CD44 (Phospho-Ser706) Antibody
- Known as:
- CD44 (Phospho-Ser706) Antibody
- Catalog number:
- 11911
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CD44 (Phospho-Ser706) Antibody
Related genes to: CD44 (Phospho-Ser706) 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 (Phospho-Ser706) Antibody
Related articles to: CD44 (Phospho-Ser706) Antibody
- Complement Factor H (FH) regulates the alternative complement pathway, and FH deficiency promotes complement activation, macrophage recruitment, and renal injury. Extracellular vesicles (EVs) mediate intercellular communication and may provide molecular signatures of tissue inflammation. We examined complement- and macrophage-associated transcriptional signatures in renal tissue and serum-, kidney-, and urine-derived EVs using a FH-deficient murine model of chronic serum sickness. Pilot kidney microarray analysis was combined with qRT-PCR and EV transcript profiling. FH deficiency increased renal expression of macrophage-associated inflammatory genes, including AIF1, MMP9, S100A10, and CD44, and the complement receptor C3aR1. EVs from FH-deficient mice lacked FH transcripts and exhibited increased complement- and macrophage-associated transcripts across serum-, kidney-, and urine-derived EV populations. EV transcriptional profiles paralleled inflammatory gene expression observed in renal tissue. FH deficiency-associated complement dysregulation produces coordinated inflammatory transcriptional signatures detectable in both kidney tissue and EVs. The concordance between intrarenal inflammatory programs and EV cargo suggests that EVs may reflect complement-mediated renal immune activity. In particular, urinary EVs may provide a non-invasive source of molecular information and potential biomarkers of complement-mediated kidney inflammation. - Source: PubMed
Publication date: 2026/09/07
Campanieri AumFraher ShaneSatheeshkumar Poolakkad SReynolds JessicaQuigg Richard JAlexander Jessy J - Osteoarthritis (OA) is the most prevalent chronic joint disorder. This study explored therapeutic mechanisms of intra-articular (i.a.) hyaluronic acid (HA), and/or dextrose prolotherapy (DPT) on surgically induced OA. Rats were divided into five groups (n = 12): control, OA, HA, DPT, and DPT + HA groups. OA group revealed increase in serum alkaline phosphatase (ALP) level, knee extension angle diameter, and CD44 immuno-expression, furthermore a decrease in cartilage thickness, chondrocyte density, and glycosaminoglycan and proteoglycan cartilage contents. Radiologically and microscopically, OA caused joint cavity narrowing, articular damage, exposed subchondral bone, and a rough surface. These parameters were modulated in HA, DPT, and DPT + HA groups. There were significant decreased ALP level (404.35, 414.97, and 318.73 U/L) (OA = 425.65 U/L), extension angle (29.25°, 47.93°, and 26.42°) (OA = 52.78°), knee diameter (7.52, 7.04, and 6.92 mm) (OA = 8.87 mm) and CD44-immunopositive chondrocyte percentage (73.27%, 16.33%, and 83.40%) (OA = 87.95%), and increased cartilage thickness (155.24, 186.83, and 230.56 μm) (OA = 115.98 μm), chondrocyte density (2.24, 3.11, and 3.21 cell × 10/μm) (OA = 2.01 cell × 10-3/μm), and glycosaminoglycan (0.653, 0.837, and 0.886) (OA = 0.485) and proteoglycan cartilage contents (0.588, 0.710, and 0.738) (OA = 0.340). There was no significant difference between HA and DPT groups except for extension angle, chondrocyte density, and glycosaminoglycan and proteoglycan contents were higher in the HA group, and CD44-immunoexpression was higher in the HA group. In conclusion, combination of i.a. HA and DPT has the upper hand in mitigation of OA parameters and is recommended for OA treatment. - Source: PubMed
Publication date: 2026/09/07
Nasr El-Din Wael AminPotu Bhagath KumarFadel Raouf AbdelrahmanAbdel Fattah Islam Omar - In this study, we developed a biodegradable CS-PLGA/pEGFP/HA ternary complex for intraocular gene therapy via intravitreal injection. In our system, plasmid-enhanced green fluorescent protein (pEGFP) was chosen as the model plasmid, chitosan (CS) was used to condense the plasmid DNA, poly(lactic-co-glycolic acid) (PLGA) provided sustained-release potential and structural protection for plasmids, and hyaluronic acid (HA) served as a ligand for targeting CD44 receptors on the surface of adult retinal pigment epithelial (ARPE-19) cells. In vitro evaluations revealed that the CS-PLGA/pEGFP/HA group exhibited higher cellular uptake, transfection efficiency, and protein expression levels compared with those of free pEGFP and CS-PLGA/pEGFP groups. Several previous studies have verified the feasibility of intravitreal plasmid delivery. Therefore, this CS-PLGA/pEGFP/HA ternary complex is a promising nonviral vector with the potential to deliver plasmids to ocular tissues and enhance protein expression in target cells. - Source: PubMed
Wang TianyiLiu YongqiXu JingfeiGao ShenghaoZhang ShimingYang Xinggang - Bladder cancer therapy is frequently limited by inefficient drug retention and adaptive immune resistance within a hypoxic tumor microenvironment. Here, we report a CD44-targeted, fully synthetic nanocomposite (HPPZC) that converts chemotherapy into a mitochondria-associated therapeutic strategy accompanied by tumor immune remodeling. Rapid microwave-assisted assembly integrates hyaluronic acid (HA), polydopamine (PDA), protamine, zinc oxide (ZnO), and camptothecin (CPT) into a structurally integrated hybrid nanocomposite with tumor targeting, while the PDA/ZnO interface functions as a redox-active platform associated with mitochondrial dysfunction and redox modulation. HPPZC induces rapid mitochondrial depolarization, elevates oxidative stress, and is associated with PINK1/Parkin-related mitochondrial quality-control and autophagy-associated turnover signatures. In vivo, HPPZC treatment prolonged local intratumoral retention and produced tumor regression. The combination of chemotherapy with mitochondrial stress and tumor immune remodeling, suppressing CXCL12 and PD-L1, promoting M1-like marker profile, and increasing CD8⁺ T-cell infiltration. This work establishes a reproducibly fabricated redox-active nanotherapeutic associated with mitochondrial stress that couples targeted chemotherapy with immune microenvironment remodeling for antitumor efficacy. - Source: PubMed
Publication date: 2026/09/05
E-Y Chuang AndrewTung Szu-YuTzou Kai-YiCai Yao-EnHsu Hao-ChengTsui Ke-HungLin Wei-XuanRethi LekshmiDong Shao-WeiNguyen Hieu TrungLiu Chia-Hung - Ferroptosis is an iron-mediated cell death process driven by lipid peroxidation, yet its antitumor potential is often counteracted by the limited endogenous HO content, the strict catalytic conditions required for the Fenton reaction, and protective autophagy. Notably, sustained autophagy drives ferritin degradation and iron release, thereby amplifying ferroptotic signaling. To exploit this mechanism, we designed a CD44-targeted nanoplatform, Cur@MG@HA, using hyaluronic acid for tumor-specific delivery. The system co-delivers glucose oxidase (GOx) and curcumin (Cur) within a Fe-Cu MOF. Following cellular uptake, GOx catalyzes the oxidation of intratumoral glucose to produce gluconic acid and HO. The acidic microenvironment promotes the Fe/Cu-mediated Fenton reaction, converting HO into OH and initiating ferroptosis. The resulting oxidative stress induces autophagy, a process further potentiated by Cur. Enhanced autophagy accelerates ferritin degradation, thereby elevating labile iron levels and establishing a self-reinforcing cycle that amplifies lipid peroxidation, culminating in ferroptotic cell death. In vitro and in vivo experiments demonstrate that the self-reinforcing cycle between autophagy and ferroptosis significantly enhances tumor suppression. This study provides a mechanistic basis for synergistic therapy through redox-metabolic modulation and suggests that targeting iron-autophagy crosstalk with nanomaterials represents a promising strategy for cancer treatment. - Source: PubMed
Publication date: 2026/09/05
Wang ChenshuoMa ZhenzhenLiu MengyuDu MengyuYao Hanchun