ArticleFrontiers in microbiology2016
Shortening of the Lactobacillus paracasei subsp. paracasei BGNJ1-64 AggLb Protein Switches Its Activity from Auto-aggregation to Biofilm Formation.
Article in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Identification of an operon and its regulator required for autoaggregation inApplied and environmental microbiology · 2023Article
- Evaluation of the Probiotic Properties ofFood technology and biotechnology · 2023Article
- Article
- RadA, a MSCRAMM Adhesin of the Dominant SymbioteBiomolecules · 2021Article
- Probiotic Characterization of Lactobacillus paracasei subsp. paracasei KNI9 Inhibiting Adherence of Yersinia enterocolitica on Caco-2 Cells In Vitro.Probiotics and antimicrobial proteins · 2020Article
- Binding activity to intestinal cells and transient colonization in mice of two Lactobacillus paracasei subsp. paracasei strains with high aggregation potential.World journal of microbiology & biotechnology · 2019Article
- Novel Aggregation Promoting Factor AggE Contributes to the Probiotic Properties ofFrontiers in microbiology · 2017Article
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Authors and funding
7 authors.
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Abstract
AggLb is the largest (318.6 kDa) aggregation-promoting protein of Lactobacillus paracasei subsp. paracasei BGNJ1-64 responsible for forming large cell aggregates, which causes auto-aggregation, collagen binding and pathogen exclusion in vitro. It contains an N-terminus leader peptide, followed by six successive collagen binding domains, 20 successive repeats (CnaB-like domains) and an LPXTG sorting signal at the C-terminus for cell wall anchoring. Experimental information about the roles of the domains of AggLb is currently unknown. To define the domain that confers cell aggregation and the key domains for interactions of specific affinity between AggLb and components of the extracellular matrix, we constructed a series of variants of the aggLb gene and expressed them in Lactococcus lactis subsp. lactis BGKP1-20 using a lactococcal promoter. All of the variants contained a leader peptide, an inter collagen binding-CnaB domain region (used to raise an anti-AggLb antibody), an anchor domain and a different number of collagen binding and CnaB-like domains. The role of the collagen binding repeats of the N-terminus in auto-aggregation and binding to collagen and fibronectin was confirmed. Deletion of the collagen binding repeats II, III, and IV resulted in a loss of the strong auto-aggregation, collagen and fibronectin binding abilities whereas the biofilm formation capability was increased. The strong auto-aggregation, collagen and fibronectin binding abilities of AggLb were negatively correlated to biofilm formation.
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