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Prediction of Host-Pathogen Interactions for Helicobacter pylori by Interface Mimicry and Implications to Gastric Cancer

  1. Author:
    Guven-Maiorov, Emine
    Tsai, Chung-Jung
    Ma, Buyong
    Nussinov, Ruth

  2. Author Address

    Cancer and Inflammation Program, Leidos Biomedical Research, Inc. Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: emine.guven-maiorov@nih.gov., Cancer and Inflammation Program, Leidos Biomedical Research, Inc. Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: tsaic@mail.nih.gov., Cancer and Inflammation Program, Leidos Biomedical Research, Inc. Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: mabuyong@mail.nih.gov., Cancer and Inflammation Program, Leidos Biomedical Research, Inc. Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA; Sackler Inst. of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. Electronic address: NussinoR@mail.nih.gov.,
    1. Year: 2017
    2. Date: Dec 8
    3. Epub Date: 2017 10 26
  2. Journal: Journal of molecular biology
    1. 429
    2. 24
    3. Pages: 3925-3941
  4. Type of Article: Article
  5. ISSN: 0022-2836
  1. Abstract:

    There is a strong correlation between some pathogens and certain cancer types. One example is Helicobacter pylori and gastric cancer. Exactly how they contribute to host tumorigenesis is however a mystery. Pathogens often interact with the host through proteins. To subvert defense, they may mimic host proteins at the sequence, structure, motif or interface levels. Interface similarity permits pathogen proteins to compete with those of the host for a target protein, and thereby alter the host signaling. Detection of host-pathogen interactions (HPIs) and mapping the re-wired superorganism HPI network - with structural details - can provide unprecedented clues to the underlying mechanisms and help therapeutics. Here, we describe the first computational approach exploiting solely interface mimicry to model potential HPIs. Interface mimicry can identify more HPIs than sequence or complete structural similarity since it appears more common than the other mimicry types. We illustrate the usefulness of this concept by modeling HPIs of H. pylori to understand how they modulate host immunity, persist lifelong, and contribute to tumorigenesis. H. pylori proteins interfere with multiple host pathways as they target several host hub proteins. Our results help illuminate the structural basis of resistance to apoptosis, immune evasion, and loss of cell junctions seen in H. pylori-infected host cells. Copyright © 2017. Published by Elsevier Ltd.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.jmb.2017.10.023
  3. PMID: 29106933
  4. View record in Web of Science®
  5. WOS: 000418979000011
  6. PII : S0022-2836(17)30505-3

Library Notes

  1. Fiscal Year: FY2017-2018
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