Rat Anti-Mouse CD44
- Known as:
- Rat Antibody toMouse CD44
- Catalog number:
- 128-10036-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD44
Related genes to: Rat Anti-Mouse CD44
- 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: Rat Anti-Mouse CD44
Related articles to: Rat Anti-Mouse CD44
- Colorectal cancer (CRC) remains therapeutically challenging due to high metastasis, recurrence, and immunotherapy resistance driven by tumor microenvironment-mediated immune evasion. Immunogenic cell death (ICD) offers a promising strategy to reshape the immune microenvironment, yet existing ICD inducers suffer from poor targeting efficiency and insufficient death signal release. Here, we constructed a calcium overload-based smart nanosystem, HA-HAP@CUR, to achieve highly efficient ICD induction via a triple-effect mechanism: hyaluronic acid (HA)-mediated CD44 targeting enables tumor-selective accumulation; pH-responsive hydroxyapatite (HAP) degradation releases Ca in the acidic tumor microenvironment; and curcumin (CUR) amplifies intracellular calcium overload by promoting endoplasmic reticulum Ca release, collectively establishing a positive feedback loop disrupting calcium homeostasis. Mechanistically, calcium overload induces mitochondrial membrane potential dissipation and sustained mPTP opening, triggering mitochondrial oxidative stress and energy metabolic disorders. This mitochondrial crisis concurrently activates caspase-3, GSDMD, and RIPK1, synergistically initiating apoptosis, pyroptosis, and necroptosis, ultimately converging into PANoptosis with potent immunostimulatory potential. This strategy, encompassing targeted accumulation, calcium storm activation, and multi-modal cell death synergy, provides a biologically precise approach to overcoming immunotherapy resistance in CRC. - Source: PubMed
Publication date: 2026/05/06
Xiao YaoYang YuxuanQiu HaosenYang JiaLiang HaoJiang ZhaojunTong XiaoLi YongyingHuang QunfengWu JiamingLin TianYu JiangLiang Min - Traditional metal-organic frameworks (MOFs) suffer from limited responsiveness to the complex tumor microenvironment, systemic toxicity from non-specific distribution, and compromised Fenton-like efficiency due to antioxidants. To address these, we propose a multi-modal synergistic strategy to functionalize MOFs and achieve chemodynamic and photothermal synergy without chemotherapeutics. A replacement MOFs system (FHMGA) integrated with hyaluronic acid, glucose oxidase, and gold nanoparticles is designed based on CD44 receptor recognition. In the acidic TME, FHMGA degrades and is reduced by overexpressed glutathione to Fe and Mn for further reaction with endogenous HO via Fenton-like reactions to generate ·OH and induce oxidative stress. Under near-infrared irradiation, gold nanoparticles exhibit high photothermal conversion efficiency, triggering local hyperthermia for thermal ablation. Simultaneously, heat enhances glucose oxidase-powered catalysis, which catalyzes glucose oxidation in cancer cells to disrupt energy metabolism and produce additional HO, further boosting Fenton-like reactions. Our results demonstrate that FHMGA exhibits significant anti-tumor efficacy with minimal systemic toxicity. The triple synergy of oxidative damage from chemodynamic therapy, thermal ablation from photothermal therapy, and metabolic disruption via glucose oxidase significantly inhibits cancer cell growth by overcoming antioxidant-mediated limitations. Self-amplifying Fenton catalysis, while responsive degradation reduces systemic toxicity. This work advances precise cancer therapy by establishing a chemotherapy-free, multi-responsive synergistic system, addressing critical bottlenecks of ferrium-based MOFs and providing a safer, more effective strategy for tumor-specific treatment. - Source: PubMed
Publication date: 2026/05/06
Xin ShengnanLiu ZheWang JinghanWu YanhuaJiang ZiyiCui JielinWang DandanGong Peiwei - Spontaneous ovarian hyperstimulation syndrome (OHSS) is closely associated with follicle stimulating hormone receptor (FSHR) functional mutations. We observed that estrildid finches naturally carry the gain-of-function FSHR p.Thr449Ala mutation found in humans, yet do not develop OHSS, thereby providing a novel and system to study aspects of OHSS prevention. Cross-species single-cell analysis revealed that macrophages, the most abundant immune cells in ovaries, play a pivotal role in OHSS progression. Macrophage depletion exacerbates the manifestations of OHSS in both birds and rats. Pharmacological activation of the G protein-coupled receptor 183 (GPR183) in ovarian macrophages, significantly alleviates OHSS symptoms. Mechanistically, GPR183 activation in macrophages maintains ovarian immune homeostasis by downregulating inflammatory factors (Interleukin 1 alpha: IL1A, Interleukin 6: IL6, Interleukin 1 beta: IL1B) and upregulating immune regulators responsive to external stimuli (sphingomyelin phosphodiesterase acid like 3A: Smpdl3a, Macrophage-expressed gene 1: Mpeg1, Epithelial stromal interaction 1: Epsti1, Unc-93 homolog B1: Unc93b1, Apolipoprotein B mRNA editing enzyme catalytic subunit 1: Apobec1). It markedly altered CD44 molecule (CD44)/Syndecan-4 (SDC4) -mediated intercellular communication between macrophages and endothelial/stromal cells, thereby modulating the ovarian microenvironment. This study identifies ovarian macrophages as a key therapeutic target for OHSS and proposes GPR183 as a novel receptor target for precision macrophage-based interventions. - Source: PubMed
Publication date: 2026/05/05
Yan XiaofeiHuang YongjieYang JiabaoMa SuLiu SongsongHuang XuanBrosius JuergenZheng HuapingYao BingChen LiLai ShanshanDeng Cheng - The fat mass and obesity-associated protein (FTO), an N6-methyladenosine (m6A) demethylase, plays a crucial role in various cancers. This study investigates its expression and functional role in bladder cancer (BCa). Analysis of TCGA data and validation in BCa cell lines revealed that FTO is significantly overexpressed in bladder cancer tissues and is associated with poor overall and disease-free survival. Functional assays demonstrated that knockdown of FTO markedly increased global m6A RNA methylation and suppressed the proliferation, migration, invasion, and colony formation of BCa cells in vitro. Furthermore, FTO depletion significantly inhibited tumor growth and experimental liver colonization in nude mouse xenograft models. Mechanistically, transcriptomic analysis of FTO-high patient tissues and FTO-knockdown cells revealed a strong association between FTO and epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) pathways. Consequently, FTO knockdown impaired the self-renewal capacity of BCa cells and downregulated the expression of key stemness genes (CD133, CD44, Nanog, OCT4). These findings suggest FTO is a critical oncoprotein that promotes bladder cancer progression and stemness-associated phenotypes, highlighting its potential as a therapeutic target and prognostic marker. - Source: PubMed
Publication date: 2026/05/02
Wu NapingHe Xiaozhou - This study aims to examine the role of exosomes derived from human urine-derived stem cells (hUSCs-Exo) in the construction of a composite structure comprising hUSCs and a porcine urethral decellularized matrix. hUSCs-derived exosomes were isolated and characterized, and hUSCs were treated with varying exosome concentrations to assess migration using scratch and Transwell assays. Dio-labeled hUSCs were seeded onto porcine urethral decellularized matrices and grouped by exosome concentration (0, 50, 100 μg/mL). Cell proliferation and distribution were examined under a fluorescence inverted microscope on days 1, 3, and 7. On day 7, samples were paraffin-embedded for histological analysis of cell integration. hUSCs with mesenchymal stem cell (MSC) properties were successfully isolated, and exosomes extracted via centrifugation. hUSCs-exosome (Exo) enhanced cell migration but did not significantly affect proliferation. Dio-labeling and H&E staining confirmed hUSC presence and attachment to the urethral matrix, while CD44 immunohistochemistry confirmed the presence and attachment of hUSCs within the scaffold. Exosomes derived from hUSCs did not significantly enhance cell proliferation in the construction of the porcine urethral decellularized matrix-hUSC complex. The specific exosomal cargo responsible for these differential effects on migration versus proliferation was not examined in this study and will be the focus of future investigations. - Source: PubMed
Publication date: 2026/05/04
Zhang Kai-YueZhong HaoMa Wei-DeYang Xiao-YanHan Li-ZhongLiu Zhi-Zhong