Ask about this productRelated genes to: PRSS23 Blocking Peptide
- Gene:
- PRSS23 NIH gene
- Name:
- serine protease 23
- Previous symbol:
- -
- Synonyms:
- SPUVE, SIG13
- Chromosome:
- 11q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-09
- Date modifiied:
- 2018-01-19
Related products to: PRSS23 Blocking Peptide
Related articles to: PRSS23 Blocking Peptide
- Epigenetic modifications have been linked to atherosclerotic cardiovascular disease and could constitute therapeutic targets. - Source: PubMed
Publication date: 2026/06/03
Ingold MarkusMüller CelineKrolevets MykhailoYapıcı ElifRapp SteffenSchuster Alexander KTesarz JonasHeinrich IsabelWeinmann-Menke JuliaStrauch KonstantinLackner Karl JKonstantinides StavrosRuf WolframAndrade-Navarro Miguel ANiehrs ChristofGori TommasoLurz PhilippWild Philipp STen Cate Vincent - Protease-activated receptor 2 (PAR) mediates oral cancer pain. Patients with metastatic (N + ) cancers report greater pain. PAR is activated by N-terminal proteolytic cleavage. Here we show that proteases encoded by genes overexpressed in N+ cancers from patients with pain (matrix metallopeptidase 1, MMP1 and serine protease 23, PRSS23) elicit protease-specific receptor redistribution (trafficking) and signaling that differs from that promoted by proteases encoded by genes not differentially expressed (transmembrane serine protease matriptase, ST14 and cathepsin S, CTSS). Mixtures of the proteases prepared to model the oral cancer microenvironment revealed that ST14-mediated PAR activation predominated at low protease concentrations. At high concentrations, MMP1 and PRSS23 prevailed over the greater potency of ST14. We propose that PAR activation in oral N+ cancers from patients with pain is driven by high levels of MMP1 and PRSS23. Our study informs design of signaling and location-specific antagonists to provide more efficacious analgesia. - Source: PubMed
Publication date: 2026/05/11
Ramírez-García Paulina DDolgalev IgorDubeykovskaya ZinaidaLatorre RoccoArbex LeticiaTu Nguyen HuuSchmidt Brian LAlbertson Donna G - Ovarian cancer metastasizes via peritoneal dissemination, requiring tumor cells to resist detachment-induced cell death (anoikis) in suspension and to reinitiate proliferation after seeding. Because disseminating ovarian cancer cells persist in malignant ascites enriched in extracellular S1 family serine proteases, we surveyed S1 protease gene expression across ovarian cancer cohorts to identify those most associated with poor outcomes. High expression of multiple family members was associated with poor survival, with HTRA3, TMPRSS12, and PRSS23 among the strongest hits. TMPRSS12 transcripts were below the limit of detection in our cell line panel, while HTRA3 depletion showed modest, histotype-dependent effects. In contrast, PRSS23 knockdown reduced proliferation and increased anoikis sensitivity in high-grade serous and clear cell ovarian carcinoma cell lines and diminished tumor establishment, dissemination, and ascites in intraperitoneal xenograft models. RNA-seq of PRSS23-depleted cells revealed a conserved program of reduced cell-cycle/DNA repair gene expression with induction of inflammatory and adhesion/epithelial-mesenchymal transition pathways. Endogenous epitope tagging demonstrated that PRSS23 is synthesized as a precursor and secreted as a processed, glycosylated protease homology domain that retains the catalytic triad yet lacks the canonical Ile16-Asp194 zymogen activation switch. In complementary biochemical assays, PRSS23 showed no detectable serine hydrolase activity in either activity-based probe labeling of conditioned media or chromogenic peptide substrate assays using the recombinant protease domain. Furthermore, protumorigenic phenotypes persisted after mutation of the putative catalytic serine. Together, these findings demonstrate protease-independent PRSS23 function in ovarian cancer peritoneal dissemination and suggest that PRSS23 may ultimately warrant reclassification as a serine pseudoprotease. - Source: PubMed
Publication date: 2026/04/14
Akhtar SharoonCoban MattMiller ErinHockla AlexandraMaina EranMehner ChristineIlic StefanPapo NivRadisky Derek CRadisky Evette S - Esophageal squamous cell carcinoma (ESCC) is a common digestive tract tumor influenced by tumor-associated macrophages (TAMs), which promote progression through M2 polarization. Analysis of GSE75241 showed that PRSS23 was significantly upregulated in ESCC samples compared with non-tumors (n = 15). Its high expression corresponded to poorer overall survival in macrophages-enriched ESCC patients (Log-rank p = 0.04). Furthermore, PRSS23 expression was elevated in ESCC tissues compared with normal controls (n = 12) and positively correlated with CD206 expression (n = 14), suggesting a potential role for PRSS23 in ESCC progression via the regulation of TAMs. PRSS23 knockdown suppressed the malignant phenotype of ESCC cells, including proliferation, migration, and invasion. In vivo, nude mice bearing PRSS23-silenced ESCC cells developed smaller tumors with fewer M2-type TAMs. Consistently, PRSS23 knockdown impaired macrophage chemotaxis and M2 polarization in co-culture with ESCC cells. Zinc finger E-box binding homeobox 1 (ZEB1) was predicted as an upstream regulator of PRSS23. Overexpression of ZEB1 increased the transcriptional activity of the PRSS23 promoter (–1110 ~ + 15 bp) by 2.55-fold compared to the vector control, confirming ZEB1 as a positive transcriptional regulator. Notably, PRSS23 knockdown rescued the promoting effects of ZEB1 overexpression on ESCC cells and macrophage M2 polarization. Further transcriptomic analysis of macrophages suggested that PRSS23 mediates M2 polarization through the Wnt/β-catenin pathway. Accordingly, PRSS23 knockdown inhibited both Wnt/β-catenin signaling and M2 polarization in co-cultured macrophages, effects that were reversed by the Wnt/β-catenin agonist SKL2001. Collectively, our findings showed that the ZEB1/PRSS23 axis promotes ESCC progression by driving M2 polarization of TAMs, offering a potential therapeutic target for ESCC treatment. - Source: PubMed
Publication date: 2026/04/10
Chen WeiChen ChanjuanHu ZhongyunLi FanfanPeng YaoZhang Mingjun - : Broodiness is a major limiting factor for reproductive efficiency in indigenous avian breeds, a phenomenon underpinned physiologically by granulosa cell (GC) apoptosis and subsequent follicular atresia. While Serine Protease 23 (PRSS23) has been implicated in mammalian ovarian remodeling, its specific regulatory function in avian follicular dynamics remains elusive. : Utilizing the Wuding chicken-an indigenous breed distinguished by robust environmental adaptability but compromised by high broodiness frequency-as a biological model, this study dissected the molecular mechanism of PRSS23-mediated follicular regression. We cloned the complete coding sequence of the Wuding chicken gene, characterized its spatiotemporal expression profile, and interrogated its function in primary GCs via gain- and loss-of-function assays. : RT-qPCR analysis revealed that is differentially expressed across the hypothalamic-pituitary-ovarian (HPO) axis, with ovarian expression being significantly upregulated during the broody period compared to the laying period. Mechanistically, overexpression significantly downregulated the expression of follicle-stimulating hormone receptor () and key steroidogenic enzymes (, , ), thereby suppressing the expression of genes governing the biosynthesis potential of progesterone and estradiol. Concurrently, overexpression was associated with transcriptional repression of components of the PI3K/AKT/mTOR signaling cascade; this transcriptional regulation further induced cell cycle arrest at the G0/G1 phase, and activated the mitochondrial apoptotic pathway characterized by upregulation and downregulation. Conversely, siRNA-mediated knockdown of alleviated these inhibitory effects, promoting GC proliferation and survival. : These findings establish as a pivotal pro-atretic factor in Wuding chickens, driving ovarian atrophy through the dual transcriptional-level inhibition of steroidogenesis and survival signaling pathways. This study identifies a potential molecular target for marker-assisted selection programs aimed at attenuating broodiness while preserving the superior meat quality traits of indigenous poultry. - Source: PubMed
Publication date: 2026/02/27
Wang CailingZhu WeiWan EnminLi JindaFan XinyangMiao Yongwang