Austral Biologicals HPP-5003 - Rabbit anti-Helicobacter pylori Cag antigen IgG fraction (polyclonal), 1 mg

Rabbit Anti-Helicobacter Pylori Cag Antigen, IgG Fraction, Polyclonal

1mg
$425.00
Skip to product information
Austral Biologicals HPP-5003 - Rabbit anti-Helicobacter pylori Cag antigen IgG fraction (polyclonal), 1 mg

Rabbit Anti-Helicobacter Pylori Cag Antigen, IgG Fraction, Polyclonal

Catalog no. HPP-5003-9
$425.00
Size1mg

IgG fraction obtained from a rabbit immunized with highly purified Cag antigen.

  • Storage: Store at -20°C.
  • Stability: At least 1 year at -20°C.
  • Biological activity: Reacts in ELISA and Western Blot (1/5,000 dilution recognizes 100 pg of Cag)
  • Formulation: Solution at 2.00 mg/mL (0.5 ml) in 0.1M Tris HCl (pH 7.5)

Publications using Austral Biologicals HPP-5003-9

The following scientific publications report use of Austral Biologicals HPP-5003-9:

  1. Enhanced ADP-heptose-dependent NF-κB activation by Helicobacter pylori CagA through cortactin-Src-dependent tyrosine phosphorylation of IKKβ. Sharafutdinov et al., Microlife 7:uqaf049 (2026).
  2. Extracts from Plectranthus asirensis and Premna resinosa inhibit Helicobacter pylori-induced epithelial cell damage, DNA double-strand breaks and inflammation. Noman et al., Gut Pathog 17(1):97 (2025).
  3. Cultivation and molecular characterization of viable Helicobacter pylori from the root canal of 170 deciduous teeth of children. Elger et al., Cell Commun Signal 22(1):578 (2024).
  4. SOX9 is regulated by AURKA in response to Helicobacter pylori infection via EIF4E-mediated cap-dependent translation. Gomaa et al., Cancer Lett 593:216939 (2024).
  5. Cortactin-dependent control of Par1b-regulated epithelial cell polarity in Helicobacter infection. Sharafutdinov et al., Cell Insight 3(3):100161 (2024).
  6. Targeting hypoxia-inducible factor-1 alpha suppresses Helicobacter pylori -induced gastric injury via attenuation of both cag -mediated microbial virulence and proinflammatory host responses. Noto et al., Gut Microbes 15(2):2263936 (2023).
  7. A single-nucleotide polymorphism in Helicobacter pylori promotes gastric cancer development. Sharafutdinov et al., Cell Host & Microbe 31(8):1345-1358.e6 (2023).
  8. CDK1 bridges NF-κB and β-catenin signaling in response to H. pylori infection in gastric tumorigenesis. Zhu et al., Cell Rep 42(1):112005 (2023).
  9. Helicobacter pylori pathogen inhibits cellular responses to oncogenic stress and apoptosis. Palrasu et al., PLoS Pathog 18(6):e1010628 (2022).
  10. Early and late genome-wide gastric epithelial transcriptome response during infection with the human carcinogen Helicobacter pylori. Sharafutdinov et al., Cell Insight 1(3):100032 (2022).
  11. Unique TLR9 Activation by Helicobacter pylori Depends on the cag T4SS, But Not on VirD2 Relaxases or VirD4 Coupling Proteins. Tegtmeyer et al., Curr Microbiol 79(4):121 (2022).
  12. Mouse Gastric Epithelial Cells Resist CagA Delivery by the Helicobacter pylori Type IV Secretion System. Shrestha et al., Int J Mol Sci 23(5):2492 (2022).
  13. Importance of cortactin for efficient epithelial NF-ĸB activation by Helicobacter pylori, Salmonella enterica and Pseudomonas aeruginosa, but not Campylobacter spp. Tegtmeyer et al., Eur J Microbiol Immunol (Bp) 11(4):95-103 (2022).
  14. Helicobacter pylori actively suppresses innate immune nucleic acid receptors. Dooyema et al., Gut Microbes 14(1):2105102 (2022).
  15. Cortactin Promotes Effective AGS Cell Scattering by Helicobacter pylori CagA, but Not Cellular Vacuolization and Apoptosis Induced by the Vacuolating Cytotoxin VacA. Sharafutdinov et al., Pathogens 11(1):3 (2022).
  16. The Helicobacter pylori type IV secretion system upregulates epithelial cortactin expression by a CagA- and JNK-dependent pathway. Sharafutdinov et al., Cellular Microbiology 23(10):e13376 (2021).
  17. Cortactin Is Required for Efficient FAK, Src and Abl Tyrosine Kinase Activation and Phosphorylation of Helicobacter pylori CagA. Knorr et al., Int J Mol Sci 22(11):6045 (2021).
  18. Helicobacter pylori CagA elicits BRCAness to induce genome instability that may underlie bacterial gastric carcinogenesis. Imai et al., Cell Host & Microbe 29(6):941-958.e10 (2021).
  19. A bacterial small RNA regulates the adaptation of Helicobacter pylori to the host environment. Kinoshita-Daitoku et al., Nat Commun 12(1):2085 (2021).
  20. Toll-like Receptor 5 Activation by the CagY Repeat Domains of Helicobacter pylori. Tegtmeyer et al., Cell Reports 32(11):108159 (2020).
  21. Helicobacter pylori CagA Protein Attenuates 5-Fu Sensitivity of Gastric Cancer Cells Through Upregulating Cellular Glucose Metabolism. Gao et al., Onco Targets Ther 13:6339-6349 (2020).
  22. Type IV secretion of Helicobacter pylori CagA into oral epithelial cells is prevented by the absence of CEACAM receptor expression. Tegtmeyer et al., Gut Pathog 12:25 (2020).
  23. Bacterial CagA protein compromises tumor suppressor mechanisms in gastric epithelial cells. Palrasu et al., J Clin Invest 130(5):2422-2434 (2020).
  24. SHP2-Independent Tyrosine Dephosphorylation of Cortactin and Vinculin during Infection with Helicobacter pylori. Knorr et al., Eur J Microbiol Immunol (Bp) 10(1):20-27 (2020).
  25. Cholesteryl α-D-glucoside 6-acyltransferase enhances the adhesion of Helicobacter pylori to gastric epithelium. Jan et al., Commun Biol 3(1):120 (2020).
  26. T4SS-dependent TLR5 activation by Helicobacter pylori infection. Pachathundikandi et al., Nat Commun 10(1):5717 (2019).
  27. Chaperone activity of serine protease HtrA of Helicobacter pylori as a crucial survival factor under stress conditions. Zarzecka et al., Cell Commun Signal 17(1):161 (2019).
  28. 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).
  29. Establishment of serine protease htrA mutants in Helicobacter pylori is associated with secA mutations. Zawilak-Pawlik et al., Sci Rep 9(1):11794 (2019).
  30. Tailor-Made Detection of Individual Phosphorylated and Non-Phosphorylated EPIYA-Motifs of Helicobacter pylori Oncoprotein CagA. Pachathundikandi et al., Cancers (Basel) 11(8):E1163 (2019).
  31. Specific high affinity interaction of Helicobacter pylori CagL with integrin αVβ6 promotes type IV secretion of CagA into human cells. Buß et al., FEBS Journal 286(20):3980-3997 (2019).
  32. α-Difluoromethylornithine reduces gastric carcinogenesis by causing mutations in Helicobacter pylori cagY. Sierra et al., Proc Natl Acad Sci U S A 116(11):5077-5085 (2019).
  33. Nod1 Imprints Inflammatory and Carcinogenic Responses toward the Gastric Pathogen Helicobacter pylori. Suarez et al., Cancer Res 79(7):1600-1611 (2019).
  34. Evaluating the origin and virulence of a Helicobacter pylori cagA-positive strain isolated from a non-human primate. Hashi et al., Sci Rep 8(1):15981 (2018).
  35. Helicobacter pylori adhesin HopQ disrupts trans dimerization in human CEACAMs. Moonens et al., EMBO J 37(13):e98665 (2018).
  36. The Helicobacter pylori type IV secretion system promotes IL-8 synthesis in a model of pediatric airway epithelium via p38 MAP kinase. Dela et al., PLoS One 12(8):e0183324 (2017).
  37. Overexpression of serine protease HtrA enhances disruption of adherens junctions, paracellular transmigration and type IV secretion of CagA by Helicobacter pylori. Harrer et al., Gut Pathog 9:40 (2017).
  38. Helicobacter pylori modulates host cell responses by CagT4SS-dependent translocation of an intermediate metabolite of LPS inner core heptose biosynthesis. Stein et al., PLoS Pathog 13(7):e1006514 (2017).
  39. Fallacy of the Unique Genome: Sequence Diversity within Single Helicobacter pylori Strains. Draper et al., mBio 8(1):e02321-16 (2017).
  40. Systematic site-directed mutagenesis of the Helicobacter pylori CagL protein of the Cag type IV secretion system identifies novel functional domains. Bönig et al., Sci Rep 6:38101 (2016).
  41. Systematic analysis of phosphotyrosine antibodies recognizing single phosphorylated EPIYA-motifs in CagA of East Asian-type Helicobacter pylori strains. Lind et al., BMC Microbiol 16(1):201 (2016).
  42. 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).
  43. Early Molecular Events in Murine Gastric Epithelial Cells Mediated by Helicobacter pylori CagA. Banerjee et al., Helicobacter 21(5):395-404 (2016).
  44. Characterisation of worldwide Helicobacter pylori strains reveals genetic conservation and essentiality of serine protease HtrA. Tegtmeyer et al., Mol Microbiol 99(5):925-944 (2016).
  45. Dramatic increase in SHP2 binding activity of Helicobacter pylori Western CagA by EPIYA-C duplication: its implications in gastric carcinogenesis. Nagase et al., Sci Rep 5:15749 (2015).
  46. Proteomic characterization of Helicobacter pylori CagA antigen recognized by child serum antibodies and its epitope mapping by peptide array. Akada et al., PLOS ONE 9(8):e104611 (2014).
  47. Helicobacter pylori CagA promotes Snail-mediated epithelial-mesenchymal transition by reducing GSK-3 activity. Lee et al., Nature Communications 5:4423 (2014).
  48. A new type of intrabacterial nanotransportation system for VacA in Helicobacter pylori. Wu et al., Medical Molecular Morphology 47(4):224-232 (2014).
  49. Electron microscopic, genetic and protein expression analyses of Helicobacter acinonychis strains from a Bengal tiger. Tegtmeyer et al., PLoS One 8(8):e71220 (2013).
  50. Functional plasticity in the type IV secretion system of Helicobacter pylori. Barrozo et al., PLoS Pathog 9(2):e1003189 (2013).
  51. 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).
  52. Helicobacter pylori CagA and gastric carcinogenesis. Zheng et al., Asian Pacific Journal of Cancer Prevention 13(12):6305-6310 (2012).
  53. Distinct repeat motifs at the C-terminal region of CagA of Helicobacter pylori strains isolated from diseased patients and asymptomatic individuals in West Bengal, India. Chattopadhyay et al., Gut Pathog 4(1):4 (2012).
  54. Effect of Helicobacter pylori cdrA on interleukin-8 secretions and nuclear factor kappa B activation. Takeuchi et al., World J Gastroenterol 18(5):425-434 (2012).
  55. Helicobacter pylori CagA triggers expression of the bactericidal lectin REG3γ via gastric STAT3 activation. Lee et al., PLoS One 7(2):e30786 (2012).
  56. Proteasome particle-rich structures are widely present in human epithelial neoplasms: correlative light, confocal and electron microscopy study. Necchi et al., PLoS One 6(6):e21317 (2011).
  57. Induction of TLR-2 and TLR-5 expression by Helicobacter pylori switches cagPAI-dependent signalling leading to the secretion of IL-8 and TNF-α. Kumar et al., PLoS One 6(5):e19614 (2011).
  58. Difluoromethylornithine is a novel inhibitor of Helicobacter pylori growth, CagA translocation, and interleukin-8 induction. Barry et al., PLoS One 6(2):e17510 (2011).
  59. Effects of blood group antigen-binding adhesin expression during Helicobacter pylori infection of Mongolian gerbils. Ohno et al., J Infect Dis 203(5):726-735 (2011).
  60. Helicobacter pylori defines local immune response through interaction with dendritic cells. Andres et al., FEMS Immunology & Medical Microbiology 61(2):168-178 (2011).
  61. A global overview of the genetic and functional diversity in the Helicobacter pylori cag pathogenicity island. Olbermann et al., PLoS Genet 6(8):e1001069 (2010).
  62. Biochemical and functional characterization of Helicobacter pylori vesicles. Olofsson et al., Mol Microbiol 77(6):1539-1555 (2010).
  63. Helicobacter pylori CagA phosphorylation status determines the gp130-activated SHP2/ERK and JAK/STAT signal transduction pathways in gastric epithelial cells. Lee et al., J Biol Chem 285(21):16042-16050 (2010).
  64. In vivo accumulation of Helicobacter pylori products, NOD1, ubiquitinated proteins and proteasome in a novel cytoplasmic structure. Necchi et al., PLOS ONE 5(3):e9716 (2010).
  65. Partial protection against Helicobacter pylori in the absence of mast cells in mice. Ding et al., Infect Immun 77(12):5543-5550 (2009).
  66. CagA and VacA polymorphisms do not correlate with severity of histopathological lesions in Helicobacter pylori-infected Greek children. Sgouras et al., J Clin Microbiol 47(8):2426-2434 (2009).
  67. Helicobacter pylori regulates cellular migration and apoptosis by activation of phosphatidylinositol 3-kinase signaling. Nagy et al., J Infect Dis 199(5):641-651 (2009).
  68. Helicobacter pylori HopQ outer membrane protein attenuates bacterial adherence to gastric epithelial cells. Loh et al., FEMS Microbiol Lett 289(1):53-58 (2008).
  69. Analysis of Helicobacter pylori isolates from Chile: occurrence of selective type 1 Lewis b antigen expression in lipopolysaccharide. Altman et al., Journal of Medical Microbiology 57(Pt 5):585-591 (2008).
  70. Cholesterol depletion reduces Helicobacter pylori CagA translocation and CagA-induced responses in AGS cells. Lai et al., Infect Immun 76(7):3293-3303 (2008).
  71. Focal adhesion kinase is a substrate and downstream effector of SHP-2 complexed with Helicobacter pylori CagA. Tsutsumi et al., Mol Cell Biol 26(1):261-276 (2006).
  72. Analysis of cell type-specific responses mediated by the type IV secretion system of Helicobacter pylori. Bauer et al., Infect Immun 73(8):4643-4652 (2005).
  73. Activation of beta-catenin by carcinogenic Helicobacter pylori. Franco et al., Proc Natl Acad Sci U S A 102(30):10646-10651 (2005).
  74. NF-kappaB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein. Brandt et al., Proc Natl Acad Sci U S A 102(26):9300-9305 (2005).
  75. Tyrosine phosphorylation of CagA from Chinese Helicobacter pylori isolates in AGS gastric epithelial cells. Zhang et al., J Clin Microbiol 43(2):786-790 (2005).
  76. Distinct diversity of the cag pathogenicity island among Helicobacter pylori strains in Japan. Azuma et al., J Clin Microbiol 42(6):2508-2517 (2004).
  77. Helicobacter pylori CagA induces Ras-independent morphogenetic response through SHP-2 recruitment and activation. Higashi et al., Journal of Biological Chemistry 279(17):17205-17216 (2004).
  78. Phosphorylation of tyrosine 972 of the Helicobacter pylori CagA protein is essential for induction of a scattering phenotype in gastric epithelial cells. Backert et al., Molecular Microbiology 42(3):631-644 (2001).
  79. Role of activated protein C in Helicobacter pylori-associated gastritis. Oka et al., Infect Immun 68(5):2863-2869 (2000).
  80. 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).

You may also like