Rat Anti-Mouse CD44, FITC-labeled
- Known as:
- Rat Antibody toMouse CD44, fluorecein-labeled
- Catalog number:
- 128-10040-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD44 FITC-labeled
Related genes to: Rat Anti-Mouse CD44, FITC-labeled
- 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, FITC-labeled
Related articles to: Rat Anti-Mouse CD44, FITC-labeled
- Aging is characterized by a progressive decline in cellular and tissue function, shaped in part by disruptions in communication between the extracellular matrix (ECM) and intracellular signaling networks. The cell surface receptor CD44 functions as a molecular hub, integrating signals from a remodeled ECM to regulate core aging programs including senescence, inflammation, and metabolic balance. This review synthesizes evidence that CD44, through its structural domains, isoform diversity, and proteolytic processing, integrates extracellular cues to modulate key pathways such as STAT3, NF-κB, and the class III PI3K complex. Mechanistically, HA-fragment engagement of CD44 activates the CD44-STAT3 axis in vascular tissue, suppressing autophagic flux and promoting endothelial senescence. Concurrently, ECM-derived ligand binding to CD44 drives NF-κB signaling that amplifies chronic inflammation in a tissue and context-dependent manner, contributing to inflammaging. Functional outcomes are context-dependent, shaped by isoform switching and γ-secretase-mediated release of CD44-ICD, which may drive degeneration or support repair and proteostasis. Emerging single-cell and spatial transcriptomics reveal spatiotemporal CD44 dysregulation across vasculature, brain, adipose tissue, kidney, and liver. This review establishes CD44 as a mechanistic link connecting ECM remodeling to nuclear responses in aging and outlines therapeutic strategies including ligand competition, antibody blockade, and γ-secretase modulation to mitigate age-related pathology and extend health span. These insights provide a coherent framework for understanding aging biology and guiding future translational interventions targeting CD44 signaling pathways effectively. - Source: PubMed
Publication date: 2026/07/22
Ali Syeda AyeshaQiang PengfeiZhou XiaojunYang XiaotingLi ShangShen YunpengChen ZhiqiangZhang Lu - Uveal melanoma (UM) is a deadly ocular malignancy with well-described genetic alterations that predict disease outcome. However, our current understanding of the biological underpinnings of high-risk uveal melanoma progression remains relatively limited. Using RNA expression profiles from 250 patients with UM, we identified 12 novel biomarkers associated with high-risk UM, with protein expression level validation of the top two candidates: the transcriptional regulator RBFOX2 and matrix protein COL9A3. Moreover, we investigated the functional contribution of COL9A3 via its overexpression in EIF1AX and BAP1 UM cell lines. Our data suggest that COL9A3 enhances cell motility and cell proliferation and alters morphology specifically in BAP1 UM cells. Furthermore, zebrafish xenograft studies revealed increased cell dissemination in a EIF1AX UM cell line upon overexpression of COL9A3, whereas a BAP1 UM cell line remained unchanged under wild-type conditions. Interestingly, RNA sequencing revealed a high-stress profile by upregulated metabolic activity and loss of protein translation due to COL9A3 overexpression. BAP1 UM appears to adapt to this stress by upregulation of plasticity markers, such as CD44, Nestin, EZH2, ABCB5, PAX3 and CD166, as a coping mechanism. These markers are known as differentiation markers during the development of melanocyte biogenesis and are implicated in plasticity in other high-risk cancers. The relationship between COL9A3 and plasticity was validated by multiplex immunohistochemistry of formalin-fixed paraffin-embedded (FFPE) tissue, which demonstrated colocalization of COL9A3, CD44 and Nestin. BAP1-UM samples presented higher levels of COL9A3, CD44 and Nestin expression than EIF1AX or SF3B1 UM samples based on the mean fluorescent intensity of each marker. A positive correlation between COL9A3 and Nestin expression in triple-positive cells, irrespective of the UM subtype, was observed. Collectively, our findings suggest that COL9A3 is a novel high-risk biomarker that may contribute to UM cell plasticity and is most prevalent in BAP1 UM. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/07/21
van den Bosch QccVerdijk R MFadlelseed Hvan den Bosch TppOwens SKennedy SKilic EBrosens E - Astrocytes (ACs) play a crucial role within the immune microenvironment of glioma, facilitating its progression. Protein succinylation, a post-translational modification, may serve as a significant regulatory mechanism. SsDNA (single-chain oligonucleotide) drugs with specific sequences for the treatment of tumors have entered clinical trials with remarkable effects. - Source: PubMed
Publication date: 2026/07/21
Sun XiaomingWang XinyuZhang SaijunLong YingWang DanniGou ChanglongZhang WenziDeng ChunleiLiu CuiChen Zhuo - Synovial mesenchymal stem cells (MSCs) are a potential therapeutic option for meniscal injuries; however, the early cellular events following MSC application remain obscure. This study aimed to characterize the morphological and molecular changes occurring during the first 24 h after application of human synovial MSCs onto a structurally disrupted meniscal surface. MSCs were seeded onto a frozen-thawed, mechanically abraded meniscal surface under non-inflammatory conditions, and MSC morphology and gene/protein expression were evaluated before adhesion and at 1 h and 24 h after seeding. Scanning electron microscopy revealed MSCs with a round morphology and pseudopodia at 1 h, but flattened cells and multilayer formation at 24 h. MSCs attaching to nonbiological substrates showed similar time-dependent morphological changes. Gene expression analysis demonstrated time-dependent changes in CD44, BMP2, PRG4, TIMP1, TSG6, and integrin-related genes, including increased ITGA2 expression and decreased ITGA11 and ITGA4 expression at 24 h. Immunofluorescence staining detected these proteins before and after adhesion. These findings indicate that synovial MSCs undergo rapid morphological and transcriptional changes during early adhesion. Although these changes may partly reflect general adhesion-related processes, the results provide a descriptive framework for understanding the early behavior of MSCs upon application to a structurally disrupted, devitalized meniscal matrix surface. - Source: PubMed
Publication date: 2026/07/21
Meguro TomokoEndo KentaroOzeki NobutakeSakamaki YurikoNakagawa YusukeKoga HideyukiSekiya Ichiro - Diffuse IDH-mutant astrocytomas are brain tumors typically diagnosed as low-grade but capable of progressing to higher grades. They exhibit three cellular states resembling astrocytes, oligodendrocytes, and neural progenitor (NPC) cells. Understanding their biology has been limited by the scarcity of relevant in vitro models. Here, we established and extensively characterized four astrocytoma cell lines (LGG275, LGG336, LGG85, LGG349) derived from IDH-mutant astrocytomas of different grades and analyzed them using multi-omics approaches. These lines display growth rates in vitro and in vivo consistent with tumor grade and recapitulate some key molecular alterations observed in patient tumors, including IDH1, ATRX, and TP53 mutations, ALT (alternative lengthening of telomeres) activation and, in more aggressive lines, MET and PDGFRA alterations. Single-cell RNA sequencing revealed three major transcriptional states (astrocyte-like, oligodendrocyte-like, and NPC-like), consistent with those described in patient tumors. A hallmark of higher-grade-derived lines (LGG85, LGG349) is the persistence of NPC-like populations without growth factors possibly reflecting tumor progression. The LGG275 line most accurately mirrors slow-growing astrocytomas. Using CD44 and GLAST, we isolated astrocyte-like (CD44⁺/GLAST⁺) cells from LGG275 that preferentially adopt a quiescent state yet retain remarkable plasticity, generating oligodendrocyte-like cells (CD44⁻/GLAST⁻). Transcriptomic and proteomic analyses revealed that astrocyte-like and oligodendrocyte-like cells populations resemble, respectively, quiescent and activated neural stem (NSC) cells from the adult subventricular zone (SVZ). Finally, we provide evidence that NOTCH signaling contributes to the regulation of cell state balance, promoting transitions toward an astrocyte-like transcriptional program while DLL3, an anti-Notch protein, expressed by oligodendrocyte-like cells, modulates both proliferation and phenotype. These cell lines represent valuable resources for dissecting lineage dynamics, heterogeneity, and progression mechanisms in IDH-mutant astrocytomas. - Source: PubMed
Publication date: 2026/07/20
Garcia LeonorGranotier-Beckers ChristinePineau DonovanSika DassouHideg SzimonettaLabadie CamilleAguilar Cázarez KasandraKundnani JignaStuani LucilleGauthier Laurent RBoussin François DMouthon Marc-AndréUrbach SergeEl Koulali KhadijaSéveno MartialRipoll ChantalDaddi KawtarVerreault MaitéIdbaih AhmedO'Connor SamanthaPlaisier Christopher LChen WeiLv Sheng-QingZhang LeiZheng MinRigau ValérieDuffau HuguesHugnot Jean-Philippe