Helicobacter pylori SabA Adhesin in Persistent Infection and Chronic Inflammation

By J. Mahdavi, B. Sondén, M. Hurtig, Farzad O. Olfat, Lina Forsberg, N. Roche, Jonas Ångström, T. Larsson, S. Teneberg, K. Karlsson and 13 more. Science, 2002

947 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/57759668a62015ec9e309f480895ce3a0eacd4f0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. B. Goodman
2. R. Peek
3. Keith T. Wilson
4. E. Kuipers
5. Lydia E. Wroblewski
6. H. Gardner
7. A. V. van Vliet
8. J. G. Kusters

In Molecular Biology

1. Ian R. Henderson
2. B. Goodman
3. H. Gardner

In Surgery

1. B. Goodman
2. R. Peek
3. Keith T. Wilson
4. E. Kuipers
5. Lydia E. Wroblewski
6. H. Gardner
7. A. V. van Vliet
8. J. G. Kusters

Citations in the corpus

• Pathogenesis of Helicobacter pylori Infection (2006, background): “SabA mediates binding to sialic acidcontaining glycoconjugates (387, 529).”
• iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “pylori to persist chronically in its host (Mahdavi et al., 2002).”
• Mucin dynamics and enteric pathogens (2011, background): “pylori can express two main adhesins for mucin carbohydrates, sialic acid-binding adhesin (SabA) and blood group antigen-binding adhesin (BabA), which vary in their expression levels in infected human populations and affect pathogenicit”
• The microbiome and cancer (2018, background): “pylori is able to drive through the thick gastric mucous layer via flagella and adhere to gastric epithelial cells through the presence of multiple adhesins, including SabA and BabA [59,60].”
• Helicobacter pylori: gastric cancer and beyond (2010, background): “pylori adhesin that binds the sialyl-Lewis x ( Le x ; also known as FUT4) antigen, which is an established tumour antigen and a marker of gastric dysplasia that is upregulated by chronic gastric inflammatio”
• Type V Protein Secretion Pathway: the Autotransporter Story (2004, background): “pylori-infected patient with gastritis (308).”
• Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk (2010, background): “pylori modulates host cell glycosylation patterns to enhance attachment and colonization (187).”
• Bacterial adhesion and entry into host cells. (2006, neutral): “…of other Lewis antigens normally expressed at low levels such as sialylated sLe x and sLe a , and H. pylori recognizes these molecules via the sialic acid binding protein (SabA) (Mahdavi et al., 2002), suggesting that H. pylori infection favors the expression of its own receptors in target tissues.”