Abcam, ab224836, Recombinant Helicobacter pylori CagA protein (Tagged)

Size: 100µg
Recombinant Helicobacter pylori CagA protein (Tagged) is a Helicobacter pylori Fragment protein, in the 918 to 1147 aa range, expressed in Escherichia coli, with >90%, suitable for SDS-PAGE, Mass Spec.
Key facts
Purity:>90% SDS-PAGE,
Expression system:Escherichia coli,
Tags:His tag N-Terminus,
Applications:Mass Spec, SDS-PAGESee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Biologically active:No,
Accession:P80200,
Animal free:No,
Carrier free:No,
Species:Helicobacter pylori,
Storage buffer:pH: 7.2 - 7.4Constituents: Tris buffer, 50% Glycerol (glycerin, glycerine)

Properties and Storage Information:
Shipped at conditions-Blue Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Helicobacter pylori CagA also known as CagA protein is a major virulence factor of the bacterium Helicobacter pylori. CagA has a molecular weight of around 120-145 kDa depending on the strain. It is expressed within the gastric environment where Helicobacter pylori colonizes the human stomach lining. The presence of CagA in the organism allows it to interact with host cells upon translocation by a type IV secretion system altering cellular pathways and signaling. This interaction gives the bacterium a mechanism to interfere with normal cellular processes.
Biological function summary
CagA protein plays a significant role in the pathogenicity of Helicobacter pylori. It forms part of a complex process involving host-pathogen interactions. Once inside the host cell CagA undergoes phosphorylation by host cell kinases. This phosphorylation enables CagA to disrupt intracellular signaling pathways leading to changes in cell morphology and increased proliferation. Notably CagA interacts with a variety of host cellular proteins such as SHP-2 leading to cytoskeletal rearrangements and pro-inflammatory responses.
Pathways
CagA influences several signaling cascades important to cell behavior. Within the MAPK/ERK pathway CagA interaction with SHP-2 leads to aberrant activation of downstream signals contributing to pathogenic effects. Additionally CagA affects the Wnt/β-catenin pathway by stabilizing β-catenin in the nucleus promoting gene transcription linked to cell proliferation. These interactions illustrate CagA's role in altering normal cellular processes thereby contributing to the pathogenic mechanisms of Helicobacter pylori infection.
CagA implicates itself in the development of gastric cancer and peptic ulcer disease. The alterations in cell signaling and morphology induced by CagA increase the risk of malignant transformation of gastric epithelial cells. Additionally CagA interferes with E-cadherin an important protein in maintaining cellular adhesion further facilitating cancer progression. By modulating host cell biology through such interactions CagA stands as an important factor in the pathogenic profile of Helicobacter pylori-related diseases.