Mouse Anti-Human CD44, FITC-labeled
- Known as:
- Mouse Antibody toHuman CD44, fluorecein-labeled
- Catalog number:
- 128-10039-1
- Product Quantity:
- 500
- 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
- Chondrosarcoma is the most common type of primary bone sarcoma in adults with a high risk of local recurrence and metastasis. Chondrosarcomas are largely resistant to chemotherapy and radiotherapy, meaning that surgery is the mainstay of treatment for most patients. Therefore, new therapeutic targets are required. Cluster of differentiation 44 (CD44) is a transmembrane protein that has roles in cell proliferation, adhesion and migration and is shown to be overexpressed in several cancer types. Consequently, this work was undertaken to understand whether CD44 could be a potential therapeutic target in chondrosarcoma. In this study, tissue sections from chondrosarcoma patients were evaluated for CD44 expression using immunohistochemical analysis. The relationship between CD44 expression in the patient tissue and overall and event-free survival was investigated. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing was used to generate a CD44 knockout chondrosarcoma cell line which was used for a spheroid invasion assay to understand the role of CD44 in chondrosarcoma cell invasion. Cox multivariate analysis of CD44 expression in chondrosarcoma patient tissue revealed that high CD44 expression was linked to decreased overall ( < 0.01) and event-free survival ( < 0.01). The observed invasion of CD44 knockout cells in the spheroid assay was less than that of the wild type cells ( < 0.001). The increased expression of CD44 in intermediate and high grade chondrosarcomas, as well as reduced invasion of CD44 knockout cells suggests that CD44 plays an important role in chondrosarcoma progression and metastasis. These findings support further investigation of CD44 as an imaging and/or therapeutic target for the management of chondrosarcoma. - Source: PubMed
Publication date: 2026/06/16
Bell ZoeChan Corey DHowarth RachelAtkinson AndreaGamie ZakareyaFrankel DanielBretcanu OanaRankin Kenneth S - : Glioblastoma (GBM) is characterized by pronounced transcriptional plasticity and a highly structured immune microenvironment, yet the molecular features associated with tumor-state transitions and immune remodeling remain incompletely understood. : We used an integrative multi-omics framework to examine how secreted phosphoprotein 1 () relates to tumor microenvironment organization in human gliomas. Single-cell analyses associated with myeloid populations, mesenchymal-like (MES-like) malignant states, inflammatory regulatory programs, and inferred ligand-receptor co-expression patterns involving - and -integrin pairs. Spatial transcriptomic analyses showed that -high regions were enriched for estimated myeloid abundance, MES-like tumor signal, and ECM/angiogenic programs, supporting an -associated spatial mesenchymal-myeloid program in GBM. Computational perturbation analyses provided network-level support for --associated stress-responsive programs. HPA immunohistochemistry provided tissue-level protein context for SPP1 and related mesenchymal/receptor-associated components. Ivy GAP analysis showed enrichment of -associated features in core-like anatomic compartments, and CODEX spatial protein imaging provided antibody-panel-based contextual support for mesenchymal-myeloid-associated features. In the TCGA-GBM cohort, elevated expression and an -associated mesenchymal signature were associated with poorer overall survival. : These findings support an inferential model in which is associated with spatial mesenchymal-myeloid organization in GBM and nominate -associated programs as candidate readouts of tumor plasticity, inflammatory myeloid remodeling, and spatial tumor microenvironment organization. - Source: PubMed
Publication date: 2026/05/28
Wang YingZhou DongHong Zhen - Leukocyte recruitment from blood into tissues involves sequential adhesive steps, including rolling and integrin-dependent arrest. VLA-4 can support firm adhesion and, in some settings, rolling interactions, whereas CD44-hyaluronan interactions have also been implicated in leukocyte rolling. Here, we used adhesion assays and parallel-plate flow chamber experiments to analyze CD44-hyaluronan-dependent monocyte interactions on ECV304 monolayers and to compare them with α4-integrin-sensitive adhesion on endothelial monolayers. WEHI 78/24 monocytoid cells interacted with ECV304 monolayers in a CD44- and hyaluronan-dependent manner, whereas adhesion to HMEC-1 and bEnd.3 monolayers was sensitive to α4-integrin blockade. Blocking CD44, adding soluble hyaluronan, or treating ECV304 monolayers with hyaluronidase reduced adhesion and rolling. Mixed primary human monocyte preparations also showed CD44-dependent adhesion and rolling on ECV304 monolayers. ECV304 cells are interpreted here not as endothelial cells, but as T24-derived, hyaluronidase-sensitive cellular monolayers useful for functional analysis of CD44-hyaluronan-dependent interactions. These findings support a substrate-dependent functional hierarchy in which CD44-hyaluronan-dependent monocyte rolling becomes detectable when α4-integrin-dependent adhesion is not dominant, while emphasizing the cell-model-based nature of the assay. - Source: PubMed
Publication date: 2026/06/13
Hubbe MarcusEibl Robert H - Heat shock protein 90 (HSP90) is a molecular chaperone essential for maintaining the stability of many oncogenic client proteins. Although several HSP90 inhibitors (HSP90i) have entered clinical trials, their use has been limited by toxicity and resistance, underscoring the need for improved therapeutic strategies. In this study, we assessed the therapeutic potential of a new HSP90i, SP11, in T-cell acute lymphoblastic leukemia (T-ALL) in vitro and in the DLA mouse model in vivo, using single-cell transcriptomic profiling. Single-cell RNA sequencing showed that SP11 treatment reduces key oncogenic drivers, including MYC, BCL2, and stemness-related genes, consistent with impaired leukemic survival programs. In the DLA mouse model, SP11-mediated HSP90 inhibition was associated with alterations in the tumor microenvironment, including increased immune cell representation and enrichment of cytokine- and antigen-presentation-related transcriptional pathways. Despite these antitumor effects, a distinct subpopulation of cells continued to express or re-express MYC and BCL2, suggesting the development of early adaptive resistance. Consistent with these findings, an SP11-resistant MOLT4 cell line maintained high levels of MYC and BCL2 at both the transcript and protein levels, maintained CD44 expression, and exhibited altered inflammatory cytokine signaling. Functional studies confirmed that pharmacological inhibition of BCL2 notably increased SP11 sensitivity, supporting a rational combination strategy. Collectively, our results show that SP11 may exert both tumor-intrinsic and immune-modulating effects and reveal transcriptionally defined adaptive cellular states linked to resistance. This study provides mechanistic in sights into responses to HSP90 inhibition and supports combination approaches for improving therapeutic outcomes in T-ALL. - Source: PubMed
Publication date: 2026/06/12
M V ShahanaR AnjithaChoudhary Bibha - Zinc is an essential trace element with a critical role in regulating immune functions. Patients with autoimmune diseases or chronic lymphatic leukemia often exhibit lower serum zinc levels. As T cells are key mediators of adaptive immunity, disturbances in zinc homeostasis can strongly affect their function. Effective T cell activity depends on directed migration to inflamed tissues, requiring coordinated cytoskeletal reorganization. This process involves the formation of a leading edge and a trailing edge (uropod) and is regulated by the ezrin-radixin-moesin (ERM) complex and its interaction with focal adhesion kinase (FAK). We investigated how zinc availability influences the expression and phosphorylation of FAK and ERM, as well as other migration-related molecules, including LFA-1 and the CD49d/CD44 complex, using Western blot, qRT-PCR, and flow cytometry in the HUT78 T cell line. Cells were cultured in media with different zinc concentrations. Zinc deficiency reduced FAK and ERM expression and decreased LFA-1 while increasing CD49d expression. Overall, these findings indicate that zinc deficiency compromises cytoskeletal remodeling and may impair T cell motility. Maintaining zinc homeostasis could thus enhance T cell migration and strengthen immune responsiveness, highlighting the potential therapeutic relevance of zinc in immune modulation. - Source: PubMed
Publication date: 2026/06/10
Dermaku AtlantidaSchoofs HannahRink LotharFischer Henrike Josephine