Mouse Anti-Human CD44
- Known as:
- Mouse Antibody toHuman CD44
- Catalog number:
- 128-10035-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD44
Related genes to: Mouse Anti-Human 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: Mouse Anti-Human CD44
Related articles to: Mouse Anti-Human CD44
- First-generation vaccine candidates against leishmaniasis, based on chemically or physically inactivated whole parasite, have attracted considerable attention owing to their feasibility, scalability of production, and comparatively low manufacturing costs. Vaccine formulations typically require immunostimulatory compounds to elicit robust cell-mediated immunity. Traditionally, adjuvants have been incorporated into vaccine formulation to augment their immunogenic potential. Recent advances over the past decade have yielded novel adjuvant system capable of stimulating both antibody-mediated and cell-mediated immune pathways. Recent advances in adjuvant development have facilitated the design of several promising vaccine candidates against leishmaniasis. Therefore, in the present study, we tested tomatine (identified as a steroidal glycoalkaloid, a saponin subgroup), for its ability to induce cell-mediated immunity that confer protection against leishmaniasis. Tomatine, a glycoalkaloid based adjuvant, possesses the ability to elicit cytotoxic T-lymphocyte responses. It shows remarkable potential as an effective adjuvant candidate for vaccine applications targeting infectious pathogens. Our results demonstrated that tomatine combined with the first-generation antigen induced durable central (CD44CD62L) and effector (CD44CD62L) memory CD4⁺ and CD8⁺ T-cell responses in both pre-challenge and post-challenge mice, indicating the development of long-lasting protective cellular immunity. Significant protective immunity was further demonstrated in the vaccinated animals, as evidenced by remarkably declined parasite burden, increased levels of T cells (CD4, CD8), IFN-γ, GM-CSF, effector molecules i.e. reactive oxygen species and nitric oxide and heightened NF-kB and iNOS gene expression. Collectively, these findings highlight tomatine as an effective immunomodulatory adjuvant capable of inducing cell-mediated protective immunity against leishmaniasis. - Source: PubMed
Publication date: 2026/09/30
Saini IshaKaur Sukhbir - Breast cancer is the most commonly diagnosed cancer worldwide and a leading cause of cancer-related mortality in women. Despite therapeutic advances, treating advanced or recurrent cases is substantially hampered by drug resistance and the immunosuppressive tumor microenvironment (TME). Here, we report a breakthrough immunotherapeutic strategy using dual-targeted extracellular vesicles from pro-inflammatory M1 macrophages, hyaluronic acid (HA), and cyclic RGD (M1EV_HA/cRGD), which function as molecular bridges to physically link natural killer (NK) cells with cancer cells. Our platform simultaneously reprograms the hostile TME while activating potent antitumor immunity. HA is incorporated to engage CD44 receptors on NK cells and cRGD peptides to bind tumor-overexpressing integrins, establishing precision dual-targeting. M1EV_HA/cRGD could physically tether NK cells directly to tumors, and deliver inflammatory cytokines and miRNAs that transform the immunosuppressive TME into a pro-inflammatory battlefield, substantially amplifying immune activation. In vitro and in vivo studies demonstrate that M1EV_HA/cRGD significantly enhances NK cell clustering at tumor sites, activation status, and cytotoxic killing of breast cancer cells. Unlike single-targeted approaches, this dual-targeting mechanism achieves simultaneous TME reprogramming and enhanced immune-tumor engagement. M1EV_HA/cRGD is a paradigm shift in solid tumor immunotherapy that directly addresses breast cancer treatment failure, can overcome therapeutic resistance, and substantially improve patient survival outcomes. - Source: PubMed
Kang Su JinBaek GichanJu SuwunKim GunheeGwak SeongjinRhee Won Jong - During the practice of diagnostic pathology, we identified a case of invasive ductal carcinoma (IDC) of the breast with lung metastases exhibiting a ductal carcinoma in situ (DCIS)-like morphology. Immunohistochemistry confirmed the presence of CK5/6, P40 and P63-positive tumor cells at the periphery of the metastatic nests. Subsequent expansion of our sample revealed similar DCIS-like morphology in lymph node metastases of other IDC cases. This study aimed to preliminarily characterize the pathological features, significance, and mechanisms of this phenomenon. - Source: PubMed
Publication date: 2026/09/30
Lin XinFan MingmeiLiu JingquanLong TingGao LingfangWu HaibinZhong YanLin WenwenWang RuianLi ZuguoChen Meihua - Progressive disease (PD) remains the dominant barrier to cure in high-risk neuroblastoma (HR-NB), driven in part by profound post-transcriptional deregulation that fuels clonal evolution, stemness, immune evasion, and therapy resistance. In this study, we define the molecular architecture of PD-associated microRNA (miR) collapse and demonstrate that radiotherapy (RT) acts as a potent post-transcriptional reprogrammer capable of reversing this trajectory. - Source: PubMed
Narayanan SivasubramaniSubramanian PoorviMohanvelu SreenidhiAravindan SheejaPeriyasamy LoganayakiAravindan Natarajan - Metastasis remains the leading cause of cancer-related mortality, a process in which circulating tumor cells (CTCs) play a central but incompletely understood role. Although most CTCs are rapidly eliminated during circulation through detachment-induced anoikis and fluid shear stress (SS)-triggered apoptosis, a subset of CTCs can survive these hostile conditions; however, the underlying mechanisms remain poorly defined. To investigate this, we developed a microfluidic circulatory system that mimics physiological SS and performed transcriptomic profiling of A549 lung cancer cells under SS, attached, and static suspension conditions. Through this approach, we identified the ROS-CD44-Ezrin axis as a potential mechanosignaling module that may contribute to CTC survival under shear stress. In this cascade, SS-induced ROS and CD44 converge to activate Ezrin via phosphorylation at Thr567. Once activated, Ezrin appears to coordinate its two canonical functions-membrane-cytoskeleton reinforcement and pro-survival signaling via PI3K/AKT/Bcl-2 and NF-κB/p38/JNK pathways-within this specific mechanobiological context to preserve cell integrity and limit apoptosis. Our findings suggest that these well-established molecular functions are differentially engaged under shear stress, revealing a context-dependent survival mechanism that may offer opportunities for therapeutic exploration, pending further validation in more clinically relevant models. - Source: PubMed
Publication date: 2026/09/03
Zhang XiaoyingZhou MuyaLi KoukouYuan MinghengTong HaiboLuo Kathy Qian