Ask about this productRelated genes to: CD44 antibody
- 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 antibody
Related articles to: CD44 antibody
- 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 - Mitoxantrone (MTX) is limited by cardiotoxicity and MDR. At the same time, graphene oxide (GO) and nano-graphene oxide (NGO) offer ultrahigh surface area, strong π-π interactions with aromatic drugs, and versatile surface chemistry, making them superior to many conventional nanocarriers for high-capacity, stimuli-responsive MTX delivery. Conventional chemotherapy remains constrained by nonspecific biodistribution, dose-limiting toxicity, and the frequent emergence of multidrug resistance. This review surveys recent advances in GO- and NGO-based nanocarriers developed for targeted delivery of mitoxantrone. The platforms examined include hyaluronic acid-Pluronic functionalization for CD44-mediated targeting and P-glycoprotein inhibition, biomimetic coatings derived from mesenchymal stem cells or cancer-cell exosomes, magnetic graphene oxide systems designed for mitochondrial delivery, hybrid gold-graphene constructs, and multi-stimuli-responsive designs that respond to acidic pH, near-infrared light, or external magnetic fields. Combination strategies that integrate chemotherapy with photothermal therapy, nitric oxide release, or immunotherapy are also considered. Molecular dynamics simulations together with in vitro and limited in vivo studies indicate high drug-loading capacities (commonly reaching 40-45 wt% and higher in selected systems), stimulus-triggered release within acidic microenvironments, improved intracellular accumulation in resistant cell lines, and enhanced antitumor activity relative to free MTX in preclinical models, frequently accompanied by reduced systemic exposure. Nevertheless, long-term biocompatibility, immunogenicity, biodegradation and clearance pathways, batch-to-batch reproducibility, scalable manufacturing, and the complete absence of clinical data remain major translational barriers. Further progress will require safer, more biodegradable graphene derivatives and rigorous toxicological characterization before these platforms can advance toward clinical evaluation. - Source: PubMed
Publication date: 2026/08/24
Talebi Haftadori ZahraMahdavian LeilaMirjafary ZohrehGhorbani Seyed Hosein - White adipose tissue is organized into anatomically and functionally distinct depots, yet the mechanisms by which intrinsic differences between subcutaneous and visceral adipose progenitor cells (APCs) contribute to depot-specific inflammatory and remodeling properties remain unresolved. Here, by directly comparing APCs isolated from subcutaneous and visceral fat, we identify distinct surface protein programs underlying their divergent functional properties. Subcutaneous APCs exhibited elevated expression of galectin-9, CD44, and CD63, defining functional programs governing immune modulation, adipogenesis, and exosome-mediated stress adaptation. Functional assays revealed that galectin-9 promotes an anti-inflammatory phenotype, CD44 quantitatively modulates adipogenic differentiation, and CD63 enhances exosome release and confers resistance to iron-induced cellular stress. Notably, several depot-specific features were not evident at the transcriptomic level, underscoring the importance of surface protein-level regulation. Together, our findings demonstrate that APC surface protein signatures distinguish subcutaneous from visceral fat, establishing a mechanistic link between depot identity, tissue remodeling, and metabolic disease susceptibility. - Source: PubMed
Publication date: 2026/08/17
Hachiya KazukiYamasaki NobuoFukai HirotoUchida YukiNozaki YukaMizunoe YuheiHigami Yoshikazu - Metastatic breast cancer remains difficult to cure, and the way B and T lymphocytes adapt across metastatic niches especially under therapy remains insufficiently defined. Clarifying compartment specific immune remodeling may help explain resistance to PD-1/PD-L1 blockade and identify actionable targets. We performed an integrated meta-analysis of single cell RNA-seq datasets from normal breast tissue, primary tumors, tumor-draining lymph nodes (TLNs), and peripheral blood mononuclear cells (PBMCs), focusing on B and Tcell states. Immune composition differed notably by compartment. Tumors were enriched for effector CD8 states (CD8 cytotoxic 20.1%; CD8 activated 13.5%), whereas TLNs preserved larger naïve and memory reservoirs (CD4 naïve 40.7%; B naïve 11.4%; B memory 12.0%) and contained a higher B cell fraction than tumors (39.6% vs. 19.5%). Post therapy, PBMCs and TLNs showed increased BTLA-HVEM (TNFRSF14) checkpoint signaling and enhanced MIF-CD74 interactions with a shift from CD44 toward CXCR4, consistent with CXCR4 driven migratory and survival programs. In TLNs, TNFRSF14 signaling was unidirectional (B→T), absent in the reverse direction, and not detected in tumors. Clinically, higher tumor CXCR4 combined with lower TNFRSF14 was associated with shorter progression free survival in TCGA-BRCA, most evident in node positive, early stage disease. To target the BTLA-HVEM checkpoint axis, we performed structure guided peptide design using the native HVEM (23-39) peptide as an active structural template, followed by docking and molecular dynamics simulations. The optimized De novo-P2 peptide showed stable and favorable interactions at the BTLA interface, supporting its potential as a competitive modulator of BTLA-HVEM signaling. These data define niche specific lymphocyte remodeling and implicate BTLA-HVEM and CXCL12-CXCR4 as candidate biomarkers and therapeutic targets linked to PD-1/PD-L1 resistance. - Source: PubMed
Publication date: 2026/08/12
Khan SajidJamil SabahatHamza MuhammadAttique ZarlishZhang Suping - Hyaluronan (HA) is a major glycosaminoglycan of the extracellular matrix that regulates cell migration, signaling, and tissue homeostasis. Its turnover is controlled by coordinated synthesis by HA synthases and degradation by hyaluronidases. Among these hyaluronidases, TMEM2, the only known transmembrane hyaluronidase, plays a unique role in HA degradation at the cell surface; however, the cellular conditions that support its activity remain incompletely understood. To address this, we developed a cell-based HA turnover assay to examine TMEM2-mediated degradation of endogenously synthesized HA, rather than exogenously added, fluorescently labeled HA used in previous studies. Using this system, we show that TMEM2 readily degrades high-molecular weight HA synthesized by co-expressed HAS3. This degradation occurs only when TMEM2 and HAS3 are co-expressed in the same cells (), whereas co-culture of TMEM2-expressing cells with HAS3-expressing cells supports little or no degradation. Interestingly, HA-binding cell surface receptors CD44 and its homolog LYVE-1 promote efficient TMEM2-mediated HA degradation even under conditions, whereas other HA-binding proteins, including TSG-6, layilin, TLR2, RHAMM, and ICAM-1, do not. These findings suggest a spatially regulated mechanism of TMEM2 activity in which capture of HA at the cell surface, mediated by CD44 or LYVE-1, contributes to efficient HA degradation by TMEM2. - Source: PubMed
Publication date: 2026/08/12
Tobisawa YukiYano FumiakiraTomioka-Inagawa RisaIrie FumitoshiKoie TakuyaYamaguchi Yu