CD44
- Known as:
- CD44
- Catalog number:
- 11-221-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD44
Related 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
- Oral squamous cell carcinoma (OSCC) is a very frequently occurring cancer type. A salivary biomarker-based noninvasive diagnostic technique helps as promising method in the early detection of cancer. This research was done to assess salivary biomarkers' diagnostic value for early OSCC identification. - Source: PubMed
Publication date: 2026/07/02
Yeladandi MounikaSuliman Nada Mohamed AhmedRastogi Jyoti GoyalBehera SasmitaMohsin Syed FareedMahabob NazargiAhmed Muzammil MoinMujoo SheetalBabaji Prashant - Fascia, the connective tissue network enveloping muscles, organs, and viscera, functions as a hyaluronan (HA)-rich adaptive interface that senses and responds to inflammatory cues. This narrative review synthesizes ECM literature across niches to examine the calcium-hyaluronan (CHA) axis, a feedback loop linking Ca² signaling to HA synthesis via HAS2 and molecular weight-dependent signaling through CD44 and RHAMM receptors. We propose that the CHA axis is constrained further by ATP/NAD-mediated feedback and functions as a rheostat regulated by four distinct constraint types (1): Mechanical loading and shear regulate HA turnover, hydration, and viscosity via YAP/TAZ and integrin mechanosensing (2). Inflammatory cytokines drive HAS2/HA accumulation during chronic irritation or injury through CD44/RHAMM signaling (3). Metabolic energy availability provides purinergic brakes via AMPK/SIRT1 that suppress synthesis when ATP is scarce (4). HA clearance mechanisms-hyaluronidases, TMEM2/CEMIP, lymphatic drainage, and interstitial fluid flow-which may be as critical as synthesis itself. This is the first review integrating the domains of research across cell types, with clinical relevance in cancer and wound healing as well as exercise physiology and longevity protocols. - Source: PubMed
Publication date: 2026/06/17
Kirkness Karen Bda Silva Fabiana CSchleip RobertCruvinel-Júnior Ronaldo HScarlata Suzanne - Patients with liver cirrhosis exhibit increased susceptibility to bacterial infections; however, the specific immune defects facilitating this vulnerability remain incompletely understood. We aimed to characterize the dysregulated intercellular crosstalk within the cirrhotic liver that compromises antibacterial defense. - Source: PubMed
Publication date: 2026/07/01
Chen RuochanLi JieZhong XiaoWang XiaoxuWu LiLi HaiLi ZhiHuang YanSun LunquanFan Xuegong - The tumor microenvironment (TME) limits durable antitumor immunity by impairing CD8 T cell responses. Memory like CD8 T cells are important for long-term immune control but are often restricted in the TME. Dendritic cells (DCs) are key regulators of T cell fate. Previous studies have shown that SHP1 in DCs fosters an immunosuppressive microenvironment and facilitates tumor immune escape. T cell factor-1 (TCF-1), encoded by Tcf7 gene, is required for central memory CD8 T cell (TCM) formation and is closely linked to canonical Wnt/β-catenin signaling. However, whether SHP1 in DCs regulates TCF-1 expression and TCM formation remains unclear. To investigate the role of DC intrinsic SHP1 in T cell immunity, SHP1 deficient DC2.4 cells and primary bone marrow derived dendritic cells (BMDCs) were co-cultured with OT-1 T cells to assess proliferation, TCM formation, cytotoxic activity, and TCF-1 expression. A DC-specific SHP1 knockout mice model was used to evaluate antitumor immunity in vivo, and Tcf7 or Ctnnb1 silencing was used to probe the TCF-1/Wnt/β-catenin axis. SHP1 downregulation in DCs markedly enhanced CD8 T cell proliferation, promoted the generation of CD62L CD44 central memory T cells, and potentiated B16-F10-OVA tumor cell killing, accompanied by increased TCF-1 expression in OT-1 T cells. In DC-specific SHP1 knockout mice, EO771 tumor growth was suppressed with concurrent increases in intratumoral IFN-γ and TCF-1 CD8 T cell frequencies. Mechanistically, we found that DC SHP1 regulates TCM formation via TCF-1, as silencing Tcf7 in OT-1 T cells abrogated this effect. SHP1-deficient DCs activated Wnt/β-catenin signaling in CD8 T cells, as shown by increased active β-catenin, total β-catenin, c-Myc and Cyclin D1, and a reduced phospho β-catenin/total β-catenin ratio. Critically, Ctnnb1 silencing in T cells abrogated the enhanced proliferation, TCM formation, and cytotoxic activity induced by SHP1-deficient DCs. DC-intrinsic SHP1 restrains central memory CD8 T cell formation via the TCF-1/Wnt/β-catenin axis. - Source: PubMed
Publication date: 2026/07/01
Li BingLu HuilinHuang JiayiLiang YushengYu WeizeWu ShunhongLei TingTan XiaomingZhang Yuan - Glioblastoma (GBM) is a highly aggressive brain tumor in which hypoxia plays a central role in driving tumor progression, cellular plasticity, and resistance to treatment. In order to mimic these pathological features under conditions, a bioprinted GBM model was developed by integrating a PDMS-based hypoxia chip with a hydrogel composed of hyaluronic acid methacrylate (HAMA) and decellularized extracellular matrix (dECM), aiming to replicate the biochemical, mechanical, and oxygen-deprived conditions of native tumors. Glioblastoma (U87) and microglia (HMC3) cells were bioprinted within the hydrogel in the core and the periphery of the compartmentalized model, respectively. Hypoxic conditions were generated passively by placing a glass barrier and monitored using a fluorescence-based probe. The model was able to reproduce the key GBM features, including pseudopalisading necrosis (central Ki67/necrotic and peripheral Ki67/proliferative cells) and a 32% increase in invasion distance under hypoxic conditions. Gene expression analysis revealed that hypoxic conditions induced the upregulation of proliferation (EGFR, Ki67), stemness (SOX2, NES), and invasion (MMP2, CD44, TGFβ) associated markers, while proteomic analysis showed increased glycolysis, HIF1 signaling, and amino acid biosynthesis. Drug testing with temozolomide (TMZ) demonstrated reduced sensitivity under hypoxic conditions, shown by a 56% increase in IC, reflecting clinically relevant therapy resistance. These findings show the ability of the model to mimic key properties of the GBM microenvironment at both phenotypic and molecular levels and offer a physiologically relevant platform to study GBM biology and evaluate therapeutic responses. - Source: PubMed
Publication date: 2026/07/01
Isik SeymaYucel DenizHasirci Vasif