Anti-Canine CD44 FITC 100 tests
- Known as:
- Antibody toCanine CD44 fluorecein 100 tests
- Catalog number:
- 11-5440-42
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Canine CD44 FITC 100 tests
Ask about this productRelated genes to: Anti-Canine CD44 FITC 100 tests
- 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
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- Metastasis remains the leading cause of cancer-related mortality, a process in which circulating tumor cells (CTCs) play a central but incompletely understood role. Although most CTCs are rapidly eliminated during circulation through detachment-induced anoikis and fluid shear stress (SS)-triggered apoptosis, a subset of CTCs can survive these hostile conditions; however, the underlying mechanisms remain poorly defined. To investigate this, we developed a microfluidic circulatory system that mimics physiological SS and performed transcriptomic profiling of A549 lung cancer cells under SS, attached, and static suspension conditions. Through this approach, we identified the ROS-CD44-Ezrin axis as a potential mechanosignaling module that may contribute to CTC survival under shear stress. In this cascade, SS-induced ROS and CD44 converge to activate Ezrin via phosphorylation at Thr567. Once activated, Ezrin appears to coordinate its two canonical functions-membrane-cytoskeleton reinforcement and pro-survival signaling via PI3K/AKT/Bcl-2 and NF-κB/p38/JNK pathways-within this specific mechanobiological context to preserve cell integrity and limit apoptosis. Our findings suggest that these well-established molecular functions are differentially engaged under shear stress, revealing a context-dependent survival mechanism that may offer opportunities for therapeutic exploration, pending further validation in more clinically relevant models. - Source: PubMed
Publication date: 2026/09/03
Zhang XiaoyingZhou MuyaLi KoukouYuan MinghengTong HaiboLuo Kathy Qian - To evaluate the therapeutic effects of arsenic trioxide (ATO) in lupus-prone mice and to determine whether SOCS1/JAK2/STAT3/IL-17A-related inflammatory regulation is relevant to human systemic lupus erythematosus (SLE) using public transcriptomic and DNA methylation datasets. Two in vivo experiments were performed using MRL/lpr mice. The first assessed the effects of ATO on hepatorenal injury and inflammatory gene expression. The second further evaluated these findings using C57BL/6 controls and MRL/lpr mice treated with ATO, 5-Azacytidine (5-Aza), or their combination. Serum biomarkers, histopathology, and the mRNA expression of the SOCS1/JAK2/STAT3 axis were analyzed. Network pharmacology was used to predict potential ATO-related targets and pathways in SLE. WGCNA was performed using the GSE4588 human CD4⁺ T-cell transcriptomic dataset to identify SLE-associated co-expression modules. Disease-context support was assessed using the GSE65391 whole-blood transcriptomic dataset. SOCS1 promoter-associated methylation was further evaluated using the GSE82218 PBMC DNA methylation dataset. ATO improved lupus-like manifestations in MRL/lpr mice, reduced anti-dsDNA antibodies, IgG, urinary protein, and hepatorenal injury markers, restored complement C3, and alleviated renal and hepatic inflammation. At the molecular level, ATO treatment was associated with reduced DNMT1 expression, increased SOCS1 expression, and decreased JAK2, STAT3, and IL-17A transcription. Network pharmacology highlighted Th17 cell differentiation as a candidate ATO-related pathway in SLE. WGCNA of the GSE4588 human CD4⁺ T-cell transcriptomic dataset identified SLE-associated co-expression modules and hub genes. STRING/Cytoscape analysis further identified hub genes including CD44, TLR4, THBS1, and TET2, suggesting disease-associated immune and inflammatory network remodeling in SLE CD4⁺ T cells. In GSE65391, JAK2 and STAT3 expression and JAK/STAT-related signatures were increased in SLE. In the GSE82218 DNA methylation cohort, SOCS1 promoter-associated CpG sites showed site-specific hypermethylation in SLE. ATO ameliorates lupus-like immune and hepatorenal injury in MRL/lpr mice, accompanied by DNMT1/SOCS1-related transcriptional changes and reduced JAK2/STAT3/IL-17A-related inflammatory transcription. Public human transcriptomic and DNA methylation data support the disease relevance of this regulatory context. - Source: PubMed
Publication date: 2026/09/29
Zhang YiChen XiaoYuShi ChenXiFu JiaYingChen XinYiShao FengXie ZhiJunYang XiaoBing - Progress in clinical requirements creates high demands for advanced biomedical materials. As a natural linear anionic polysaccharide, hyaluronic acid (HA) exhibits favorable properties such as outstanding biocompatibility, non-immunogenicity, enzyme-triggered degradation and CD44-targeting ability, attracting widespread interest in tissue engineering, drug delivery and organ chip. However, due to the wide particle size distributions, the inability to construct complex microarchitectures, and common toxic organic solvent residues, the traditional fabrication methods severely obstruct the performance of HA materials. Moreover, these drawbacks prevent HA materials from meeting rigorous biomedical standards and restrict the clinical application in precision medicine. What's more, microfluidic technology can overcome the above manufacturing limitations, enabling the fabrication of highly monodisperse HA materials with distinct microstructures to support co-loading and spatiotemporally controlled release of multiple therapeutics. While existing reviews cover HA biomaterials, general microfluidic fabrication, and its biomedical applications, a systematic framework integrating microfluidic engineering with HA properties remains absent. To fill this gap, this review establishes an integrated design framework for microfluidic-engineered HA materials, bridging processing parameters, precise microstructural control and programmable biomedical functions. This work summaries microfluidic configurations and operating parameters, discusses HA modification and crosslinking strategies adapted to microfluidic processes, analyses structure-function relationships, and describes typical biomedical applications. Moreover, the critical challenges involving clinical translation, large-scale production and artificial intelligence-assisted optimization are also highlighted. In conclusion, this work establishes a systematic guideline for developing microfluidic engineered HA materials, offering theoretical support to basic research and industrial translation. - Source: PubMed
Publication date: 2026/09/28
Xu FenglanGao YangLi SenpengZheng HuiyuanXin HuanWang YangqingLi BoSun WentaoMa Qingming - The malignant progression of nonsmall cell lung cancer (NSCLC) is closely related to cancer stemness. Histone deacetylase 4 (HDAC4) plays a regulatory role in lung cancer, but its effect on NSCLC stemness remains unclear. This study aimed to investigate the role and mechanism of HDAC4 in NSCLC stemness. - Source: PubMed
Chen ChangxianJiang XiaomingYao ZhenwuSun JiaxueZhang LijuXu MingyuBao WeiminLiu Weijun - Andrographolide (AG) has been reported for its anticancer activity. However, it is classified as a class IV in the biopharmaceutics classification system (BCS). Therefore, AG possesses low bioavailability due to its low solubility and permeability. In this study, hyaluronic acid-coated chitosan nanoparticles (Hyalo-CS-NPs) were formulated to enhance AG delivery and allow the active targeting of CD44 receptors overexpressed on breast cancer cells. Results showed optimized AG-Hyalo-CS-NPs with a size of 388.2 ± 1.41 nm, a zeta potential of -25.7 ± 1.58 mV, and an entrapment efficiency of 95.3%±1.01%. In vitro release profile revealed a sustained pH-responsive release from coated and uncoated CS-NPs with greater AG release under acidic conditions that mimic the tumor microenvironment. The MTT assay demonstrated the sharpest decline in the MCF-7 cell viability. Moreover, flow cytometry studies illustrated a significant apoptosis compared to uncoated nanoparticles and AG suspension. In addition, biochemical marker evaluation showed upregulating of the pro-apoptotic protein Bax and downregulating of Bcl-2, HER2, and Cyclin D1, confirming the underlying mechanism of the anticancer activity. Finally, confocal imaging showed higher intracellular uptake from coated and uncoated CS-NPs by 2.2-fold and 1.85-fold, respectively. In conclusion, AG-Hyalo-CS-NPs is a smart, targeted nanoplatform that improves AG anticancer efficacy in breast cancer management. - Source: PubMed
Publication date: 2026/09/27
Shoala Sohaila AAbbas HaidyElbedaiwy Heba MShamaa Marium MElsheikh Manal A