Proc Natl Acad Sci USA 2005, 102:8327–8332.PubMedCrossRef 76. Goding J: Monoclonal antibodies: principles

and practice : production and application of monoclonal antibodies in cell biology, biochemistry and immunology. 3rd edition. Academic Press, London; 1996. 77. Sturgill-Koszycki S, Schlesinger PH, Chakraborty P, Haddix PL, Collins HL, Fok AK, Allen RD, Gluck SL, Heuser J, Russell DG: Lack of acidification in Mycobacterium phagosomes produced by exclusion OSI-906 cost of the vesicular proton-ATPase. Science 1994, 263:678–681.PubMedCrossRef 78. Domingue GJ, Woody HB: Bacterial persistence and expression of disease. Clin Microbiol Rev 1997, 10:320–344.PubMed 79. Hines ME, Styer EL: Preliminary characterization of chemically generated Mycobacterium avium subsp. paratuberculosis cell wall deficient forms

(spheroplasts). Vet Microbiol 2003, 95:247–258.PubMedCrossRef 80. Sechi LA, Ahmed N, Felis GE, Duprè I, Cannas S, Fadda G, Bua A, Zanetti S: Immunogenicity and cytoadherence of recombinant heparin binding haemagglutinin (HBHA) of Mycobacterium avium subsp. paratuberculosis: functional promiscuity or a role in virulence? Vaccine 2006, 24:236–243.PubMedCrossRef 81. Rahman A, Srivastava Selleckchem Nirogacestat SS, Sneh A, Ahmed N, Krishnasastry MV: Molecular characterization of tlyA gene product, Rv1694 of Mycobacterium tuberculosis: a non-conventional hemolysin and a ribosomal RNA methyl transferase. BMC Biochem 2010, 11:35.PubMedCrossRef Competing interests The study does not present any conflict of interest for the authors. Authors’ contributions Conceived and designed the experiments: AC, VR. Performed the experiments: AC, VR. Analyzed the data: AC, VR. Contributed reagents/materials/analysis tools: AC, VR. Contributed strains/ Instruments tools: LAS, SZ . Wrote the paper: AC, VR. All authors read and approved the final manuscript.”
“Background Helicobacter pylori infection increases the risk of peptic ulcers and gastric adenocarcinoma of

the human stomach [1–3]. H. pylori adherence to the gastric epithelium and deliver effectors to induce inflammation [4, 5]. One of the best-studied adhesins is the blood group antigen binding adhesin (BabA), which binds Lewis b (Leb) and related ABO antigens [6, 7]. Putative adhesin, BabB, is encoded by babB, which shares Etofibrate nearly identical N- and C-terminal sequences with babA[7, 8]. The reversed chromosomal www.selleckchem.com/products/oligomycin-a.html locations of babA and babB between strain J99 and 26695 prove the recombination events between these two genes [9, 10]. The two genes also show both geographic and allelic variation [11]. Moreover, the duplication of babA or babB gene is mediated by gene conversion between the different chromosomal loci [12–14]. Bäckström et al. [14] demonstrated that the silent babA gene of a Leb-nonbinding strain can be activated by recombination into the babB gene.