Methods: This study developed the specialized software LanthMS. The software exhaustively enumerates all possible lanthipeptide structures derived from given peptide sequences and assigns multidimensional scores by comprehensively comparing theoretical spectra against experimental MS/MS data, thereby predicting the most probable structures.

Results: Using this approach, two novel lanthipeptides, amyA and amyC, were identified, from the Bacillus amyloliquefaciens WS-8 strain.

Discussion: The LanthMS tool developed and validated in this study provides an automated solution for the structural elucidation of lanthipeptides. It not only significantly reduces the difficulty and subjectivity of manual interpretation but also deeply integrates computational structural prediction with experimental mass spectrometry data. This establishes a key technological framework for accelerating the discovery of lanthipeptides with novel activities and guiding their rational engineering.

Conclusion: As a specialized in silico prediction tool, LanthMS substantially reduces the burden of manual interpretation, enhances the efficiency and accuracy of structural confirmation, and serves as a powerful engine for rapidly exploiting and engineering lanthipeptides with novel activities.

Methods: Cell viability and mRNA expression were measured in GA-treated HepG2 cells with or without the addition of GPHyp. The half-maximal inhibitory concentration (IC₅₀) of GPHyp for inhibiting TAGE formation and for inhibiting lysozyme glycation crosslinking was evaluated.

Results: Only GPHyp significantly suppressed cell death and interleukin-8 (IL-8) mRNA expression in GA-treated cells. The IC₅₀ for TAGE production and inhibitory effect on lysozyme crosslinking demonstrated that GPHyp exhibited stronger anti-glycation effects than its metabolite amino acids and peptides. The addition of GPHyp also resulted in increased GA consumption. Analysis of the changes in GA concentrations during the reaction revealed that the addition of GPHyp significantly reduced GA levels within the first hour.

Discussion: These results suggest that GPHyp possesses potent GA-scavenging activity and inhibits TAGE production, contributing to the CTP-mediated reduction in serum TAGE levels and to improvements in vascular elasticity.

Conclusion: The anti-glycation effect of GPHyp may support a healthy lifestyle and warrant further investigation.

Methods: Five NCBP derivatives (NCBP-1 to NCBP-5) were generated using a green tag-assisted peptide synthesis (TAPS) strategy, combined with site-directed mutagenesis and terminal modification. The peptides were characterized by MS and HPLC and subsequently evaluated for antibacterial activity against ten bacterial strains, salt tolerance, and cytotoxicity in RAW 264.7 murine macrophages. Molecular docking was performed to assess binding interactions.

Results: NCBP-1 was identified as the lead derivative, demonstrating potent antibacterial activity (MIC 8 μg·mL-¹) and low cytotoxicity. It also exhibited moderate anti-inflammatory activity in LPSstimulated RAW 264.7 macrophages. Its antibacterial mechanism was further supported by favorable molecular docking interactions with E. coli outer membrane LPS (PDB ID: 4RHB).

Discussion: The combined approach successfully identified NCBP-1 as a potent antibacterial candidate. Its activity against Gram-negative bacteria is likely related to LPS binding, as suggested by the docking results. Further studies would be needed to fully elucidate its mechanism of action.

Conclusion: NCBP-1 represents a promising lead for the development of novel antibacterial agents, particularly for treating Gram-negative bacterial infections.

Method: Recombinant hGPRC6A constructs were engineered by substituting the native signal peptide and modifying the ICL3 region. The optimized receptor was expressed in mammalian cells, purified using detergent solubilization and chromatography, and analyzed by negative-staining Electron Microscopy (EM) followed by Two-Dimensional (2D) classification.

Results: Signal peptide substitution and ICL3 modification markedly improved the membrane expression of hGPRC6A. Negative-staining EM revealed well-defined particles, and 2D class averages displayed an overall architecture characteristic of canonical class C GPCRs.

Discussion: We demonstrate that engineering of the signal peptide and ICL3 region promotes proper cell surface expression of GPRC6A. This strategy provides a useful approach for the expression and purification of other GPCRs that are difficult to traffic to the plasma membrane.

Conclusion: We established an effective expression and purification strategy for hGPRC6A that restores membrane localization and yields well-defined particles consistent with class C GPCR architecture. These results provide a foundation for future high-resolution structural and functional studies of hGPRC6A.

Methodological advances have progressively deepened our insight. DNA-based sequencing (metagenomics) catalogues microbial genes but reveals only potential functions. RNA-based sequencing (metatranscriptomics) highlights active gene expression, but instability of transcripts and poor correlation with protein activity limit its predictive value. Metabolomics measures small-molecule end products, providing direct evidence of microbial biochemistry and identifying disease-linked metabolites such as urolithin A, trimethylamine N-oxide, and equol. These approaches together have transformed microbiome science, but they remain incomplete.

A critical and underutilised dimension is peptidomics: the systematic analysis of endogenous peptides in the gut and circulation. Enabled by peptide-enriching, protease-inhibiting workflows and high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS), peptidomics directly captures unstable signaling peptides and proteolytic fragments that are often invisible to conventional proteomics. Coupled with emerging gut-specific peptide databases, such as MetaPep, and Artificial Intelligence (AI) assisted de novo sequencing and spectral prediction for non-human peptides, this provides a concrete technical route to reading out the functional peptide layer of the microbiome. Peptidomics can capture functional signals of host-microbiome interaction, reveal context-specific biomarkers, and provide mechanistic insight into disease. Recent studies demonstrate that peptide-level resolution uncovers microbial contributions to gut inflammation, modulates the gut-brain axis, and enables peptide-based disease stratification in conditions such as inflammatory bowel disease. However, despite these promising examples, peptidomics remains largely absent from mainstream microbiome research. Integrating peptidomics with existing genomic, transcriptomic, and metabolomic approaches will generate a more complete and functional picture of the microbiome. This shift will accelerate biomarker discovery, refine diagnostics, and expand the search for peptide-based therapeutics, positioning peptidomics as an essential next step in microbiome science.

This decision follows a thorough investigation that identified inconsistencies in the reported work, along with directives received from the authors’ institution. In light of these concerns, the integrity and reliability of the data presented in the article can no longer be assured. Therefore, the findings of this study should not be cited or relied upon as a scientific reference.

This retraction has been made in agreement with the Editor-in-Chief.

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