Rat Anti-Mouse CD44
- Known as:
- Rat Antibody toMouse CD44
- Catalog number:
- 128-10036-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD44
Related genes to: Rat Anti-Mouse 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: Rat Anti-Mouse CD44
Related articles to: Rat Anti-Mouse CD44
- Gastric cancer is an aggressive malignancy with poor prognosis due to complex pathogenesis, underscoring the need for biomarkers and targets. Core Binding Factor Beta Subunit (CBFB) has regulatory roles across cancers and shows promise, but its prognostic significance and mechanisms in gastric cancer remain unclear. - Source: PubMed
Publication date: 2026/04/30
Zhou QiWang LuWang Meng-HanYuan Yao-HongGuo JianChen BoZhang Ji-ZheWang Mi-Zhu - Pancreatic cancer (PC) is one of the most insidious malignant tumors with aggressive metastasis and ineffective treatments. Although gemcitabine (GEM) is the gold standard for PC, the acquired resistance and severe myelosuppression limit clinical utility. It has been found that abnormal aerobic glycolysis may be responsible for drug resistance in PC. Disulfiram (DSF), a commonly used anti-alcoholic drug, possesses potent anti-tumor activity combined with copper. Nevertheless, poor water solubility and neurotoxicity restrict clinical applications. Therefore, our group modified the structure of DSF and synthesized a novel compound CPD12C15, which exhibited stronger anti-tumor activity and lower neurotoxicity than DSF. Nanoparticles with excellent release properties, modified with hyaluronic acid (HA) targeting CD44, which is highly expressed on pancreatic cells, can evade the removal of natural defense system and enhance tumor-targeting ability. Herein, CPD12C15 was loaded into HA-modified PLGA nanoparticles (HPC-NP) in order to improve the sustained release properties and active targeting ability. Our research revealed that CPD12C15 combined with Cu (HPC-NP/Cu) could inhibit tumor proliferation, migration, invasion and induce apoptosis by suppressing the aerobic glycolysis pathway, which further inhibited cell stemness and drug resistance in vivo and in vitro, suggesting that it may be a potential strategy for PC treatment. - Source: PubMed
Publication date: 2026/04/27
Feng YafeiLv HuaiyouWang YinglinZhao GuozhiYan ChongzhengSun FengqinLi GenjvLi YuhanFu YaqingLi YizheZhao ZhongxiLi Kangqi - Cancer stemness is a major therapeutic challenge in oncology. This study investigated the functional role and molecular mechanism of cell division cycle-associated 8 (CDCA8) in non-small cell lung cancer (NSCLC) stem cells. In this study, NSCLC and paracancerous tissues were collected. The lung adenocarcinoma cell line A549 and the lung squamous cell carcinoma cell line NCI-H520 were used. The stem-like cell population in A549 and NCI-H520 was isolated by CD44+ fluorescence-activated cell sorting. Gene expression was detected by quantitative real-time PCR, western blotting, and immunohistochemical staining. Cell stemness was assessed by biomarker (SOX and NANOG) expression detection, colony formation assay, and sphere-formation assay. Cell migration and invasion ability were determined by the Transwell experiment. Our results showed that CDCA8 expression was higher in NSCLC tissues than in paracancerous tissues. CDCA8 overexpression enhanced stemness properties, as evidenced by increased biomarker expression and colony formation, larger sphere size, and enhanced migratory/invasive capacity. Conversely, CDCA8 knockdown had the opposite effect. Mechanistically, we identified Y-box binding protein 1 (YBX1) as a direct binding protein of CDCA8 mRNA that positively regulated CDCA8 expression. YBX1 overexpression had a similar effect to CDCA8. Furthermore, recovery experiments revealed that the stemness-promoting effect of YBX1 was reversed by CDCA8 knockdown. These findings were further validated in xenograft models, confirming that the YBX1/CDCA8 axis promoted tumorigenesis in vivo. Collectively, our study reveals that YBX1 enhances cell stemness and metastasis of NSCLC by promoting CDCA8 expression. Our findings established a new mechanism that maintains NSCLC stemness and may provide novel biomarkers. - Source: PubMed
Wu XiaominHu YuyouJi XiuyuZhao Yi - Rapid and accurate HIV detection is crucial for early diagnosis and viral load (VL) monitoring in individuals receiving antiretroviral therapy (ART). To address the challenge of limited sample volume, we developed a novel immunomagnetic sample preparation method to isolate HIV-1 virions from 25 μL of plasma─about one-tenth of a small finger-prick sample. Immunomagnetic conjugates were produced by coupling antimouse IgG magnetic beads with mouse IgG antibodies targeting host- and virus-derived antigens on the HIV surface. In buffer spiked with inactivated HIV-1 grown in the HUT-78 cell line, these conjugates achieved capture efficiencies of 45-97%. Optimization of conjugate concentrations (0.71-5.71 mg/mL) improved capture efficiency by 19%, with 15 min identified as the optimal capture time. In spiked plasma (25 μL), immunoconjugates targeting different surface antigens captured inactivated HIV-1 across inputs of 148-53,145 RNA copies/25 μL (5,920-2,125,800 RNA copies/mL) with consistent efficiencies ranging from 41% to 100%. In clinical specimens from individuals living with HIV with VLs ranging from 100,000 to >1 million copies/mL, capture efficiencies varied from 5% to 60% depending on the conjugate used. Notably, combining CD44 and CD46 targeting conjugates, which recognize different surface markers, did not enhance virion capture, suggesting the coexpression of targeted antigens on HIV-1. Together, our results established immunomagnetic isolation as a promising approach for HIV-1 sample preparation, enabling more accessible, sensitive, and rapid VL quantification. - Source: PubMed
Publication date: 2026/04/29
Gulati Gaurav KPanpradist NuttadaLutz Barry RLai James J - Recent studies have shown that dengue virus (DENV) infection during pregnancy is linked to adverse pregnancy outcomes, presenting an emerging clinical challenge with poorly understood pathogenic mechanisms. Uterine vascular remodeling, a critical determinant of successful pregnancy, is predominantly regulated by uterine natural killer (uNK) cells. In this study, we explored the effect of uNK cells on uterine injury in a DENV-induced adverse pregnancy mouse model. Transcriptomic analysis revealed significant dysregulation of uterine vascular remodeling and immune response-related gene expression after DENV-2 infection. Histopathological analysis revealed vascular remodeling disorders characterized by the preservation of vascular smooth muscle and a high level of tight junction protein in the vascular wall, accompanied by abnormal dilation of the lumen. These structural abnormalities coincided with a marked increase in uNK cell infiltration in the uterus. Moreover, the depletion of NK cells with anti-Asialo-GM1 mitigated uterine vascular damage and improved pregnancy outcomes. Single-cell RNA sequencing revealed a subpopulation of uNK cells (uNK2) that is characterized by upregulated expression of cytotoxicity-related genes. We further revealed that monocytes/macrophages (Mon_Macro) serve as intermediates in uNK2-mediated neutrophil (NE) recruitment. The SPP1-CD44 signaling axis is the dominant pathway governing uNK2-Mon_Macro crosstalk, and activated Mon_Macro2 can secrete chemokines such as CXCL2 to recruit NE. These findings provide valuable insights into the pathogenesis of DENV-induced uterine injury and facilitate the development of targeted therapeutic interventions for DENV-associated gestational disorders.IMPORTANCEDengue virus (DENV), a globally prevalent mosquito-borne virus, increasingly threatens maternal health because its infection is linked to adverse pregnancy outcomes. However, the mechanisms underlying DENV-induced damage to the uterus remain elusive. This study revealed impaired uterine vascular remodeling and abnormal vascular dilation followin DENV-2 infection. Notably, uterine natural killer (uNK) cells are the critical pathological determinants of vascular injury in the uterus. Mechanistically, uNK cells may influence monocytes/macrophages (Mon_Macro) through SPP1-CD44 signaling to drive neutrophil infiltration, leading to uterine damage and adverse pregnancy outcomes. Successful depletion of NK cells reduces vascular damage and improves pregnancy outcomes. These findings provide critical mechanistic insights into DENV-2-induced uterine pathological lesions, fundamentally advancing our understanding of mosquito-borne virus-associated gestational diseases. The identified molecular cascades not only reveal the etiological landscape of pregnancy complications but also establish therapeutic measures for intervention strategies in mosquito-borne viral disorders. - Source: PubMed
Publication date: 2026/04/29
Xue FeiyangFan DongyingWang HanYang YilinHe ShiqiZhang HaoSong ZhengranZhang YingyingGao NaWang PeigangAn JingSheng Ziyang