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Animal venoms contain many peptides with high specificity and selectivity against their protein targets, a characteristic which makes venoms an invaluable source of potential drugs. High-sensitivity mass spectrometry (MS)- based peptidomic platform has evolved as a predominant method for natural peptide drug discovery due to its strength for direct and rapid identification of peptides and peptide-associated post-translational modifications (PTMs). In this study, we used cell-affinity assays combined with nanoLC-MS/MS based peptidomics to identify cancer cell binding peptides (CBPs) from Bufo Bufo gargarizans. We identified 76 potential cell binding peptides and 237 non-affinity peptides in venom extracts from Asiatic toads, and some were verified with MS-parallel reaction monitoring (PRM) mode. These peptides were further analyzed and internalized within human cells and some demonstrated anti-tumor properties in vitro. These specific peptides might be used as templates for peptide-based drug design or optimization.
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http://dx.doi.org/10.1016/j.jpba.2021.114354 | DOI Listing |
ACS Biomater Sci Eng
September 2025
Materials Engineering, McGill university, Montreal H3A0C5, Canada.
Transcutaneous devices such as dental implants frequently fail due to infections at their interfaces with epithelial tissues. These infections are facilitated by the lack of integration between the devices and the surrounding soft tissues. This study aims to improve epithelial integration through surface modification of a transcutaneous implant material (polyetheretherketone (PEEK)).
View Article and Find Full Text PDFBlood Adv
September 2025
BC Cancer, Vancouver, British Columbia, Canada.
Classical Hodgkin Lymphoma (CHL) is characterized by a complex tumor microenvironment (TME) that supports disease progression. While immune cell recruitment by Hodgkin and Reed-Sternberg (HRS) cells is well-documented, the role of non-malignant B cells in relapse remains unclear. Using single-cell RNA sequencing (scRNA-seq) on paired diagnostic and relapsed CHL samples, we identified distinct shifts in B-cell populations, particularly an enrichment of naïve B cells and a reduction of memory B cells in early-relapse compared to late-relapse and newly diagnosed CHL.
View Article and Find Full Text PDFSci Signal
September 2025
Department of Pathology, Microbiology and Immunology, New York Medical College, Valhalla, NY, USA.
Replication of HIV-1 requires the coordinated action of host and viral transcription factors, most critically the viral transactivator Tat and the host nuclear factor κB (NF-κB). This activity is disrupted in infected cells that are cultured with extracellular vesicles (EVs) present in human semen, suggesting that they contain factors that could inform the development of new therapeutics. Here, we explored the contents of semen-derived EVs (SEVs) from uninfected donors and individuals with HIV-1 and identified host proteins that interacted with HIV Tat and the NF-κB subunit p65.
View Article and Find Full Text PDFPLoS Genet
September 2025
Department of Biochemistry, Indian Institute of Science, Bengaluru, Karnataka, India.
Tropomyosin is an actin-binding protein (ABP) which protects actin filaments from cofilin-mediated disassembly. Distinct tropomyosin isoforms have long been hypothesized to differentially sort to subcellular actin networks and impart distinct functionalities. Nevertheless, a mechanistic understanding of the interplay between Tpm isoforms and their functional contributions to actin dynamics has been lacking.
View Article and Find Full Text PDFACS Chem Neurosci
September 2025
Department of Medical Biology, Faculty of Medicine, Bahçeşehir University, Istanbul 34353, Turkey.
IL-17A is a pro-inflammatory cytokine that significantly contributes to the pathogenesis of autoimmune diseases, including multiple sclerosis (MS). Previous studies have suggested that PARP-1 inhibitors can modulate IL-17A-mediated inflammation, prompting the investigation of Niraparib, an FDA-approved PARP-1 inhibitor, as a potential therapeutic agent for MS. In this study, we hypothesized that Niraparib could disrupt the interaction between IL-17A and its receptor, IL-17RA.
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