Anti-Human_Mouse CD44 FITC 50 ug
- Known as:
- Antibody toHuman_Mouse CD44 fluorecein 50 ug
- Catalog number:
- 11-0441-81
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human_Mouse CD44 FITC 50
Related genes to: Anti-Human_Mouse CD44 FITC 50 ug
- 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: Anti-Human_Mouse CD44 FITC 50 ug
Related articles to: Anti-Human_Mouse CD44 FITC 50 ug
- Oral squamous cell carcinoma (OSCC) is a significant public health issue. While tobacco and alcohol are established risk factors, the role of human papillomavirus (HPV) in oral carcinogenesis remains debated. Cancer stem cells (CSCs) are implicated in tumor aggressiveness and therapy resistance. This study investigated the correlation between HPV infection, CSC marker expression (CD44, CD98, ALDH1), and clinicopathological parameters in tongue SCCs. - Source: PubMed
Publication date: 2026/08/16
da Silva Adriely PrimoSartori Beatriz Gomes Carreirade Barros Gigliotti Vendramini CarolinaNunes Adauto José FerreiraNogueira Maria Renata Sales - Pancreatic tumors are characterized by a prominent desmoplastic stroma that can account for up to 90% of the tumor. Given the marked upregulation of CD44, a family of transmembrane glycoproteins, in pancreatic cancer-associated fibroblasts (CAFs), we investigated its role in regulating myofibroblastic and inflammatory CAF phenotypes. Conditional deletion of Cd44 in fibroblastic cells in Cd44;PdgfrβCreER mice significantly reduced tumor growth and was associated with a significant reduction in intratumoral regulatory T cells (T). Consistently, in human CAFs CRISPR/Cas9-edited to delete CD44, the fibroblasts' morphology changed drastically: CAFs lost their elongated phenotype and adopted a round shape, reflecting their inactivation. This was accompanied by a significant downregulation of activation markers, unresponsiveness to exogenous stimuli, and reduced contractile activity. Furthermore, CD44 ablation decreased extracellular matrix production and altered the immunomodulatory cytokine secretion, highlighting its role in both fibrosis and immune regulation. Finally, CD44-deficient CAFs exhibited a reduced capacity to suppress anti-tumor immune responses by failing to induce immunosuppressive programs in dendritic cells (DCs) and by increasing cytotoxic T cell (CTL)-mediated tumor cell killing. Collectively, we identify CD44 as a regulator of CAF activation and immunosuppressive function, linking stromal remodeling to immune evasion in pancreatic cancer and supporting CD44 as a potential therapeutic strategy to reprogram the tumor stroma and enhance anti-tumor immunity. - Source: PubMed
Publication date: 2026/08/15
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Publication date: 2026/08/10
Shi JinfengZhang XueqianYang LinxingWang WeiLiu LinglingLu TianXu XingXu YanRen ShiyuLuo Ruifeng - The high rates of recurrence and metastasis in colorectal cancer (CRC), coupled with its immunosuppressive tumor microenvironment (TME), severely constrain patient survival. To overcome the limitations of monotherapies, this study developed a multifunctional targeted nanoplatform (RLHMnH). This system consists of a hyaluronic acid (HA)-modified hollow manganese dioxide (H-MnO) nanocarrier co-loaded with the anti-angiogenic drug Regorafenib (Reg) and the nitric oxide precursor L-Arginine (L-Arg) for synergistic triple therapy against CRC. The platform leverages HA-mediated CD44 receptor targeting to achieve enhanced tumor accumulation. Within the TME, the H-MnO framework undergoes rapid responsive decomposition. On one hand, Within the acidic and GSH-rich TME, H-MnO undergoes reductive degradation to release Mn, concomitantly depleting GSH and disrupting redox homeostasis. The released Mn further catalyzes Fenton-like conversion of endogenous HO into highly cytotoxic ·OH, thereby inducing oxidative damage and tumor cell apoptosis. On the other hand, the concomitantly released Reg effectively blocks tumor angiogenesis by inhibiting the VEGFR2 signaling pathway, while L-Arg generates nitric oxide, synergistically reversing drug resistance, alleviating hypoxia, and activating anti-tumor immunity. Both in vitro and in vivo experiments demonstrated that RLHMnH, through integrating the triple synergistic mechanisms of CDT, anti-angiogenesis, and gas therapy, achieved a remarkable tumor inhibition rate of ∼75% in a CT26 xenograft model and potently suppressed CT26 cell viability to below 20% at 72 h, showcasing significant suppression of CRC. This study provides an innovative nano-carrier-based synergistic strategy to overcome the current therapeutic bottlenecks in CRC treatment. - Source: PubMed
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Publication date: 2026/02/28
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