TPP1 (Tripeptidyl Peptidase 1)

Tumor uptake was 2.48 ± 0.05% ID/g, 1.81 ± 0.20% ID/g, and 0.96 ± 0.09% ID/g at 30, 60, and 90 min, respectively. Collectively, these results suggest that [18F]-AlF-Asp2-TPP-1 is a promising PET imaging agent for monitoring PD-L1 expression in tumors and may serve as a valuable tool for guiding PD-L1-targeted immunotherapy.

TPP1, induced by H. pylori, promoted GC metastasis by enhancing ERS via interaction with GRP78. Targeting the TPP1/ERS axis may offer a novel therapeutic strategy for GC.

TPP1 emerges as a compelling diagnostic indicator and a potential treatment focus in esophageal cancer, with Elbasvir offering promise as a novel therapeutic agent.

TRF1-TIN2-TPP1-POT1 tightly associates with telomeres, whereas TRF2-RAP1 binds more dynamically, facilitating the recruitment of co-factors that protect chromosome ends. Altogether, our work provides mechanistic insight into shelterin function in telomere maintenance and advances our understanding of telomeric chromatin architecture.

Moreover, the dual-targeting radiotracer demonstrated potential for ultrasmall tumor imaging and could be combined with X-ray irradiation to further enhance PET imaging contrast, thereby improving tumor-targeting efficiency. These findings suggest that [64Cu]-PEG-RGD-TPP-1 is a promising noninvasive tracer for detecting tumors expressing PD-L1 and/or integrin avβ3, with the prospect of clinical implementation.

The high-OXPHOS-macrophage-related prognostic signature derived from scRNA-seq data provides valuable insights into GC patient stratification. NPC2, LY96, and TPP1, highly expressed in TAMs, were implicated in promoting tumor growth and immune escape, offering potential targets for novel therapeutic interventions.

Metformin has been shown to inhibit cancer cell proliferation, migration, and invasion while inducing apoptosis and inhibiting the expression of PD-L1...Both in vitro and in vivo experimental results demonstrated that this tumor cell membrane-based drug delivery system significantly prolonged the half-life of TPP1, maintained its ability to activate T cells and promote IFN-γ secretion, and effectively inhibited tumor growth. Our constructed nanodelivery system could provide a promising therapeutic platform for co-delivery of peptides and small-molecule inhibitors in cancer therapy.

APPFs may play an important role in the regulation of tumor immune microenvironment in GC and warrant further exploration. The predictive model based on APPFRGs effectively predicts the prognosis and tumor immune status of GC.

NFt1 treatment induced autophagic traits by suppressing the PI3K/AKT/mTOR pathway, thereby enhancing TFEB transactivity. These findings demonstrated the therapeutic promise of NFt1 in the effective management of HCC.

These findings suggest that p53K382me1 may be an early step in tumor initiation, especially in inflammation-induced CRC, and could serve as a functional biomarker and therapeutic target in adjuvant setting for advanced CRCs.

The newly associated proteins indicated the involvement of complement (C1S and C1R), microglia (SIRPA, SIGLEC9 and PRSS8) and lysosomes (CLN5) in Alzheimer's disease; the interleukin-6 pathway (CTF1) in Parkinson's disease; lysosomes (TPP1), blood-brain barrier integrity (MFAP2) and astrocytes (TNFSF13) in amyotrophic lateral sclerosis; and blood-brain barrier integrity (VEGFB), oligodendrocytes (PARP1), node of Ranvier and dorsal root ganglion (NCS1, FLRT3 and CDH15) and the innate immune system (CR1, AHSG and WARS) in multiple sclerosis. Our study demonstrates how harnessing large-scale genomic and proteomic data can yield new insights into the role of the plasma proteome in the pathogenesis of neurodegenerative diseases.

Overall, we identified inflammation-related changes in the BALF as a common toxic mechanism for the combustion particles. Our protein-based approach enables sensitive detection of inflammatory protein changes across different matrices enhancing understanding of exhaust particle toxicity.