CD44 (HCAM) Antibody
- Known as:
- CD44 (HCAM) Antibody
- Catalog number:
- MAB348C
- Product Quantity:
- 0.5 ml
- Category:
- -
- Supplier:
- INNOVEX
- Gene target:
- CD44 (HCAM) Antibody
Related genes to: CD44 (HCAM) 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 (HCAM) Antibody
Related articles to: CD44 (HCAM) Antibody
- Extracellular matrix (ECM) disorder was considered as the result of fibrosis, but it is recently recognized that fibrotic ECM initiates a self-reinforcing circuit and contributes to development of fibrosis. Versican, an ECM component, participates in cell-ECM interaction and ECM regeneration. In pleura, versican is primarily derived from pleural mesothelial cells (PMCs). However, the role and mechanism of versican in pleural fibrosis remained unknown. In this study, versican and versican-mediated pleural viscoelasticity was found elevated in both human and murine pleural fibrotic tissues. Versican knockdown by shRNA prevented increases of viscoelasticity as well as pleural fibrosis. High level of versican and viscoelasticity promoted mesothelial to mesenchymal transition (MesoMT) in PMCs. Mechanistically, increased viscoelasticity induced pleural fibrosis through CD44/USP10/Smad4 mechanotransduction pathway. In conclusion, these results revealed that excessive versican in fibrotic pleural ECM enhanced ECM viscoelasticity, and consequently promoted progression of pleural fibrosis. - Source: PubMed
Publication date: 2026/04/23
Jia Zi-HengHe Xin-LiangCui Xiao-LinLi QianCheng Pei-PeiZhao Li-QinYe Shu-YiHu Shi-HeLian Chen-YueZhang He-DeLiang Li-MeiSong Lin-JieYu FanXiong LiangXiang FeiWang XiaorongWang MengDai XiyongYe HongMa Wan-Li - Despite serving as a radical alternative to surgery for inoperable colorectal hepatic metastases patients, thermal ablation faces local tumor progression rates up to 25% from residual tumors, seriously compromising treatment efficacy and survival of patients. We constructed hyaluronic acid (HA)-modified nanoparticles as carriers for the hydrophobic necrosis-avid agent I-hypericin (I-Hyp), enabling tumor necrosis-targeted radiotherapy. I-Hyp was synthesized via iodogen-catalyzed electrophilic substitution and loaded into amphiphilic block copolymer hyaluronan-b-poly(ε-caprolactone) (HA-PCL) using dialysis, yielding HA-PCL@(I-Hyp) nanoparticles (HP-NPs). HP-NPs were characterized in terms of size, stability, and drug release. Biodistribution and antitumor efficacy were evaluated in rodent models (nude mice and SRG rats bearing HT-29 subcutaneous tumors) with residual tumors induced by incomplete microwave ablation. HP-NPs showed 84.32% encapsulation efficiency, a uniform spherical shape with a hydrodynamic diameter of 75.66 nm, and rapid cytosolic degradation, enabling the release of I-Hyp in necrotic regions. After intravenous injection into animals with residual tumors, HP-NPs accumulated in tumor tissue through the enhanced permeability and retention effect and CD44/HA receptor-ligand interactions. The released I-Hyp remained selectively in necrotic areas, delivering localized β-radiation to the surrounding residual tumor tissue and significantly inhibiting tumor growth via induction of apoptosis. In conclusion, HP-NPs enable targeted radiotherapy to residual tumor tissue after ablation for colorectal metastases by leveraging necrosis avidity and CD44-mediated HA endocytosis, effectively reducing post-ablation tumor progression. This nanoplatform shows potential for clinical translation in colorectal metastasis treatment. - Source: PubMed
Publication date: 2025/11/07
Bao HanWang NingZhu XiaowenChen SongWang YangHan XiangjunZhong Hongshan - Melanoma is a highly aggressive skin cancer with biologically distinct subtypes. Acral melanoma (AM), a rare but particularly aggressive form, often presents with lymph node (LN) metastasis at diagnosis. Despite its clinical severity, the mechanisms underlying its metastatic behavior remain unclear. Emerging studies suggest the tumor microenvironment as a key driver of metastatic niche formation, but its specific role in AM progression is not well characterized. To investigate the role of the tumor microenvironment in AM progression, we performed single-cell RNA sequencing (scRNA-seq) on tumor tissues and matched adjacent normal samples from treatment-naïve AM patients, comparing cases with (LN) and without (LN) lymph node metastasis. Key transcriptomic findings were validated by immunofluorescence staining. Functional relevance was tested by conducting in vitro and in vivo assays. An independent validation cohort was employed to confirm key observations and evaluate prognostic associations. Our results reveal preferential SPP1 signaling pathways, including autocrine amplification within secreted phosphoprotein (SPP) 1 macrophages and their interactions with S100A8 melanoma cells via the SPP1-CD44 axis. S100A8 melanoma cells emerged as the predominant malignant subpopulation in LN metastatic tumors (56.3% versus 34.7% in non-metastatic cases). Clinically, elevated SPP1 expression emerged as an independent predictor of poor overall survival. In vivo, anti-SPP1 therapy induced a macrophage phenotype switch and significantly reduced tumor burden. Together, these findings indicate that LN AM is characterized by an SPP1 macrophage-driven immunosuppressive microenvironment and highlight the SPP1-CD44 axis as a promising therapeutic target for limiting AM dissemination. - Source: PubMed
Publication date: 2026/04/22
Liang YaoZheng YuliCai ZhimouShi ZhangruiShen MaoqiaYu RuixinWang FangCao XiaolongXu Rui - - Source: PubMed
Poluzzi ChiaraNastase Madalina-VivianaZeng-Brouwers JinyangRoedig HeikoHsieh Louise Tzung-HarnMichaelis Jonas BBuhl Eva MiriamRezende FlaviaManavski YosifBleich AndréBoor PeterBrandes Ralf PPfeilschifter JosefStelzer Ernst H KMünch ChristianDikic IvanBrandts ChristianIozzo Renato VWygrecka MalgorzataSchaefer Liliana - Renal tubular epithelial cells (TECs) are major targets of drug-induced kidney injury, a cause of acute kidney injury (AKI). Although TEC regeneration aids recovery, maladaptive repair promotes fibrosis and chronic kidney disease (CKD). CD44 has been reported to localize predominantly to dilated/atrophic TECs in the fibrotic lesions of rat CKD models, suggesting enrichment in failed-repair TECs, but its dynamics during the AKI-to-CKD transition are unclear. We examined CD44 across rat models spanning adaptive repair and AKI-to-CKD transition induced by renal ischemia/reperfusion (I/R; 30 or 60min) or cisplatin nephrotoxicity (2 or 6mg/kg, i.p.) through day 28. In the AKI-to-CKD transition settings (I/R 60min and cisplatin 6mg/kg), CD44 was induced in dilated/atrophic TECs before fibrosis. Re-analysis of mouse I/R single-cell RNA-seq confirmed Cd44 enrichment in maladaptive TEC clusters. In the cisplatin model, serum CD44 rose early and remained elevated after conventional markers normalized, paralleling renal CD44 induction. Microarray profiling of microdissected dilated/atrophic TECs revealed a matrix-associated signature. Immunohistochemistry showed reduced aquaporin 1, vimentin induction, and that CD44 tubules remained enclosed by a laminin-positive basement membrane. Pathway analysis predicted CD44 as a putative upstream regulator of fibrosis-related genes including Fn1; increased Fn1 mRNA in dilated/atrophic TECs with peritubular fibronectin accumulation suggested a possible tubular contribution to matrix deposition. Together, these findings support tissue CD44 as a candidate marker of maladaptive tubular repair during the AKI-to-CKD transition and suggest serum CD44 as a candidate circulating indicator in cisplatin nephrotoxicity. - Source: PubMed
Publication date: 2026/04/20
Matsushita KoheiAkane HirotoshiAkagi Jun-IchiMorikawa TomomiMizuta YasukoOgawa KumikoToyoda Takeshi