Category:Team A-Squared

toxin molecule that attaches to the surface and gets inserted into the cell where it accumulates and effects the normal trafficking of the cells resulting in the death of that cell

Fig. 3 Shows were NikR is located and it regulates Ni.

Figure 1 shows the genes used to identify RND efflux pumps in H. hepaticus which are highly homologous in other bacteria. Table 3 shows the minimal inhibitory concentration (MIC) of various compounds with wild-type and mutant HefA. The mutant HefA resulted in a significant drop in MIC for amoxicillin and bile acids. These data support that HefA is a multi-drug efflux pump which transports toxic compounds outside of the cell.

Figure 4 demonstrates the presence of SabA and other proteins as major phospholipid components in H. pylori vesicles. Figure 6 demonstrates the presence of receptor-binding adhesins like SabA on the surface of H. pylori vesicles. Figure 7 shows the SabA adhesion–receptor specificity operating in the vesicle–tissue interaction.

Fig. 7 shows southern hybridization of peb1A conversion; Fig. 8 shows PCR of peb1A fragment

Figure 8 shows PCR of peb1A fragment of both campylobacter strains. It displays the importance of the conservation of the peb1A gene in C. jejuni.

Figure 4 shows the southern blot of the chromosomal DNA of a cytotoxic H. pylori strain and a non-cytotoxic strain of H. pylori.

Table 3 shows that the minimal inhibitory concentration (MIC) of amoxicillin is higher in bacteria that contain HefA than the mutant bacteria without HefA. This suggests that HefA contributes to amoxicillin resistance.

Figure 3 shows DNA catalysis which can be recognized in known members of mammalian deoxyribonuclease 1 (DNase 1).