P, and Moll R. Telomerase activity of Merkel cell carcinomas and Merkel cell carcinoma-derived cell cultures. Archives of Dermatological Research, 2001 (293), 397-406.
  • Stoppler H, Malercyzk C, Block K, Aigner A, and Czubayko F. The human papillomavirus (HPV) 16 E6 oncoprotein leads to an increase in gene expression of the angiogenic switch molecule FGF-BP in non-immortalized human keratinocytes. Oncogene, 2001 (20) 7430-7436.
  • Moller A, Malerczyk C, Volker U, Stoppler H, and Maser E. Monitoring daunorubicin-induced alterations in protein expression in pancreas carcinoma cells by two-dimensional gel electrophoresis. Proteomics, 2002 (2) 697-705.
  • Kehmeier E, Ruhl H, Voland B, Conrad Stoppler M, Androphy E, and Stoppler H. Cellular steady state levels of the "high risk" but not the "low risk" human papillomavirus (HPV) E6 proteins are controlled by proteasome-dependent degradation and independent of their p53 and E6AP binding capabilities. Virology, 2002 (299) 72-87.
  • Alfke H, Stoppler H, Nocken F, Heverhagen J, Kleb B, Czubayko F, and Klose KJ. In vitro MR Imaging of regulated gene expression. Radiology, 2003 (228) 488-492.
  • Greengauz-Roberts O, Stöppler H, Nomura S, Yamaguchi H, Goldenring JR, Podolsky RH, Lee JR, and Dynan WS. Saturation labeling with cysteine-reactive cyanine fluorescent dyes provides increased sensitivity for protein expression profiling of laser microdissected clinical specimens. Proteomics, 2005 (5) 1746-1757
  • Hsu. S, Dickinson DP, Qin H, Lapp C, Lapp D, Borke J, Walsh DS, Bollag WB, Stöppler H, Yamamoto T, Osaki T, Schuster G. Inhibition of Autoantigen Expression by (-)-Epigallocatechin-3-gallate (the Major Constituent of Green Tea) in Normal Human Cells. The Journal of Pharamcology and Experimental Therapeutics, 2005 (315) 805-811
  • Hsu S, Dickinson DP, Qin H, Borke J, Ogbureke K, Winger J, Camba A, Bollag WB, Stoppler H, Sharawy M, and Schuster G. Green Tea Polyphenols Reduce Autoimmune Symptoms in a Murine Model for Humans Sjogren's Syndrome and Protect Human Salivary Acinar Cells from TNF--Induced Cytotoxicity via p38 MAPK Activation. Autoimmunity, 2007 (40) 138-147
  • Stephen Hsu, Haiyan Qin, Douglas Dickinson, Ding Xie, Wendy B. Bollag, Hubert Stoppler, Henna Pearl, Anna Vu, Margaretta Watkins, Meredith Koehler, and George Schuster. Expression of caspase 14 reduces tumorigenicity of skin cancer cells. In Vivo, 2007 (21) 279-283