CD44
- Known as:
- CD44
- Catalog number:
- 11-221-M001
- Product Quantity:
- 1.0 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD44
Ask about this productRelated genes to: 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: CD44
Related articles to: CD44
- Surgical stress reprograms monocyte/macrophage populations, rendering patients more susceptible to infections and impairing postoperative recovery. However, the underlying mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/07/11
Hua QingYao YutingShi XintongWu ShufeiZhu XiaoyanXu Pingbo - Carbohydrate-functionalized nanocarriers have moved from a decorative surface-modification concept to a molecular drug-delivery strategy in which glycan ligands, polysaccharide shells and synthetic glycopolymers are engineered to negotiate tumor recognition, receptor clustering, endocytosis, intracellular trafficking and stimulus-triggered release. The field is scientifically attractive because cancer cells and tumor-associated stromal cells remodel their glycocalyx, overexpress selected carbohydrate-recognizing receptors and display altered metabolic demand; however, the translation of glycoengineered nanomedicine remains limited by low tumor delivery efficiency, heterogeneous receptor density, competitive off-target uptake by liver and macrophages, batch-to-batch variation in ligand density and insufficient quantitative reporting. This review re-frames carbohydrate-mediated cancer drug delivery as an evidence-weighted design problem. It integrates receptor-density data, particle-size boundaries, ligand-density ranges, release-rate targets, in vitro uptake metrics, pharmacokinetic endpoints and preclinical efficacy readouts into a quantitative framework. Special attention is given to hyaluronic acid-CD44, galactose/GalNAc-ASGPR, mannose-CD206, sialylated glycan-siglec/selectin, beta-galactoside-galectin and glucose/GLUT-related approaches, with emphasis on what the available data can and cannot prove. The central conclusion is that molecular glycoengineering is most defensible when carbohydrate chemistry is linked to measurable receptor engagement, competitive inhibition, uptake kinetics, intracellular drug exposure and statistically stronger antitumor benefit rather than to generic claims of active targeting. The framework explicitly links anomeric configuration, glycosidic linkage, branching, sulfation/acetylation, epitope display and glycan-protein hydration to receptor-specific pharmacological outcomes, thereby shifting the emphasis from general nanomedicine performance to carbohydrate structure-activity relationships required for a carbohydrate-chemistry readership. - Source: PubMed
Publication date: 2026/07/03
Singh Dilpreet - Acute kidney injury (AKI) is a clinical syndrome with high incidence and mortality involving oxidative stress, ferroptosis, and inflammation, yet there are no clinically effective interventions. Herein, HA@PDA@EGCG nanoparticles were constructed using polydopamine (PDA) as carriers, loaded with epigallocatechin gallate (EGCG) via π-π stacking, and further surface-modified with hyaluronic acid (HA) through electrostatic interaction. The nanoparticles had uniform morphology with a size of approximately 50 nm and an EGCG loading capacity of 15.4 ± 0.8%. They exhibited prominent broad-spectrum antioxidant activity and hydrogen peroxide-responsive EGCG release, with a cumulative release rate of 58.2 ± 2.2% within 2 h and close to 80% at 12 h. Cellular uptake and in vivo distribution confirmed the efficient CD44 receptor-mediated internalization of the nanoparticles by human kidney-2 (HK-2) cells as well as renal-targeted accumulation. Reactive oxygen species (ROS) staining, mitochondrial morphology and apoptosis assays showed that the nanoparticles effectively scavenged ROS, alleviated mitochondrial damage, and inhibited cell apoptosis. In a cisplatin-induced in vivo AKI model, HA@PDA@EGCG significantly restored renal function: blood urea nitrogen and creatinine decreased to 12.3% and 27.2% of model group levels, respectively, while alleviating renal pathological damage and inflammation. Mechanistically, HA@PDA@EGCG inhibited ferroptosis by downregulating acyl-CoA synthetase long-chain family member 4 (ACSL4) to suppress lipid synthesis, chelating ferrous ions, and stabilizing glutathione peroxidase 4 (GPX4) protein. Collectively, HA@PDA@EGCG achieved renal protection by ameliorating oxidative stress, suppressing inflammation and inhibiting ferroptosis through multiple pathways, offering a novel strategy for targeted AKI therapy. - Source: PubMed
Publication date: 2026/07/11
Zhang JiekeLi YafangTian ChaoyingZhang XiaodiGuo JialingLiu ChenxinWu LigangDu BinCheng Genyang - Cancer stem cells (CSCs) are a small population of cells within a tumor which perform stem cell like functions including self-renewal, differentiation and initiation. This narrative review aims to provide an overview of the role of CSCs in resistance to standard treatment and metastasis in breast cancer, potential treatment strategies including latest clinical trials, and the clinical implications for CSCs in the management of breast cancer. The most established breast CSC markers (CD44+/CD24- and ALDH1) are most prevalent in basal-like cancers, the most aggressive subtype of breast cancer. The most implicated CSC pathways include Hedgehog, Notch, CXCR1, and Wnt. Previous phase I/II trials targeting these pathways associated with breast CSCs have shown mixed results; no CSC-specific drug has reached phase III trial in breast cancer. To maximize the potential benefit of CSC-targeted therapy, it would be important to select or enrich patients with CSC markers or CSC-associated pathway activation. It would also be critical to develop combination strategies that overcome plasticity and/or immune invasion, and preferentially destroy CSCs with limited impact on healthy stem cells. Overall, breast CSCs may have greater clinical implications but require further research and development to realize their full clinical potential. - Source: PubMed
Publication date: 2026/07/11
Wu Wesley Oliver - Heart failure is associated with the accumulation of reactive lipid peroxidation-derived aldehydes, such as acrolein, which form immunogenic protein adducts in the heart. Histidyl dipeptides, including carnosine (β-alanine-histidine), can covalently sequester these aldehydes. We tested whether increasing myocardial carnosine through β-alanine supplementation reduces aldehyde stress, limits the immunogenicity of aldehyde-modified proteins, and improves cardiac function during pressure overload-induced heart failure. - Source: PubMed
Publication date: 2026/07/10
Doelling BenjaminChaudhari MamataHoetker DavidBrittian KennethNong YibingStephan Jonah KJouja IbrahimJanis Helen IMitchell ThomasWysoczynski MarcinBhatnagar AruniJones Steven PBaba Shahid P