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
- Gastric cancer is a heterogeneous disease in which cancer stem cell-associated properties may contribute to tumor heterogeneity and progression. This study aimed to establish paired normal and tumor gastric organoids, characterize stemness-related gene expression, and explore its association with organoid formation. - Source: PubMed
Publication date: 2026/08/31
Yoo Yie-RiJeong KyoungyunYoo JaeunKim Hyun MyongShin Ji-YeonKang Min KyuPark KyoyoungKim Sa-HongKim ChungyoonKim JeesunPark Young SukKong Seong-HoLee Hyuk-JoonYang Han-KwangPark Do Joong - Minichromosome maintenance protein 2 (MCM2) is a key regulator of DNA replication and has been implicated in tumor progression. While previous studies have demonstrated its role in lung cancer stem cells (CSCs), its role in breast cancer remains unclear. This study aimed to investigate whether MCM2 regulates CSCs and epithelial-mesenchymal transition (EMT) in breast cancer. - Source: PubMed
Publication date: 2026/08/31
Kim Rae-Kwon - Natural killer (NK) cell-based immunotherapies are promising for cancer treatment due to their ability to eliminate cancer cells independently of antigen presentation and "off-the-shelf" utility. However, molecular determinants governing tumor susceptibility to NK cytotoxicity remain incompletely understood. Here we employ CRISPR activation (CRISPRa) screening to identify cancer cell surface regulators of NK killing. Using a surfaceome-focused library, we screen human and murine cancer cell lines co-cultured with NK cells, identifying known and novel ligands modulating NK cytotoxicity. Screens reveal established factors including CD43 and previously uncharacterized regulators CD44, PDPN, and Siglec-1/CD169. Validation with orthogonal approaches confirm that disruption of these factors alters NK killing susceptibility in vitro and in humanized mouse models. Mechanistically, we find that CD43-mediated NK resistance operates independently of its proposed interaction with Siglec-7, and that targeting CD43 on NK cells or CAR T cells substantially enhances cytotoxic activity against leukemia. These results establish gain-of-function surfaceome screening as a powerful tool for identifying therapeutic targets for NK cell-based immunotherapy. - Source: PubMed
Publication date: 2026/08/06
Dinesh Ravi KWang XiaotongMohammad Imran AGunasekaran PariStiklioraitis KostasVillafuerte Jeremy RRao AnirudhHernandez-Lopez Rogelio ASunwoo John BCong Le - Ferroptosis therapy holds great potential in metastatic cancer treatment. Whereas, Dickkopf-related protein-1 (DKK1) that highly expressed in various tumors might contribute to low ferroptosis sensitivity of tumor cells, which imposed restrictions on ferroptosis therapy. Our research revealed that DKK1 inhibition could sensitive tumor cells to ferroptosis by obstructing the cystine-GSH-GPX4 axis and the CoQ-FSP1 axis. Moreover, DKK1 inhibition facilitated dormancy of tumor cells, thereby inhibiting their metastatic proliferation. Encouraged by that, a strategy combining DKK1 inhibition with ferroptosis induction was innovatively proposed for metastatic cancer treatment. And a sulfated hyaluronic acid (SHA)-functionalized liposome co-encapsulating DKK1 inhibitor (Gallocyanine) and ferroptosis inducer (RSL3) was developed for this purpose. The constructed SLip/G+R simultaneously targeted primary tumors, circulating tumor cells and tumor metastases by not only binding to P-selectin/CD44 on tumor cells, but also hitchhiking on activated platelets with tumor cells tendency. Particularly, SLip/G+R increased P-selectin/CD44 on tumor cells through DKK1 inhibition, providing more targets for itself and enhancing the targeting effect in a "self-promoting" manner. Due to the self-promoting ferroptosis amplification, SLip/G+R exerted excellent anti-tumor and anti-metastasis efficacy. Overall, this study provided a new idea for efficiently eliminating metastatic tumor cells. It is conducive to promoting the development of ferroptosis therapy, and is of great significance for metastatic cancer treatment. - Source: PubMed
Publication date: 2026/09/02
Guo RongLiu YingkeYin ZhaoruChen ShuangYe YunxiaJi XuxuZhang ZhengkunWang DingxueLi ManLiu Ji - Activated hepatic stellate cells (aHSCs) play a central role in liver fibrosis by promoting excessive extracellular matrix (ECM) deposition, while oxidative products in fibrotic livers perpetuate their activation. The treatment of liver fibrosis remains challenging because the ECM barrier limits drug uptake by aHSCs. To overcome this challenge, we developed high-density lipoprotein (HDL) nanoparticles loaded with silybin (SIL), and modified them with chondroitin sulfate (CS) and bromelain (BRO). The resulting formulation, denoted as BRO/CS-SIL@HDL nanoparticles (BCSH), was designed to enhance hepatic enrichment, facilitate penetration through the collagen-rich ECM, and enable CD44 receptor-mediated targeting. BCSH showed efficient internalization even in the presence of a collagen barrier. BCSH treatment markedly reduced inflammation, oxidative stress, collagen deposition, and HSC activation. Then RNA seq was further performed to explore the potential molecular mechanisms underlying the therapeutic effects of the nanoparticles, revealing alterations in multiple signaling pathways and biological processes related to liver fibrosis. In conclusion, these results suggest that BCSH represents a promising therapeutic strategy for liver fibrosis. - Source: PubMed
Publication date: 2026/09/02
Zhao YuxinLiu KaiXie LongLuo JiaGu HuanLi Xiaofang