Product Description
Size: 100µL
Rabbit Polyclonal E. coli heat labile toxin A antibody. Suitable for IP, WB and reacts with Escherichia coli samples. Cited in 5 publications. Immunogen corresponding to Native Full Length Protein corresponding to Escherichia coli eltA.
Key facts
Host species:Rabbit,
Clonality:Polyclonal,
Isotype:IgG,
Carrier free:No,
Reacts with:Escherichia coli,
Applications:WB, IPSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Native Full Length Protein corresponding to Escherichia coli eltA.P06717,
Specificity:ab188541 reacts with LT and cholera toxin.
Properties and Storage Information:
Form-Liquid, Purity-Whole antiserum, Storage buffer-pH: 6 - 8.5Preservative: 0.09% Sodium azide, Shipped at conditions-Blue Ice, Appropriate short-term storage duration-1-2 weeks, Appropriate short-term storage conditions-+4°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.
The LT subunit (A + B) also known as heat-labile enterotoxin is a heteromeric protein complex produced by enterotoxigenic Escherichia coli (ETEC). The protein consists of two distinct subunits A and B with the A subunit approximately weighing 27 kDa and the B subunit being about 11.6 kDa. The B subunit forms a pentameric ring that binds to the GM1 ganglioside receptors on the host cell surface. In contrast the A subunit possesses enzymatic activity that modifies intracellular pathways. ETEC which expresses this protein colonizes the intestinal mucosa leading to diarrhea commonly referred to as traveler's diarrhea.
Biological function summary
The LT subunit interacts with the host cell membrane where the B subunit facilitates the entry of the A subunit into the cytosol. Upon entry the A subunit enzymatically modifies the Gs alpha subunit of the adenylate cyclase complex resulting in increased cyclic AMP levels. This elevation in cyclic AMP leads to altered ion transport across the intestinal epithelial cells causing water and electrolyte imbalance. The LT subunit functions within a larger toxin complex and collaborates with additional bacterial factors to disrupt host cell processes.
Pathways
The mechanisms involving the LT subunit impact the cAMP signaling pathway important for regulating many cellular processes. Changes in cAMP levels induced by LT alter the activity of the protein kinase A (PKA) which subsequently affects the phosphorylation of various substrates. The changes also impact chloride channels such as CFTR (cystic fibrosis transmembrane conductance regulator) leading to ion imbalance and diarrhea. The interactions link the LT subunit function to other key proteins such as G proteins that regulate intracellular signaling.
The LT subunit's activity connects it to enteric infections primarily caused by ETEC strains leading to diarrheal illness. This protein interacts with the host's Gs alpha subunit and CFTR contributing to the pathology of the disease. Additionally there have been studies exploring the LT subunit’s potential role in vaccine development as it evokes a strong immune response. Research also examines the subunit as an adjuvant in mucosal vaccines due to its ability to enhance immune responses without causing disease.
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Collaboration
Tony Tang
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