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
- Gastric cancer (GC) with peritoneal metastases (PM) and positive peritoneal cytology (CY+) is associated with extremely poor prognosis, and most patients are considered unsuitable for surgical treatment. We evaluated a response-adapted strategy combining repeated intraperitoneal paclitaxel perfusion via videolaparoscopy (RIPPENC-VLP) with systemic chemotherapy in patients with GC and low-volume PM. - Source: PubMed
Publication date: 2026/08/27
de Souza Filho OdilonRondinelli ReinaldoAccetta Antônio CarlosAlbagli RafaelRego Alexandre Gabriel SilvaPalladino AlexandreGuedes Cristiano DuqueVieira Claudia Cristine RochaThuler Luís Claudio SantosDiniz ClaudiaDos Santos Everton CruzAbdelhay Eliana - Alzheimer's disease (AD) involves complex changes, including synaptic dysfunction, neuroinflammation, and metabolic impairment, yet the role of lipid raft-associated gene networks in these processes remains unclear. In this study, we performed an integrative transcriptomic analysis using the GSE5281 dataset and validated the findings in an independent cohort (GSE33000). By combining differential expression analysis with weighted gene co-expression network analysis, we identified 72 lipid raft-associated genes linked to mitochondrial, synaptic, and immune-related pathways. Using network analysis and machine learning approaches (LASSO and SHAP), we further identified eight key biomarkers (CBL, CD44, EZR, FAS, FYN, ITGB1, MAPK1, and TGFBR1) that showed strong diagnostic performance and consistent results across datasets. Functional analysis revealed increased inflammatory signaling, including pyroptosis and cytokine pathways, alongside reduced oxidative phosphorylation and synaptic activity. Interestingly, immune profiling showed only minor differences in immune cell infiltration, but clear activation of multiple immune pathways, such as Th2 and Treg signaling, CD8⁺ T-cell signatures, and IL-6/IL-10-mediated inflammation. These immune changes were strongly associated with lipid raft-related biomarkers. Overall, our findings suggest that lipid raft dysregulation may act as a key link between immune activation, mitochondrial dysfunction, and synaptic impairment in AD. - Source: PubMed
Publication date: 2026/08/14
Hsu Chun-HsienJallow Amadou WurrySaleem FatimaChau Vu Thi MinhLin Yung-Feng - Objective To investigate the effect of polyphyllin I on MCF-7 spheroids enriched with cancer stem cells and to preliminarily observe its effect on the hybrid epithelial-mesenchymal transition (EMT) state and its regulatory role on cell stemness. Methods MCF-7 spheroids were cultured under serum-free,non-adherent conditions.Cell viability,invasion,and key protein expression were assessed through the cell counting kit-8 assay,Transwell assay,and Western blot,respectively.The CD44/CD24 cell population was analyzed by flow cytometry. Results The MCF-7 spheroids exhibited high proliferative and invasive capacities,co-expressing the epithelial marker E-cadherin and the mesenchymal marker vimentin,which is indicative of a hybrid EMT state and high stemness.Polyphyllin I treatment significantly suppressed the viability and invasion of MCF-7 spheroids.From a mechanism perspective,polyphyllin I downregulated the E-cadherin/vimentin ratio,significantly reduced the levels of stemness-associated proteins CD44 antigen,aldehyde dehydrogenase 1 family member A1,as well as the ratio of phosphorylated signal transducer and activator of transcription 3 to total signal transducer and activator of transcription 3.Simultaneously,polyphyllin I decreased the proportion of CD44/CD24 cells.No significant changes were observed in key proteins of the intrinsic apoptosis pathway. Conclusions Polyphyllin I reshapes the hybrid EMT state in MCF-7 spheroids,which is accompanied by the disruption of their high stemness equilibrium.This compound may reduce cellular stemness through the EMT remodeling process,thereby exerting antitumor effects,and this mechanism is independent of the intrinsic apoptosis pathway. - Source: PubMed
Liu TongLi Yuan - Red blood cell (RBC)-camouflaged nanocarriers provide a biomimetic strategy to reduce immune clearance and improve tumour-directed drug delivery. Here, we engineered an RBC-camouflaged albumin nanoplatform co-loaded with oxaliplatin (Oxa) and zinc oxide nanoparticles (nZnO), termed C-Alb, for colorectal cancer therapy. The optimized formulation exhibited a uniform hydrodynamic size of 139.3 ± 2.5 nm, a zeta potential of -17.6 ± 2.3 mV, efficient Oxa/nZnO loading, good colloidal stability, and pH-responsive Oxa/Zn release, with enhanced release under acidic/reductive tumour-mimicking conditions. RBC membrane cloaking preserved vesicular morphology and key membrane-associated components, including glycoproteins, sialic acid, CD47, CD55, and CD59, while reducing macrophage uptake. In CT26 cells, C-Alb enhanced cytotoxicity (IC₅₀ = 4.27 μM), increased caspase 3/7 activation, and induced ICD-associated calreticulin exposure, ATP secretion, and HMGB1 release. These responses promoted M1 macrophage polarization, dendritic cells maturation, and macrophage-mediated phagocytosis of treated tumour cells. The formulation also downregulated CD44 and reduced CT26 adhesion and migration. In CT26 tumour-bearing mice, RBC coating prolonged systemic exposure, reduced RES-associated accumulation, enhanced tumour Oxa deposition, improved antitumour efficacy, and maintained acceptable systemic tolerability. Therefore, C-Alb integrates immune-evasive delivery, Oxa/nZnO co-delivery, ICD-associated immune activation, and improved in vivo antitumour performance. - Source: PubMed
Publication date: 2026/08/27
Hamdi MohamedAbdel-Bar Hend MohamedElmowafy EnasElKashlan Akram MMansour MaiAl-Jamal Khuloud TAwad Gehanne A S - Spinal cord injury (SCI) is a devastating condition that results in long-term functional impairments due to loss of tissue and limited regeneration. Investigating the factors that regulate the post-SCI response is critical to understanding the pathophysiology of this condition and developing treatments. One molecule of interest in the post-SCI response is CD44. CD44 is cell-surface protein with a well-established role in regulating cellular functions including cell migration and proliferation. CD44 is expressed in many cells that play a role in the post-SCI microenvironment but the effect of global CD44 KO on SCI outcomes has not previously been tested. Here, we investigate that role in a mouse unilateral cervical contusion SCI model. We predicted that CD44 KO would exert a predominant effect on glial progenitor/cell recruitment, inhibiting astroglial scar formation and thereby increasing lesion expansion and exacerbating locomotor deficits. In contrast, we found that CD44 KO mice exhibited increased numbers of astrocytes at the lesion epicenter, developed a more compact astroglial scar by 28 days after injury, showed improved locomotor function, and exhibited decreased recruitment of acutely activated immune cells vs WT mice. Together, these findings highlight the role of CD44 in diverse cell populations after SCI as a critical point of further investigation to understand the post-SCI response. - Source: PubMed
Publication date: 2026/08/27
Creasman DanaBenavente FranciscaNishi RebeccaAnderson Aileen