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MMI Faculty

Markus Stein, PhD

Markus Stein, PhD
Dept. of Medical Microbiology & Immunology
University of Alberta
Faculty of Medicine & Dentistry
1-17 Medical Sciences Building
T6G 2H7 Edmonton, AB

Ph : (780) 492-5495
Fx : (780) 492-7521




  • Assistant Professor, Dept. of Medical Microbiology & Immunology
  • AHFMR Scholar
  • Member of the Canadian Association of Gastroenterology



My major research interest is to understand the complex interactions between the human pathogen Helicobacter pylori and the eukaryotic cells.

Helicobacter pylori is associated with the development of several gastric diseases including peptic ulcer disease (PUD), MALT-lymphoma and adenocarcinoma. Strains with an increased pathogenicity contain additional virulence factors encoded on the chromosome in a region that was designated as the cag pathogenicity island. Encoded in cag are a type IV secretion system (TFSS), the CagA virulence factor and proteins with unknown function.

We recently demonstrated that CagA is an effector molecule that is translocated into the host cell via the TFSS. CagA is then phosphorylated on tyrosine residues by members of the Src-kinase family and induces signaling pathways that lead to dramatic morphological changes of the host cell. This effect depends on the association of CagA with proteins that are crucial components of oncogenic pathways (Src-kinases, Shp-2 phosphatase).

My laboratory investigates:

  1. the molecular signals that allow recognition and translocation of CagA through the TFSS,
  2. the interactions of CagA with host cell signaling complexes following translocation, and
  3. the identification of novel type IV effectors.

Our research will provide new knowledge about the function of TFSS, broaden our understanding of the molecular basis of gastric diseases triggered byH. pylori, and may result in the identification of novel targets for drug development.

H. pylori host signaling pathways

Picture: host signaling pathways induced by Helicobacter pylori



  • Hugo Diaz (Postdoctoral Fellow)




Selected Publications:

  1. DeVinney, R., M. Stein, D.J. Reinscheid, A. Abe, S. Ruschkowski, and B.B. Finlay. Enterohemorrhagic Escherichia coli O157:H7 produces Tir, which is translocated to the host cell membrane but is not Tyrosine phosphorylated. Infect Immun, 67: 2389-98 1999
  2. Stein, M., R. Rappuoli, and A. Covacci. Tyrosine phosphorylation of the Helicobacter pylori CagA antigen after cag-driven host cell translocation. PNAS, 97: 1263-1268 2000
  3. Censini, S., M. Stein, and A. Covacci. 2001. Cellular responses induced after contact with Helicobacter pylori. Curr Opin Microbiol, 4: 41-46 (review) 2001
  4. Stein, M., R. Rappuoli, and A. Covacci. 2001. The cag pathogenicity island. Helicobacter pylori. Physiology and Genetics, ASM Press, Washington, DC (Book Chapter) 2001
  5. Stein, M., F. Bagnoli, Halenbeck, R., Rappuoli, R., Fantl, W., and A. Covacci. 2002. c-Src / Lyn kinases activate Helicobacter pylori CagA through tyrosine-phosphorylation of the EPIYA motifs. Molecular Microbiology, 43: 971-980 2002

U.S. Patents:

6,355,254 USA. Pathogenic Escherichia coli associated protein EspA. Finlay; B. Brett; Kenny; Brendan; Stein; Markus; Donnenberg; Michael S.; Lai; Li-Ching. Issue Date: March 12, 2002