Ask about this productRelated genes to: Cpa3 Blocking Peptide
- Gene:
- CPA3 NIH gene
- Name:
- carboxypeptidase A3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3q24
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-13
- Date modifiied:
- 2015-12-16
Related products to: Cpa3 Blocking Peptide
Related articles to: Cpa3 Blocking Peptide
- : Allergic conjunctivitis (AC) is the most common inflammatory disease affecting the ocular conjunctiva. Tacrolimus (TCR), a potent calcineurin inhibitor, is limited by poor aqueous solubility and low ocular bioavailability. This study aimed to develop TCR-loaded cubosomes (TCR-Cubs) incorporated into HPMC/PVP K90 dissolving microneedles (MNs) to enhance their therapeutic efficacy. : TCR-Cubs were prepared using a modified top-down fragmentation method with glyceryl monooleate and poloxamer 407, optimized via Box-Behnken design, and incorporated into dissolving MNs. The system was evaluated in vitro, ex vivo, and in vivo using a rabbit model of allergic conjunctivitis. : The optimized formulation exhibited the smallest particle size (210 ± 0.91 nm), polydispersity index (0.29 ± 0.03), zeta potential (-21 ± 0.87 mV), and the highest entrapment efficiency (% 93.3 ± 0.45). The optimized formulation was incorporated into MNs via micro molding. Scanning electron microscopy (SEM) confirmed well-defined, sharp microneedles, with low height reduction (<10%) by mechanical testing and high penetration efficiency (>85-90%). In vitro release studies revealed sustained drug release of (~75-80%) over 24 h, compared to (~40%) from the TCR suspension, following diffusion-controlled kinetics. Ex vivo permeation studies showed a (~2-3-fold) enhancement in corneal drug flux. In vivo pharmacodynamic evaluation using an ovalbumin-induced allergic conjunctivitis model demonstrated significant reductions in inflammatory mediators, including inflammatory markers (TNF-α, IL-1β, IL-6, NLRP3), which were reduced by (~50-75%), with modulation of CPA3, BCL2, and TGF-β1 by qRT-PCR. Histopathology and TLR4 analysis confirmed reduced inflammation without irritation. : This dual-delivery system offers a promising, non-invasive platform for enhanced ocular delivery of tacrolimus with superior anti-inflammatory efficacy in allergic conjunctivitis. - Source: PubMed
Publication date: 2026/04/09
Elhabal Sammar FathyShoela Mai SHassan Fatma EAwad AbdelGhany Morsy SuzanAllam ShadyAldeeb Reem Abd ElhameedTaha Amal AnwarMostafa Abd El Galil RaniaM Emam AmrElzohairy Nahla AWanas HanaaHamdan Ahmed Mohsen Elsaid - Asthma is a chronic inflammatory respiratory disease characterized by significant heterogeneity, which complicates accurate patient classification and management. With the aim of defining new, reliable biomarkers, we previously evaluated the potential of 94 genes to differentiate allergic asthma (AA) from nonallergic asthma (NA) based on their expression in peripheral blood mononuclear cells (PBMCs). Here, the most promising biomarkers were further analyzed in a 2-year longitudinal cohort of 24 healthy controls (HCs), 18 NA patients, and 51 AA patients. - Source: PubMed
Publication date: 2026/03/26
Cremades-Jimeno LucíaLópez-Ramos MaríaBaos SelenFernández-Santamaría Rubénde Pedro María AMahíllo-Fernández IgnacioRosales-Ariza CristinaOlaguibel José MDel Pozo VictoriaCaballero María LLuna-Porta Juan AQuirce SantiagoBarroso BlancaBetancor DianaValverde-Monge MarcelaSastre JoaquínCárdaba Blanca - Allergic rhinitis, a common chronic inflammatory condition characterized by T-cell imbalance and mast cell hyperactivity, had not been investigated for the role of Lyn kinase within mast cells and its effects on T helper cell differentiation. α-Linolenic acid (ALA), a dietary supplement, exerts anti-allergic and anti-inflammatory effects. This study investigated the function of Lyn kinase in mediating mast cell-promoted Th17 cell differentiation during ALA treatment for allergic rhinitis. - Source: PubMed
Publication date: 2026/03/09
Wang YuejinYuan YujuanLuo ShiqiongWang ChaoGong LingDu HongfenJi XiaolanDing YuanyuanZhang Tao - Biomolecular condensates are membraneless bodies that organize biochemical reactions typically within cells. However, the roles of condensates in extracellular space-where conditions differ substantially from intracellular space-remain poorly understood. Here we report that mast cell extracellular granules (MCEGs), a stable membraneless entity, are condensates assembled through electrostatic interactions between glycosaminoglycans and polyamines. Disrupting polyamine synthesis or trafficking blocks MCEG formation and compromises the storage of proteases and cytokines. Granules reconstituted with heparin and spermine are sufficient to enrich mediators such as carboxypeptidase A3 (CPA3) and tumor necrosis factor (TNF), maintaining an elevated pH and higher concentrations of calcium and zinc compared to the extracellular milieu. This unique environment enhances CPA3 enzymatic activity. Furthermore, the granules increase TNF binding and its bioactivity toward endothelial cells. Together, we reveal MCEGs as functionally active biomolecular condensates with distinct biochemical and immunological properties; MCEGs are formed through sugar-metabolite interactions, expanding the mechanisms of condensate assembly beyond classical protein-protein and protein-RNA interactions. - Source: PubMed
Publication date: 2026/02/27
Xiong YiweiTomares Dylan TGuo JianjianSato KazukiZeng LonghuiTian YuanSu MaohanAlbis AvaPant AvnikaPappu Rohit VSu Xiaolei - Triple-negative breast cancers (TNBCs) are among the most aggressive breast tumors, due not only to the absence of clinically functional biomarkers used in other molecular subtypes, but also their marked heterogeneity and pronounced migratory and invasive behavior. The search for new molecules of interest for risk prediction, diagnosis and therapy stems from the class of long non-coding RNAs (lncRNAs), which often display context-dependent ("dual") functions and tissue specificity. Among them, lncRNA LINC01133 stands out for its dysregulation across cancer, although its molecular role in TNBC remains unclear. In the present study, we used the human TNBC cell line Hs578T to generate a cell panel comprising the parental line (Hs578T_wt), the control line (Hs578T_ctr), and the LINC01133 knockout line (Hs578T_ko). Subsequently, we performed bulk RNA-Seq to identify KO-associated Differentially Expressed Genes (DEGs) using as the primary contrast. Functional interpretation was achieved by Over-Representation Analysis (ORA) using Gene Ontology. We then conducted a comparative patient-cohort analysis using TCGA-BRCA Basal-like/TNBC cases (TCGA/BRCA n = 1098; Basal-like/TNBC n = 199), classified with the AIMS algorithm, and evaluated concordance between KO-associated signatures and patient tumor expression patterns via trend-based analyses across the LINC01133 expression levels and associated genes. A total of 265 KO-dominant DEGs were identified in Hs578T_ko, reflecting transcriptional changes consistent with tumor progression, with enrichment of pathways associated with LINC01133 knockout including cell adhesion, cell-cell interactions, epithelial-mesenchymal transition (EMT), and extracellular matrix (ECM) remodeling. The main DEGs included , , , , , , , , , and with additional candidates, such as and the lncRNA gene , which have been implicated in migration/invasion, ECM remodeling, or signaling across multiple tumor contexts. Translational analyses in TCGA-BRCA basal-like tumors suggested a descriptive association in which lower LINC01133 levels were accompanied by shifts in the expression trends of genes linked to ECM/EMT programs and modulation of genes related to cell adhesion and protease inhibition. : These results suggest a transcriptional model in which LINC01133 is associated with TNBC-related gene expression programs in a concentration-dependent manner, with loss of LINC01133 being associated with a transcriptomic shift toward pro-migratory/ECM remodeling signatures. While functional validation is required to establish causality, these data support LINC01133 as a molecule of interest in breast cancer research. - Source: PubMed
Publication date: 2026/01/24
Teodoro Júnior LeandroJesus-Ferreira Henrique César deSogayar Mari CleideNishiyama-Jr Milton Yutaka