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Last update 08 May 2025

XPNPEP1

Last update 08 May 2025

Basic Info

Synonyms

Aminoacylproline aminopeptidase, Cytosolic aminopeptidase P, sAmp

+ [11]

Introduction

Metalloaminopeptidase that catalyzes the removal of a penultimate prolyl residue from the N-termini of peptides, such as Arg-Pro-Pro (PubMed:11106490, PubMed:18515364, PubMed:35165443). Contributes to the degradation of bradykinin (PubMed:11106490).

Drugs associated with XPNPEP1

CQ31

Target

PEPD x XPNPEP1

Mechanism

PEPD inhibitors [+1]

Active Org.

Memorial Sloan Kettering Cancer Center

Originator Org.

Memorial Sloan Kettering Cancer Center

Active Indication

Inflammation

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CQ80

Target

PEPD x XPNPEP1

Mechanism

PEPD inhibitors [+1]

Active Org.

Memorial Sloan Kettering Cancer Center

Originator Org.

Memorial Sloan Kettering Cancer Center

Active Indication-

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with XPNPEP1

100 Translational Medicine associated with XPNPEP1

0 Patents (Medical) associated with XPNPEP1

114

Literatures (Medical) associated with XPNPEP1

07 Apr 2025·Gastroenterology

TL1A/DR3 signaling regulates the generation of pathogenic Th9 cells in experimental Crohn's disease.

Article

Author: Osme, Abdullah ; Buttó, Ludovica F ; Pizarro, Theresa ; Bamias, Giorgos ; Gomez-Nguyen, Adrian ; Cominelli, Fabio ; Menghini, Paola ; Aladyshkina, Natalia ; Chan, Ricky ; Wargo, Hannah L ; De Santis, Stefania ; Buela, Kristine-Ann

BACKGROUND AND AIMSDeath receptor 3 (DR3) and its ligand, tumor necrosis factor-like ligand 1A (TL1A), regulates the balance between effector and regulatory T cells in IBD. While IL-9-secreting Th9 cells are linked to ulcerative colitis, their role in Crohn's disease (CD) is unclear. We investigated the role of DR3 signaling in Th9 cell differentiation in mouse models of CD-like ileitis and colitis.METHODSPolarized Th9 cells with functional DR3 and DR3-deficient Th9 cells from SAMP WT (Th9_WT) and DR3^-/-×SAMP (Th9_KO) mice, respectively, were characterized and adoptively transferred into Rag2^-/- and SAMPxRag2^-/- recipients. Expression of Th9-associated molecules from experimental mice and IBD patients/controls was compared.RESULTSTh9_WT possess a pro-inflammatory profile compared to Th9_KO cells; conversely, ablation of DR3 signaling generates anti-inflammatory responses, as reflected by increased IL-10-producing cells in DR3^-/-×SAMP mice. RNA-seq and phosphoproteomic analyses show that inflammatory pathways are robustly activated in Th9_WT than in Th9_KO cells, while Th9 cells are detected in SAMP mice in vivo and Th9-related genes display the same expression patterns in both experimental ileitis and IBD patients. Finally, in the T-cell adoptive transfer model, Th9_KO cells are less colitogenic than Th9_WT, while IL-9 blockade diminishes the severity of intestinal inflammation, indicating a crucial role of functional DR3 receptor in the pathogenicity of Th9 cells.CONCLUSIONSWe demonstrate that functional DR3 receptor is essential for Th9 cell pathogenicity, revealing a new mechanism by which TL1A/DR3 signaling drives experimental CD-like ileitis. The TL1A/DR3/Th9 pro-inflammatory pathway may offer a novel therapeutic target for patients with CD.

01 Mar 2025·Prostate International

Sex hormones, blood metabolites and proteins mediating the causal associations between gut microbiota and prostatic diseases: evidences from Mendelian randomization study

Article

Author: Liu, Tianrui ; Wang, Zhige ; Zhang, Yang ; Zhang, Xiangyu ; Wang, Kun ; Meng, Jialin ; Mei, Yunyun ; Li, Hao ; Chen, Yiding ; Yang, Feixiang

BackgroundThe causal relationships between the gut microbiota and prostate cancer, prostatitis, and benign prostatic hyperplasia remain uncertain. We intend to identify the causal connections between the gut microbiota and prostatic diseases and investigate the potential mechanisms involved.MethodsA two-sample Mendelian randomization (MR) analysis was conducted to elucidate the impact of 196 gut microbiota on prostatic diseases risk. Reverse MR, linkage disequilibrium regression score (LDSC), and colocalization analyses were performed to strengthen causal evidence. Phenome-wide MR (Phe-MR) analysis was used to evaluate the potential side effects of targeting the detected gut microbiota. We designed a two-step MR study to assess the mediating effects of sex hormones, blood metabolites, and proteins.ResultsAccording to the MR analyses, 31 bacterial taxa were causally associated with prostatic diseases, of which 23 types were newly identified. In addition, Alphaproteobacteria restrained prostate cancer, Ruminococcaceae UCG009 prevented prostatitis, and Clostridiales posed a risk for benign prostatic hyperplasia. LDSC and colocalization analyses indicated that the detected associations were not confounded by genetic correlation or LD from common causal loci. In the mediation analysis, we identified 53 mediators linking the gut microbiota to prostatic diseases, with a specific emphasis on the critical roles played by sex hormones and blood metabolites, and identified 34 proteins that may be used as therapeutic targets, especially FGFR1 and XPNPEP1.ConclusionsOur study represents the first comprehensive exploration of the causal effects of the gut microbiota on prostatic diseases and reveals the mediating effects of sex hormones and blood metabolites on the "gut-prostate axis."

01 Feb 2025·Journal of Affective Disorders

Genomics-driven integrative analysis highlights immune-related plasma proteins for psychiatric disorders

Article

Author: Wang, Shukang ; Guo, Ping ; Zhou, Xiang ; Sun, Xiubin ; Liu, Shuai ; Liu, Lu ; Yan, Ran ; Gong, Weiming ; Xue, Fuzhong ; Yuan, Zhongshang

BACKGROUNDGenome-wide association studies (GWAS) have identified numerous variants associated with psychiatric disorders. However, it remains largely unknown on how GWAS risk variants contribute to psychiatric disorders.METHODSThrough integrating two largest, publicly available, independent protein quantitative trait loci datasets of plasma protein and nine large-scale GWAS summary statistics of psychiatric disorders, we first performed proteome-wide association study (PWAS) to identify psychiatric disorders-associated plasma proteins, followed by enrichment analysis to reveal the underlying biological processes and pathways. Then, we conducted Mendelian randomization (MR) and Bayesian colocalization (COLOC) analyses, with both discovery and parallel replication datasets, to further identify protein-disorder pairs with putatively causal relationships. We finally prioritized the potential drug targets using Drug Gene Interaction Database.RESULTSPWAS totally identified 112 proteins, which were significantly enriched in biological processes relevant to immune regulation and response to stimulus including regulation of immune system process (adjusted P = 1.69 × 10^-7) and response to external stimulus (adjusted P = 4.13 × 10^-7), and viral infection related pathways, including COVID-19 (adjusted P = 2.94 × 10^-2). MR and COLOC analysis further identified 26 potentially causal protein-disorder pairs in both discovery and replication analysis. Notably, eight protein-coding genes were immune-related, such as IRF3, CSK, and ACE, five among 16 druggable genes were reported to interact with drugs, including ACE, CSK, PSMB4, XPNPEP1, and MICB.CONCLUSIONSOur findings highlighted the immunological hypothesis and identified potentially causal plasma proteins for psychiatric disorders, providing biological insights into the pathogenesis and benefit the development of preventive or therapeutic drugs for psychiatric disorders.

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XPNPEP1

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