ArticleBiochemical and biophysical research communications2010
Biochemical and functional analysis of TIR domain containing protein from Brucella melitensis.
Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Progress in brucellosis immune regulation inflammatory mechanisms and diagnostic advances.European journal of medical research · 2025Review
- ThemicroLife · 2025Review
- A Chimeric Peptide Derived from a Bacterial Effector Protein Attenuates TLR-2/4-Mediated Production of Pro-Inflammatory Cytokines and Enhances the Cellular Availability of Gentamicin.Journal of inflammation research · 2025Article
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- Review
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- Host F-Box Protein 22 Enhances the Uptake of Brucella by Macrophages and Drives a Sustained Release of Proinflammatory Cytokines through Degradation of the Anti-Inflammatory Effector Proteins of Brucella.Infection and immunity · 2022Article
- Characterization of genome-wide microRNAs and their roles in development and biotic stress in pear.Planta · 2019Article
- Cytoplasmic Linker Protein CLIP170 Negatively Regulates TLR4 Signaling by Targeting the TLR Adaptor Protein TIRAP.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- TheThe Journal of biological chemistry · 2017Article
- AThe EMBO journal · 2017Article
- Bacillus anthracis TIR Domain-Containing Protein Localises to Cellular Microtubule Structures and Induces Autophagy.PloS one · 2016Article
- Establishment of Chronic Infection: Brucella's Stealth Strategy.Frontiers in cellular and infection microbiology · 2016Review
- Type IV secretion system of Brucella spp. and its effectors.Frontiers in cellular and infection microbiology · 2015Review
- The Brucella TIR domain containing proteins BtpA and BtpB have a structural WxxxE motif important for protection against microtubule depolymerisation.Cell communication and signaling : CCS · 2014Article
- Comparative phylogenomics and evolution of the Brucellae reveal a path to virulence.Journal of bacteriology · 2014Article
- Crystal structures of the Toll/Interleukin-1 receptor (TIR) domains from the Brucella protein TcpB and host adaptor TIRAP reveal mechanisms of molecular mimicry.The Journal of biological chemistry · 2014Article
- A Staphylococcus aureus TIR domain protein virulence factor blocks TLR2-mediated NF-κB signaling.Journal of innate immunity · 2014Article
- Two TIR-like domain containing proteins in a newly emerging zoonotic Staphylococcus aureus strain sequence type 398 are potential virulence factors by impacting on the host innate immune response.Frontiers in microbiology · 2014Article
- A TIR domain protein from E. faecalis attenuates MyD88-mediated signaling and NF-κB activation.PloS one · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Toll/interleukin-1 like receptors are evolutionarily conserved proteins in eukaryotes that play crucial role in pathogen recognition and innate immune responses. Brucella are facultative intracellular bacterial pathogens causing brucellosis in animal and human hosts. Brucella behave as a stealthy pathogen by evading the immune recognition or suppressing the TLR signaling cascades. Brucella encode a TIR domain containing protein, TcpB, which suppresses NF-kappaB activation as well as pro-inflammatory cytokine secretion mediated by TLR2 and TLR4 receptors. TcpB targets the TIRAP mediated pathway to suppress TLR signaling. With the objective of detailed characterization, we have over expressed and purified TcpB from Brucella melitensis in native condition. The purified protein exhibited lipid-binding properties and cell permeability. NF-kappaB inhibition property of endogenous TcpB has also been demonstrated. The data provide insight into the mechanism of action of TcpB in the intracellular niche of Brucella.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.