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• W2511344593 abstract "Type III secretion systems (T3SSs) are sophisticated multiprotein injection machines of Gram-negative bacteria, which translocate multiple effector proteins from the bacterial cytosol directly into the cytosol of targeted host cells. The effector translocation is essential for the pathogenesis of a wide range of Gram-negative bacterial pathogens. Several of the known anti-inflammatory effectors have attracted attention as potential drug candidates. A new concept is emerging to employ bacterial proteins to modulate inflammatory responses in humans without a requirement for their particular ‘parent’ bacteria. Instead of targeting individual cytokines or receptors stoichiometrically, it might be beneficial to address inflammatory signaling pathways upstream of cytokine production to more broadly inhibit inflammatory responses by dampening the expression of signaling molecules. Bacterial pathogens have developed intriguing virulence mechanisms, including several sophisticated nanomachines, for injecting effector proteins to manipulate host immune signaling pathways for their own benefit. Therefore, bacterial genomes harbor a wealth of information about how to manipulate the defense systems of the host. Current understanding addresses virulence mechanisms mostly as targets for antimicrobials. We propose a change of paradigm by exploiting bacterial effectors not as targets but as tools for the directed manipulation of host signaling – for the benefit of the host. Recently, effector proteins have been identified that autonomously translocate into host cells, representing a novel class of cell-penetrating peptides (CPPs) or effectors (CPEs). Moreover, autonomous cell penetration overcomes a major hurdle in pharmacology by transducing specific therapeutic agents to intracellular targets. Bacterial pathogens have developed intriguing virulence mechanisms, including several sophisticated nanomachines, for injecting effector proteins to manipulate host immune signaling pathways for their own benefit. Therefore, bacterial genomes harbor a wealth of information about how to manipulate the defense systems of the host. Current understanding addresses virulence mechanisms mostly as targets for antimicrobials. We propose a change of paradigm by exploiting bacterial effectors not as targets but as tools for the directed manipulation of host signaling – for the benefit of the host. Recently, effector proteins have been identified that autonomously translocate into host cells, representing a novel class of cell-penetrating peptides (CPPs) or effectors (CPEs). Moreover, autonomous cell penetration overcomes a major hurdle in pharmacology by transducing specific therapeutic agents to intracellular targets. a malfunction of the immune system, where components of the immune system mistakenly attack healthy tissues in the body. disorder in which a patientʼs humoral immune system is activated against the body's own protein. product derived from living sources for prevention, treatment, or cure of diseases. generally these are relatively short peptides having the ability to cross cell membranes, either alone or in combination/association with a bioactive cargo. bacterial effector proteins that have the ability to enter host cells without the requirement of additional bacterial factors. combinatorial approach of fusing variable CPPs with a ʻtool-box’ of functional peptide sequences. a type of protein secreted by cells of the immune system that mediate the communication and response of and between cells. translocation of peptides and proteins across membranes. the ensemble of known active microbial effector proteins. the uptake of extracellular substances into the cell by active transport. the ensemble of biological structures and mechanisms that protects the body from foreign substances and pathogens. a reaction of living tissues to infection, irritation, or other injury. a disease caused by entry of a microbial organism (bacterium, protozoan, fungi, or virus) into the body of the host where it grows and replicates. over-reaction of the innate immune system and its subsequent downstream signaling. a biological agent that causes disease. a protein export system that transports newly synthesized proteins to the extracellular space. continuous or discontinuous stretch of amino acids increasing the specificity of a compound for particular cells, tissues, or subcellular sites. a protein export system in the cell wall of Gram-negative bacteria that acts as a ‘molecular syringe’ or ‘nanomachine’ and injects effector proteins directly into the host cell cytoplasm. a microbial component that can manipulate and/or damage host cells, thereby increasing the probability of infection and disease." @default.
• W2511344593 created "2016-09-16" @default.
• W2511344593 creator A5034946687 @default.
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• W2511344593 date "2017-02-01" @default.
• W2511344593 modified "2023-10-15" @default.
• W2511344593 title "Cell-Penetrating Bacterial Effector Proteins: Better Tools than Targets" @default.
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• W2511344593 doi "https://doi.org/10.1016/j.tibtech.2016.08.002" @default.
• W2511344593 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27592802" @default.
• W2511344593 hasPublicationYear "2017" @default.
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