Mouse Anti-Human CD44, FITC-labeled
- Known as:
- Mouse Antibody toHuman CD44, fluorecein-labeled
- Catalog number:
- 128-10039-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD44 FITC-labeled
Related genes to: Mouse Anti-Human CD44, FITC-labeled
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: Mouse Anti-Human CD44, FITC-labeled
Related articles to: Mouse Anti-Human CD44, FITC-labeled
- Chagas disease, caused by Trypanosoma cruzi, is characterized by a complex interplay between parasite persistence and host-driven immunopathology. Although the IL-33/ST2 axis is known to regulate type 2 immunity and tissue repair, its contribution to tissue homeostasis during chronic infection remains poorly understood. Using ST2-deficient (ST2) and wild-type BALB/c mice followed for up to 100 days postinfection, we investigated the role of IL-33/ST2 signaling in coordinating hepato-intestinal response and systemic immunity. ST2 deficiency induced coordinated systemic disturbances, including platelet expansion and hyperalbuminemia. At the tissue level, loss of ST2 exacerbated hepatic inflammation and fibrotic remodeling. In the colon, ST2 mice displayed increased nitric oxide production and enhanced parasite clearance, but developed marked structural alterations. Our findings suggest that IL-33/ST2 signaling is associated with regulatory programs. ST2 deficiency was associated with a reduction in patrolling monocytes, suggesting impaired homeostatic endothelial monitoring. This profile also coincided with inflammatory monocyte-derived dendritic cell differentiation and lowered macrophage regulatory activity. This altered profile was associated with amplified IL-12-driven Th1 and cytotoxic T-cell responses while impairing IL-10-associated regulatory niches, resulting in multiorgan inflammation. These findings suggest that IL-33/ST2 signaling may contribute to immunoregulatory balance during T. cruzi infection and identify this axis as a candidate pathway for future mechanistic and therapeutic investigation. - Source: PubMed
Cardozo Marcelo EduardoCirilo Tatyane Martinsda Rocha Rihs José BryanSouza Jorge Lucas Nascimentode Brito Duval IsabelaAntunes-Porto Ana Rafaelado Amaral Luisa Vitor BragaOliveira Fernando Bento RodriguesRicci Mayra Fernandade Oliveira Santos Laura LisSantana Lívia Fernanda DiasSilva Luiza PinheiroAmorim Chiara Cássia OliveiraLemos Gabriela Gomes MonteiroJunior Getulío Mota E Silvada Silva Oliveira IzabelaDos Reys Marina Possade Oliveira Ana Laura GrossiCassali Geovanni DantasMagalhães Luisa Mourão DiasBueno Lilian LacerdaMachado Fabiana SimãoFujiwara Ricardo Toshio - Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Targeting cancer cells using functionalized nanoparticles has gained attention. In this study, the anticancer potential of Iron oxide NPs functionalized with Glucose and co-conjugated with Hyaluronic acid and trans-Chalcone (FeO@Glu-HA-TC NPs) and their influence on the expression of the lncRNAs ANRIL and ANCR was investigated. The synthesized NPs were characterized by FT-IR, XRD, SEM, EDS, DLS, zeta potential, TGA and VSM analysis. Viability level of the HepG2 and HDF cell lines was studied by MTT assay and cell cycle phases and apoptosis/necrosis percentage and ROS levels in the HepG2 cell treated with FeO@Glu-HA-TC NPs were determined. Relative expression of the lncRNAs ANCR and ANRIL was determined by Real-Time PCR assay. The NPs were spherical, moderately agglomerated, with an average particle diameter of 42.05 nm, surface charge of -56.8 mV, hydrodynamic size of 150.9 nm and saturated magnetization at 38.88 emu/g. Fe₃O₄@Glu-HA-TC NPs exhibited greater cytotoxicity toward HepG2 cells compared to normal HDF cells with an IC of 255 and 488.79 µg/mL, respectively. Exposure to the NPs caused an apparent blockage at the sub-G1 phase, notably elevated early and late apoptosis (as observed in a representative flow cytometry experiment), and induced ROS generation by approximately 3.4-fold. In addition, treatment with FeO@Glu-HA-TC NPs significantly upregulated the lncRNA ANCR (1.52-fold) while slight downregulation the ANRIL (0.89-fold). The present work provides evidence that Fe₃O₄@Glu-HA-TC NPs induce cytotoxicity, cell cycle arrest, and apoptosis in HepG2 cells, with associated ROS generation and lncRNA expression changes. However, mechanistic validation (e.g., antioxidant rescue, lncRNA functional assays) is needed to establish causality. It should be noted that while hyaluronic acid functionalization was employed as a rationale for potential CD44-mediated uptake, direct evidence of receptor-mediated targeting was not obtained in this study. - Source: PubMed
Publication date: 2026/07/04
Daghari MaryamSalehzadeh AliPourahmad AfshinYari Reza - Silicosis is an incurable fibrotic lung disease caused by crystalline silica exposure. Aberrant activation of lung fibroblasts into pathological fibroblasts is a hallmark of silicosis. CTHRC1 has been considered a novel fibroblast activation biomarker. This study sought to explore CTHRC1's role in silicosis and determine the signaling pathways it modulates. A combination of transcriptomic analysis of clinical samples, LC-MS/MS, Co-IP, and cationic nanoliposome-based techniques was utilized. In vitro models of lung fibroblast activation induced by TGF-β1, PDGF or recombinant CTHRC1 (rCTHRC1), as well as in vivo models of pulmonary fibrosis induced by silica or bleomycin in mice were established. RNA sequencing, Western blot, RT-qPCR, AlphaFold2 analyses and rescue experiments using siCTHRC1, siCD44, CTHRC1 plasmids, and the PI3K activator 740 Y-P were performed to explore the underlying mechanisms. CTHRC1 is a significantly dysregulated gene implicated in myogenesis and ECM-related pathways. Mechanistically, lymphoid enhancer-binding factor 1 (LEF1) exerts its transcriptional regulator role by binding to the CTHRC1 promoter region in TGF-β1-activated fibroblasts. Further, CTHRC1 mediates its pro-fibroblast-to-myofibroblast transition function by directly binding to the CD44 receptor. AlphaFold2 analyses revealed the binding between CTHRC1 and CD44 is accomplished by three critical CD44 residues: Arg41, Asn172, and Trp650. Rescue experiments demonstrated that the CTHRC1-CD44 complex exerts its pro-fibrotic effects through AKT signaling. In vivo, liposomal Cthrc1 siRNA mitigated fibrogenesis in both silica- and bleomycin-induced mouse fibrosis models. Our results uncover a previously unrecognized role of the LEF1-CTHRC1-CD44 axis in silicosis and highlight the therapeutic target potential of CTHRC1 in fibrotic lung diseases. - Source: PubMed
Publication date: 2026/07/04
Wang TingSun WenqingYang QingyanJia XinyingLian WenxiuMeng FanqingChen JingyuXu ShangchengLiu YiNi Chunhui - Selective intracellular activation of anticancer agents while minimizing toxicity toward non-target tissues remains a major challenge in drug delivery systems (DDSs) and prodrug design. In this study, we designed a hyaluronic acid-based prodrug system, HA-Ns-Dox, that integrates receptor-mediated cellular uptake with intracellular glutathione (GSH)-responsive activation. A doxorubicin (Dox) prodrug modified with a 2-nitrobenzenesulfonyl (Ns) group was synthesized and subsequently conjugated to hyaluronic acid (HA) via click chemistry to generate HA-Ns-Dox with both CD44-targeting capability and GSH-responsive activation properties. HA-Ns-Dox formed stable nanosized assemblies in aqueous solution and exhibited high stability under low-GSH conditions mimicking extracellular environments, whereas concentration-dependent activation of Dox was observed under high-GSH conditions mimicking intracellular reductive environments. In vitro studies demonstrated that HA-Ns-Dox was selectively internalized into the CD44-high human breast cancer cell line MDA-MB-231, accompanied by intracellular prodrug activation and nuclear accumulation of Dox. In contrast, cellular uptake and activation were minimal in the CD44-low cell line MCF-7, and cytotoxicity was significantly suppressed even at high concentrations. Cytotoxicity studies further revealed that HA-Ns-Dox exhibited significant antiproliferative activity in CD44-high cells while substantially reducing toxicity toward non-target cells. Collectively, these findings demonstrate the potential of combining CD44-targeted delivery with GSH-responsive prodrug activation to improve cancer cell selectivity. - Source: PubMed
Publication date: 2026/07/04
Yukimura TomonaSeki TomohiroSeki Toshinobu - Hepatocellular carcinoma (LIHC) features a complex tumor microenvironment (TME) where tumor-associated neutrophils (TANs) show significant plasticity. The role of aggrephagy-selective autophagy of protein aggregates-in shaping neutrophil heterogeneity and LIHC progression remains poorly understood. - Source: PubMed
Publication date: 2026/07/04
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