Polyclonal CD44
- Known as:
- Polyclonal CD44
- Catalog number:
- pc-016
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal CD44
Related genes to: Polyclonal 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: Polyclonal CD44
Related articles to: Polyclonal CD44
- Conventional nanocarriers often face challenges of insufficient tumor specificity and poor cellular internalization. To overcome these limitations, we developed an all-in-one prodrug nanoplatform based on hyaluronic acid (HA) that synergistically integrates active targeting, pH-responsive charge reversal, and controlled drug release. Doxorubicin (DOX) was covalently conjugated to oxidized HA via a pH-sensitive imine bond, while a charge-reversal polymer (PLL-DMMA) was grafted onto the HA backbone. This design enables CD44-mediated active targeting toward cancer cells. Crucially, the nanoplatform exhibits a smart charge-reversal characteristic: maintaining a negative surface charge (-32.8 mV) at physiological condition (pH 7.4) for extended circulation, while switching to positive (+16.5 mV) in the acidic tumor microenvironment (pH 6.5) to enhance cellular uptake. In vitro studies demonstrated significantly improved internalization in CD44-overexpressing MKN-45 cells compared to SNU-216 cells with low CD44 expression. The release profile showed high stability at pH 7.4 (<5% release in 5 days) and rapid drug release at endo/lysosomal pH (61.6% at pH 5.0). Cytotoxicity assays confirmed enhanced efficacy of the charge-reversed formulation, with lower IC values in both cell lines. This multifunctional prodrug nanoplatform represents a promising strategy for precision cancer chemotherapy through synergistic enhancement of tumor targeting and intracellular drug delivery. - Source: PubMed
Publication date: 2026/06/05
Yan YulongShi JingZheng ZhenqiaoShi XiaojingZhao Xubo - Cuproptosis, has attracted increasing attention in cancer therapy due to its apoptosis-independent mechanism and potential to overcome drug resistance. However, current copper-mediated nanotherapeutics are still limited by low drug-loading efficiency and insufficient therapeutic versatility. Herein, a tumor microenvironment-responsive nanoplatform, HA-SiO@ESCu-Hemin (SNECHA), was developed for combined cuproptosis-photothermal therapy. Dendritic SiO nanoparticles were sequentially loaded with elesclomol-copper complex (ESCu) and hemin, followed by hyaluronic acid (HA) coating to achieve CD44-mediated tumor targeting and HAase/pH-responsive drug release. After internalization, ESCu induced cuproptosis through FDX1-mediated copper reduction, Fe-S cluster disruption, and DLAT-associated proteotoxic stress, while hemin enabled 808 nm laser-triggered photothermal therapy. SNECHA showed efficient near-infrared photothermal conversion with an efficiency of 46.69% and increased to 57.3 °C. In addition, it exhibited enhanced cellular uptake, selective cytotoxicity toward A549 cells with IC value of 103.2 nM under laser illumination, and significantly improved antitumor efficacy. In vivo results further demonstrated enhanced tumor accumulation, superior tumor growth inhibition, and favorable preliminary biosafety. This work provides a targeted nanotherapeutic strategy for enhanced cancer treatment through cuproptosis-photothermal combination therapy. - Source: PubMed
Publication date: 2026/06/02
Li XiaojieLi ChunlinLiu DiWang Yonglian - Image-guided laser interstitial thermal therapy (LITT) is a minimally invasive cytoreductive treatment for recurrent gliomas and tumors in eloquent regions. This technique was adapted to develop an image-guided glioblastoma (GBM) ablation model of recurrence. The efficacy of imaging biomarkers for evaluating tumor ablation and recurrence was evaluated by comparing the cytopathology and molecular signatures of primary and recurrent tumors. - Source: PubMed
Publication date: 2026/06/05
Nagaraja Tavarekere NBartlett SeamusCabral GlauberAcharya Prabhu CMorosini NataliaDatta IndraniHasselbach LauraSingh JaspreetParasar ParveenAyloo BhargavAvritt FaithSpanick Katelynn GGowda PranavideCarvalho Ana CNoushmehr HoutanKnight Robert ABrown Stephen LEwing James RLee Ian Y - A healthy cardiovascular system requires a healthy endothelium. The endothelium is a central regulator of hemostasis, vascular permeability, inflammation, blood pressure, and, perhaps most fundamentally, blood flow. It is therefore of no surprise that endothelial dysfunction underlies many of the vascular complications that occur in metabolic disease (e.g. peripheral artery disease, vascular retinopathy, and coronary artery disease). Endothelial function is often assessed using flow mediated dilation (FMD), and in their recent study, Power and colleagues provide novel insight into the mechanisms by which FMD is impaired in type 2 diabetes (T2D). In T2D, loss of FMD is driven, in part, by the shedding of the glycocalyx (). This hair-like structure on the surface of the endothelium maintains an erythrocyte-free zone, preserves redox homeostasis, mitigates inflammation, and senses shear stress. The glycocalyx is a complex matrix made up of proteoglycans, glycoproteins, glycolipids, and glycosaminoglycans, and each of these components plays an essential role in its functions. Power and colleagues found patients with T2D had impaired FMD and elevated plasma hyaluronan, suggesting glycocalyx shedding. Hyaluronan is a glycosaminoglycan in the glycocalyx that works in concert with CD44 to propagate flow-induced signaling. Notably, they found endothelial CD44 expression was decreased in the db/db model of T2D. Using isolated mouse mesenteric arteries, they demonstrated cleavage of hyaluronan with hyaluronidase or blocking the binding site of hyaluronan on CD44 blunted FMD. Similarly, knockdown of CD44 in cultured endothelial cells blunted shear stress induced increases in intracellular calcium and endothelial nitric oxide synthase. Together these data demonstrate the importance of hyaluronan-CD44 signaling for endothelial mechanotransduction. Building on their previous work which reported upregulation of a disintegrin and metalloprotease 17 (ADAM17) in arteries from patients with T2D, they found elevated plasma ADAM17 activity in their patient population and increased endothelial ADAM17 expression in db/db mice. They therefore investigated whether cleavage of CD44 by ADAM17 contributes to impaired FMD in T2D. They found both activation and overexpression of ADAM17 blunted the response to shear stress in cultured endothelial cells. Furthermore, ADAM17 overexpression cleaved CD44 as demonstrated by reduced cell-surface CD44 and increased CD44 in the supernatant. Similar results were achieved when endothelial cells were treated with recombinant ADAM17, and recombinant ADAM17 was sufficient to impair CD44-hyaluronan binding . Perhaps most importantly, recombinant ADAM17 was sufficient to blunt FMD in isolated mouse mesenteric arteries. Altogether these data suggest ADAM17 upregulation contributes to the endothelial dysfunction observed in patients with T2D. These studies build on previous work implicating ADAM17 as a driver of endothelial dysfunction in metabolic disease and provide a novel mechanism by which ADAM17 impairs endothelial-dependent vasodilation. Previous work has demonstrated ADAM17 cleaves glypican-1, a proteoglycan component of the glycocalyx, thereby blunting FMD, and ADAM17 cleaves the insulin receptor, blunting insulin-dependent vasodilation. Still questions remain regarding how ADAM17 activity impacts other functions of the glycocalyx and how other flow-sensing mechanisms such as piezo channels may compensate in these conditions. The use of endothelial-specific ADAM17 knockout mice offers an exciting avenue to pursue these questions . Altogether, ADAM17 may be a promising target to preserve or restore the endothelial glycocalyx and endothelial function in T2D. Vascular dysfunction gives rise to major T2D comorbidities such as nephropathy, neuropathy, and cardiovascular disease. Continued efforts to investigate the mechanisms that drive endothelial dysfunction may offer new therapeutic targets to treat or prevent these comorbidities, thereby decreasing mortality and improving quality of life for patients with T2D. - Source: PubMed
Publication date: 2026/06/05
Dunaway Luke S - The homing of hematopoietic stem/progenitor cells (HSPCs) and leukemic cells is a multistep process governed by complex spatiotemporal interactions between adhesion molecules under shear stress. While the molecular and biological mechanisms of this process have been extensively studied, the precise nanoscale spatial organization of adhesion molecules that influences homing efficiency remains relatively poorly understood. In particular, the roles of the cell surface topography and its morphological changes during homing in shaping the spatial organization of adhesion molecules remain elusive. This is partly due to the lack of imaging techniques that simultaneously capture both nanoscopic cell surface morphology and the spatial distribution of the adhesion molecules. Here, we develop a microfluidics-based super-resolution (SR) imaging platform that enables the three-dimensional (3D) mapping of the cell surface morphology and the spatial distribution of the adhesion molecules during HSPC and leukemic cell rolling, which were fixed in situ under shear flow, by integrating total internal reflection fluorescence microscopy (TIRFM) with single-molecule localization microscopy (SMLM). We reconstruct the cell surface morphology, which is critical to the homing, using TIRFM, and precisely overlay the spatial distribution of adhesion molecules, including CD44, PSGL-1, and actin cytoskeleton, determined by 3D-SMLM, on the topographic map. We show distinct nanoscopic localizations of adhesion molecules on the microvilli of HSPCs/leukemic cells and their reorganization under shear stress during cell rolling, at a spatial resolution of approximately 30 nm. The approach offers a powerful means to elucidate the complicated interplay between cell surface morphology and ligand-receptor interactions. - Source: PubMed
Publication date: 2026/06/04
Alghamdi AbdullahAldehaiman Mansour MSerag Maged FNozue ShuhoCiocanaru Ioana-AndreeaAbuZineh KarmenMerzaban Jasmeen SHabuchi Satoshi