Rat Anti-Mouse CD44, Biotinylated
- Known as:
- Rat Antibody toMouse CD44, Biotinylated
- Catalog number:
- 128-10038-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD44 Biotinylated
Related genes to: Rat Anti-Mouse CD44, Biotinylated
- 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: Rat Anti-Mouse CD44, Biotinylated
Related articles to: Rat Anti-Mouse CD44, Biotinylated
- Chromoblastomycosis (CBM) is a chronic, neglected tropical fungal infection. Its immunopathogenesis, particularly the mechanism underlying its chronicity, remains poorly understood. - Source: PubMed
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Lei KexinTian JieZhang LuGong ZhuoqingLiu WenjieWan ZheWang YangLi RuoyuDong BilinWang Xiaowen - Injectable sodium hyaluronate (NaHA) is extensively utilized in aesthetic medicine as a dermal hydrating agent. However, there are few standardized, human-relevant preclinical methods that can reliably evaluate the moisturizing performance of those products. Existing animal and simplified cell-based models show restricted physiological relevance and insufficient sensitivity. To address this gap, we established a depot-mimicking reconstructed human full-thickness skin (RhFS) platform incorporating an inclusion-based intradermal delivery strategy. Instead of conventional mixing, this strategy mimics the clinical 'depot effect' of intradermal injection, allowing for the simultaneous assessment of cellular responses and tissue-level hydration dynamics. It forms a localized NaHA depot within the dermal compartment of RhFS and preserves spatial hydration gradients, which are lost when NaHA is mixed homogenously. The platform integrates physicochemical characterization of polymer-bound water states with cellular and tissue-level functional readouts. By quantifying key biomarkers, including CD44, aquaporin-3 (AQP3) and natural moisturizing factors (NMFs), our results demonstrate that the inclusion-based delivery strategy significantly outperforms conventional mixing approaches in activating epidermal hydration pathways. Crucially, this platform effectively distinguished the moisturizing efficacy of multiple commercial NaHA formulas, thereby revealing a structure-activity relationship between water-binding states and biological outcomes. Overall, this study presents a reproducible, mechanism-informed and human-relevant framework for preclinical performance evaluation of NaHA-based injectable biomaterials and provides a sensitive alternative to conventional animal-based approaches. - Source: PubMed
Publication date: 2026/02/09
Shi JianfengXu WennaLiu HongfuShan FengjuanWang RuiKe LinnanHan QianqianLu Yong - Chronic obstructive pulmonary disease (COPD) is characterized by incomplete recovery of airflow blockage; however, effective therapeutic agents that can prevent lung function deterioration are limited. East Asian herbal treatments have gained attention for their potential benefits in managing COPD. This study aimed to evaluate the inhibitory effects of Gyeongok-go (GOG) on lung injury in a COPD mouse model. Lipopolysaccharide (LPS)-induced alveolar macrophage (MH-S) cells were treated with GOG (50, 100, 200, and 400 μg/mL), and analyzed using enzyme-linked immunosorbent assay (ELISA). C57BL/6 mice were challenged with cigarette smoke extract and LPS and then treated with vehicle only, dexamethasone (3 mg/kg), or GOG (100, 200, or 400 mg/kg). Bronchoalveolar lavage fluid (BALF) or lung tissues were analyzed using cytospin, ELISA, real-time PCR, flow cytometry, hematoxylin and eosin, and Masson's trichrome staining. Treatment with GOG decreased tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 expression in LPS-challenged MH-S cells. In COPD mice, GOG significantly decreased the elevated numbers of neutrophils, total cells, macrophages, and Gr-1/Siglec-F, Gr-1/CD11b, and CD44/CD62L cells. It also downregulated the expression of TNF-α, IL-17A, macrophage inflammatory protein-2 (MIP2), and CXC chemokine ligand-1 in BALF. GOG also inhibited the increase in , , and mRNA expression. Moreover, GOG prevented the increase in the number of total cells, neutrophils, Gr-1/Siglec-F, Gr-1/CD11b, CD44/CD62L, and CD21/CD35/B220 cells in lung tissues. Notably, GOG decreased the severity of lung injury. Overall, these findings indicate that GOG alleviates lung injury, suggesting its potential in the treatment of COPD. - Source: PubMed
Publication date: 2026/04/14
Yang Won-KyungChoi Jin KwanKim Seung-HyungLee Su WonLyu Yee RanPark Yang-Chun - Non-small-cell lung cancer (NSCLC) constitutes approximately all lung cancers (LCs), and metastasis remains a major challenge in its treatment, thus necessitating the detection of novel molecular players involved in this process. In this study, we performed a comprehensive analysis of microarray and RNA-seq cohorts extracted from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to identify differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) and associated them with metastasis-related genes involved in brain metastasis (BM) in NSCLC. We thus identified differentially expressed metastatic genes (DEMGs) and constructed a protein-protein interaction network (PPIN) using these DEMGs. These DEMGs were further analyzed for associations with patient age, gender, and tumor stage, and the significant impact of specific genes on overall survival (OS) was assessed to determine the prognostic significance of the identified targets. We finally constructed a three-node microRNA (miRNA) feed-forward loop (FFL) involving miR-23b-3p, CD44, and five transcription factors (TFs) [EOMES, FOS, FOSL1, GLIS3, TP63] specific to NSCLC metastasis. Further mutational analysis of these FFL elements revealed that all were altered in the patient samples analyzed. Thus, our study identified potential genomic drivers that may play crucial roles in NSCLC BM. Overall, it provides valuable insights for the discovery of novel therapeutic targets in the management of NSCLC metastasis. However, further in vitro and in vivo experimentations are needed to justify the prognostic role of NSCLC biomarkers in BM pathogenesis. - Source: PubMed
Publication date: 2026/04/17
Singh PrithviDohare RavinsSarwar TariqueAlharbi Hajed Obaid ARahmani Arshad Husain - Immune thrombocytopenia (ITP) is an autoimmune disease. Megakaryocyte dysfunction caused by autoimmune response can lead to thrombocytopenia, and the underlying mechanism is still unclear. Single-cell sequencing analysis revealed the heterogeneity of CD34 + HSPCs in bone marrow between ITP patients and healthy groups. Pre-B cell population 1 (pre-B1) showed a significantly lower percentage contribution in ITP groups, and the underlying mechanism involves cell cycle-, cell apoptosis- and cell death-related pathways. The number of eosinophil-basophil mast cell progenitors (EBMPs) is significantly increased in ITP patients and the DEGs of the EBMPs in ITP patients were significantly enriched in immune-related pathways. Further, immunofluorescent staining and Western blot assay highlight C-X-C Motif Chemokine Ligand 8 (CXCL8) and Interferon Regulatory Factor 1 (IRF1) expression were significantly increased in the EBMPs of ITP patients. Furthermore, cell-cell communication analysis identified an impaired LGALS9-CD44 axis between EBMP cells and MkP1 cells in ITP patients, suggesting that targeting the LGALS9-CD44 interaction might hold promise as a therapeutic approach for ITP. Our observations indicate that ITP patients exhibit an elevated proportion of EBMP cells alongside a reduced proportion of pre-B1 cells. CXCL8 and IRF1 are potentially associated with EBMP cell dysfunction and the ITP disease process. Furthermore, the diminished LGALS9-CD44 axis between EBMP and MkP1 cells may contribute to ITP progression, suggesting a direction for future therapeutic investigation. - Source: PubMed
Publication date: 2026/04/15
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