Catalog Number: 21231222
Size: 100 ug
Format: Dry Powder
Reactivity: Immune assay with AmeriDx® H. pylori antibodies: mouse anti H. pylori antibody (Item No ADX7031CADA), mouse anti-CagA antibody B21231237 and B21231238.
QC Testing: Concentration Measurement, SDS-PAGE Analysis
Formulation and Purity
Recombinant protein (2d domain, 596D-1150T of protein accession no AAF17598.1, including 5 EPIYA motifs) over-expressed in E coli strain BL21, and affinity purification from cell pellet by Ni-NTA resin, and dialysis against 1x PBS. The protein is > 97% pure, as determined by SDS-PAGE. The concentration is measured by Nanodrop.
Storage Buffer: In PBS before lyophilized
Preparation and Storage
Upon received, save at freezer immediately if not used. After initial reconstitution with DI water (50-100uL), aliquot if necessary, and save the product at -80°C for future use.
Cytotoxin associated gene A (CagA) gene is one of 31 putative genes in cag Pathogenicity Island (PAI) that is a 40-kb segment being incorporated into H. pylori genome by horizontal transfer, and cagA gene only exists in one subgroup of H. pylori . CagA can translocate from H. pylori into H. pylori-attached gastric epithelial cells via the bacterial type IV secretion system, and manipulate many host cellular functions, including cytoskeletal function, cell-to-cell adhesion, and intracellular signal transduction  . These myriad activities and interactions promote host cells ulceration and malignancy. CagA is also a highly antigenic protein that is associated with a prominent inflammatory response by eliciting interleukin-8 production .
The purified protein is part of full length CagA protein (about 1248 aa), as shown in Figure 1, the 2d domain is at the C-terminal of CagA protein, harboring two exotoxin regions and five EPIYA motifs.
Figure 1. Recombiant CagA 2d domain position on CagA protein sequence (a) and structure (b)
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Please refer to for technical protocols.
1. Hatakeyama M, Higashi H. Helicobacter pylori CagA: a new paradigm for bacterial carcinogenesis. Cancer Sci. 2005;96(12):835-43. Epub 2005/12/22. doi: 10.1111/j.1349-7006.2005.00130.x. PubMed PMID: 16367902.
2. Tegtmeyer N, Ghete TD, Schmitt V, Remmerbach T, Cortes MCC, Bondoc EM, et al. Type IV secretion of Helicobacter pylori CagA into oral epithelial cells is prevented by the absence of CEACAM receptor expression. Gut Pathog. 2020;12:25. Epub 2020/05/22. doi: 10.1186/s13099-020-00363-8. PubMed PMID: 32435278; PubMed Central PMCID: PMCPMC7222478.
3. Varga MG, Butt J, Blot WJ, Le Marchand L, Haiman CA, Chen Y, et al. Racial Differences in Helicobacter pylori CagA Sero-prevalence in a Consortium of Adult Cohorts in the United States. Cancer Epidemiol Biomarkers Prev. 2020. Epub 2020/08/29. doi: 10.1158/1055-9965.EPI-20-0525. PubMed PMID: 32856604.
4. Yamaoka Y. Mechanisms of disease: Helicobacter pylori virulence factors. Nature reviews Gastroenterology & hepatology. 2010;7(11):629-41. Epub 2010/10/13. doi: 10.1038/nrgastro.2010.154. PubMed PMID: 20938460; PubMed Central PMCID: PMCPMC3137895.
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