Viral Antigens
Product List
Shiga Like Toxin 1
Shiga Like Toxin-1 Subunit B Recombinant
The Shiga Like Toxin 1 protein is fused to a 6xHis tag at its N-terminus and purified by proprietary chromatographic technique.
Shiga Like Toxin 2
Shiga Like Toxin-2 Subunit B Recombinant
The Shiga Like Toxin 2 protein is fused to a 6xHis tag at its N-terminus and purified by proprietary chromatographic technique.
Introduction
Shiga-like toxins (SLTs), also known as verotoxins, are a group of bacterial AB5 protein toxins that inhibit protein synthesis in sensitive eukaryotic cells . These toxins are produced by certain strains of Escherichia coli (E. coli) and are similar to the Shiga toxin produced by Shigella dysenteriae. There are two main types of Shiga-like toxins: Stx1 and Stx2, with several subtypes within each group .
Shiga-like toxins are potent inhibitors of protein synthesis. They consist of an A subunit, which has enzymatic activity, and a B subunit pentamer, which binds to the cellular receptor globotriaosylceramide (Gb3) . These toxins are primarily expressed by pathogenic strains of E. coli and are found in tissues such as the intestines, kidneys, and brain . The expression of these toxins is regulated by the bacterial genome and can be influenced by environmental factors.
The primary biological function of Shiga-like toxins is to inhibit protein synthesis in host cells, leading to cell death . These toxins play a crucial role in the pathogenicity of E. coli infections, contributing to symptoms such as bloody diarrhea and hemolytic-uremic syndrome (HUS) . They also interact with the host immune system, inducing inflammatory responses and modulating immune signaling pathways .
Shiga-like toxins exert their effects by binding to the Gb3 receptor on the surface of target cells . After binding, the toxins are internalized and transported to the endoplasmic reticulum, where the A subunit cleaves a specific adenine residue from the 28S rRNA of the 60S ribosomal subunit . This action halts protein synthesis and triggers cell death. Additionally, Shiga-like toxins can activate various cellular stress responses, including apoptosis and autophagy .
The expression and activity of Shiga-like toxins are tightly regulated by the bacterial genome. Transcriptional regulation involves the activation of specific promoters in response to environmental signals . Post-translational modifications, such as proteolytic cleavage, are also crucial for the activation and function of these toxins . The regulation of Shiga-like toxins ensures their production is optimized for bacterial survival and pathogenicity.
Shiga-like toxins have several applications in biomedical research and clinical settings. They are used as tools to study protein synthesis and cellular stress responses . In diagnostics, assays detecting Shiga-like toxins help identify pathogenic E. coli strains in clinical samples . Therapeutically, research is ongoing to develop inhibitors that neutralize these toxins and prevent their harmful effects in infected individuals .
Throughout the life cycle of pathogenic E. coli, Shiga-like toxins play a critical role in establishing infection and causing disease . During the initial stages of infection, these toxins help the bacteria evade the host immune system and colonize the intestines . As the infection progresses, the toxins contribute to tissue damage and systemic complications, such as HUS . Understanding the role of Shiga-like toxins in the bacterial life cycle is essential for developing effective treatments and preventive measures.
