Anti-Helicobacter Pylori Cag Antigen, IgG Fraction, Monoclonal
100 µg
$425.00
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Anti-Helicobacter Pylori Cag Antigen, IgG Fraction, Monoclonal
Catalog no.
HPM-5001-5
$425.00
IgG fraction from a mouse monoclonal antibody obtained by immunization of highly purified H. pylori Cag antigen (Clone 8C6/F13).It recognizes the Cag protein in a H. pylori extract.
- Storage: Store at -20°C.
- Stability: At least 1 year at -20°C.
- Biological activity: Reacts in ELISA and Western blot (1:10,000 - 1:15,000 dilution).
- Formulation: Solution at 1.0 mg/mL in PBS(pH 7.4)
Publications using Austral Biologicals HPM-5001-5
The following scientific publications report use of Austral Biologicals HPM-5001-5:
- Helicobacter pylori Exploit Short-Chain Fatty Acids-Induced CAPZA1 Overexpression to Emerge CD44v9-Positive Stemness. Tsugawa et al., Gastro Hep Adv 5(3):100860 (2026).
- NF-kB-dependent activation of STAT3 by H. pylori is suppressed by TFF1. Soutto et al., Cancer Cell Int 21(1):444 (2021).
- TIFA has dual functions in Helicobacter pylori-induced classical and alternative NF-κB pathways. Maubach et al., EMBO Rep 22(9):e52878 (2021).
- Cholesteryl α-D-glucoside 6-acyltransferase enhances the adhesion of Helicobacter pylori to gastric epithelium. Jan et al., Commun Biol 3(1):120 (2020).
- CagA Effector Protein in Helicobacter pylori -Infected Human Gastric Epithelium in Vivo: From Bacterial Core and Adhesion/Injection Clusters to Host Cell Proteasome-Rich Cytosol. Necchi et al., Toxins (Basel) 11(11):E618 (2019).
- CAPZA1 determines the risk of gastric carcinogenesis by inhibiting Helicobacter pylori CagA-degraded autophagy. Tsugawa et al., Autophagy 15(2):242-258 (2019).
- Unusual Manifestation of Live Staphylococcus saprophyticus, Corynebacterium urinapleomorphum , and Helicobacter pylori in the Gallbladder with Cholecystitis. Backert et al., Int J Mol Sci 19(7):E1826 (2018).
- Pathogen-induced ubiquitin-editing enzyme A20 bifunctionally shuts off NF-κB and caspase-8-dependent apoptotic cell death. Lim et al., Cell Death Differ 24(9):1621-1631 (2017).
- Metabolic labelling of cholesteryl glucosides in Helicobacter pylori reveals how the uptake of human lipids enhances bacterial virulence. Jan et al., Chem Sci 7(9):6208-6216 (2016).
- A specific A/T polymorphism in Western tyrosine phosphorylation B-motifs regulates Helicobacter pylori CagA epithelial cell interactions. Zhang et al., PLoS Pathog 11(2):e1004621 (2015).
- Systematic analysis of phosphotyrosine antibodies recognizing single phosphorylated EPIYA-motifs in CagA of Western-type Helicobacter pylori strains. Lind et al., PLoS One 9(5):e96488 (2014).
- Presence of terminal EPIYA phosphorylation motifs in Helicobacter pylori CagA contributes to IL-8 secretion, irrespective of the number of repeats. Papadakos et al., PLoS One 8(2):e56291 (2013).
- CagA C-terminal variations in Helicobacter pylori strains from Colombian patients with gastric precancerous lesions. Sicinschi et al., Clin Microbiol Infect 16(4):369-378 (2010).
- Polymorphism in the CagA EPIYA motif impacts development of gastric cancer. Jones et al., J Clin Microbiol 47(4):959-968 (2009).
- Cholesterol depletion reduces Helicobacter pylori CagA translocation and CagA-induced responses in AGS cells. Lai et al., Infect Immun 76(7):3293-3303 (2008).
- Helicobacter pylori and idiopathic thrombocytopenic purpura. Franceschi et al., Annals of Internal Medicine 140(9):766-767 (2004).
- Functional analysis of the cag pathogenicity island in Helicobacter pylori isolates from patients with gastritis, peptic ulcer, and gastric cancer. Backert et al., Infect Immun 72(2):1043-1056 (2004).
- Intracellular and interstitial expression of Helicobacter pylori virulence genes in gastric precancerous intestinal metaplasia and adenocarcinoma. Semino-Mora et al., J Infect Dis 187(8):1165-1177 (2003).
- Altered states: involvement of phosphorylated CagA in the induction of host cellular growth changes by Helicobacter pylori. Segal et al., Proc Natl Acad Sci U S A 96(25):14559-14564 (1999).