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Gene Review

babA  -  hypothetical protein

Helicobacter pylori J99

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Disease relevance of babA

  • Several putative H. pylori virulence genes, i.e., cag, vacA, babA, or dupA, as well as host-related genetic factors like IL-1beta and TNFalpha-gene polymorphism, have been proposed as risk factors for duodenal ulcer [1].
  • Helicobacter pylori babA encodes an outer membrane protein that binds to fucosylated Lewis b blood group antigen [2].
  • None of cagA, iceA1, babA, and vacA s1/m1 were associated with peptic ulcer [3].
  • The genetic status of cagA, vacA subtype, iceA1, and babA, and the relationship to gastroduodenal diseases were assessed in Helicobacter pylori isolates in Korea. Seventy-six strains of H. pylori were isolated from the antrum and the corpus of 41 adult patients (22 with peptic ulcer and 19 with gastritis) [3].

High impact information on babA

  • Absence of babA and duplication of babB was also seen in H. pylori isolates derived from human clinical samples, suggesting that this gene conversion event is not unique to experimentally infected rhesus monkeys [4].
  • In either case, strains lacking babA did not adhere to Lewis B, which is expressed on macaque gastric epithelium [4].
  • PCR and DNA sequence analysis showed extensive genotypic diversity in babA and babB across different strains, as well as within a strain colonizing an individual patient [5].
  • There was a significant association between the presence of babA and the presence of cagA (P = 0.0001) [2].
  • Expression of a BabA protein and the Lewis b-binding phenotype were not dependent on the chromosomal locus of babA [2].

Biological context of babA

  • Therefore, the aim of this study was to investigate the status of H. pylori strains regarding the babA and iceA alleles, as well as the cagA genotype, to reveal any association between these genotypes and clinical outcomes in Brazilian patients [6].
  • Although babA and babB 5' and midregion segment phylogenies show strong interstrain similarity, the 3' segments show strong intrastrain similarity, indicative of concerted evolution [7].

Other interactions of babA

  • We hypothesize that diverse profiles of babA and babB reflect selective pressures for adhesion, which may differ across different hosts and within an individual over time [5].

Analytical, diagnostic and therapeutic context of babA

  • Microarray analysis showed that H. pylori recovered from challenged macaques had deleted babA, a member of a large family of paralogous outer membrane proteins (OMPs) that mediates attachment of H. pylori to the Lewis B blood group antigen on gastric epithelium [4].


  1. Helicobacter pylori and Non-Malignant Diseases. Matysiak-Budnik, T., Laszewicz, W., Lamarque, D., Chaussade, S. Helicobacter (2006) [Pubmed]
  2. Multiple chromosomal loci for the babA gene in Helicobacter pylori. Hennig, E.E., Allen, J.M., Cover, T.L. Infect. Immun. (2006) [Pubmed]
  3. Genotyping CagA, VacA subtype, IceA1, and BabA of Helicobacter pylori isolates from Korean patients, and their association with gastroduodenal diseases. Kim, S.Y., Woo, C.W., Lee, Y.M., Son, B.R., Kim, J.W., Chae, H.B., Youn, S.J., Park, S.M. J. Korean Med. Sci. (2001) [Pubmed]
  4. Modification of Helicobacter pylori outer membrane protein expression during experimental infection of rhesus macaques. Solnick, J.V., Hansen, L.M., Salama, N.R., Boonjakuakul, J.K., Syvanen, M. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  5. Genotypic profile of the outer membrane proteins BabA and BabB in clinical isolates of Helicobacter pylori. Colbeck, J.C., Hansen, L.M., Fong, J.M., Solnick, J.V. Infect. Immun. (2006) [Pubmed]
  6. Prevalence of Helicobacter pylori cagA, iceA and babA2 alleles in Brazilian patients with upper gastrointestinal diseases. Gatti, L.L., Módena, J.L., Payão, S.L., Smith, M.d.e. .A., Fukuhara, Y., Módena, J.L., de Oliveira, R.B., Brocchi, M. Acta Trop. (2006) [Pubmed]
  7. Concerted evolution between duplicated genetic elements in Helicobacter pylori. Pride, D.T., Blaser, M.J. J. Mol. Biol. (2002) [Pubmed]
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