Anti_Human, mab CD50 Source Mouse
- Known as:
- Anti_Human, mab CD50 Source Mouse
- Catalog number:
- 101-M309
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CD50 Source Mouse
Related genes to: Anti_Human, mab CD50 Source Mouse
- Gene:
- ICAM3 NIH gene
- Name:
- intercellular adhesion molecule 3
- Previous symbol:
- -
- Synonyms:
- CDW50, ICAM-R, CD50
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-19
- Date modifiied:
- 2016-01-15
Related products to: Anti_Human, mab CD50 Source Mouse
Related articles to: Anti_Human, mab CD50 Source Mouse
- TM4SF1, a small transmembrane glycoprotein, has been implicated in tumor progression across multiple cancers. However, its functional and regulatory roles in esophageal cancer, particularly esophageal squamous cell carcinoma (ESCC), remain unclear. This study aims to characterize TM4SF1 expression in an ESCC cell line, KYSE150, determine its biological role in tumor cell phenotypes, and profile miRNA changes after knockdown and perform in silico target or pathway analyses. First, gene expression was analyzed in the KYSE150 cell line by qRT-PCR. shRNA-mediated knockdown was applied to the KYSE150 cells, followed by proliferation, migration, and apoptosis assays. MiRNA sequencing followed by bioinformatic analyses predicted microRNAs and potential genes targeting TM4SF1, which also included putative composite pathways and gene ontologies. gene expression was significantly upregulated in the KYSE150 cells compared to EC109 ESCC and HET1A cells, a normal esophageal epithelial cell. Functional bioassays revealed that knockdown significantly reduced cell proliferation (MTT and CCK-8 assays) by 46%, while reducing wound closure at 24 h by 30.5% with recovery by 48 h and increased 90% of caspase 3/7 activity. The exploratory sequencing of miRNAs revealed the ten most differentially expressed miRNAs (hsa-miR-6510-3p, hsa-miR-675-5p, hsa-miR-524-5p, hsa-miR-9902, hsa-miR-520f-3p, hsa-miR-3192-5p, hsa-miR-1973, hsa-miR-3614-5p, hsa-miR-501-3p, and hsa-miR-1298-5p), whereas bioinformatic analyses predicted 54 target gene predictions, including TP53, RB1, and ICAM3, and 13 composite pathways that encompassed processes such as apoptosis, cell adhesion, and metabolic regulation. This study provides preliminary and useful insights into the role of TM4SF1 within the KYSE150 ESCC cell-line model and provide a basis for future validation in additional ESCC models, alongside initial investigations into its molecular mechanisms, and underscores the necessity of further validation in diverse cells and models and possible therapeutic implications. - Source: PubMed
Publication date: 2026/04/22
Stephen AnnatashaWu Yuan SengRahim Nur SyafiqahTune Bernadette Xin JieLee Michelle FeliciaKhan AbbasSim Maw ShinHashim Najihah MohdVelaga Appalaraju - Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by dysregulated immune responses and impaired epidermal barrier function. A major therapeutic challenge is the identification of molecular targets capable of coordinately regulating both processes. Here, we identify dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) on keratinocytes as one such target. We demonstrate functional expression of DC-SIGN on keratinocytes and show that its engagement by a synthetic heparin analogue-exemplified by the oligosaccharide octaparin-produces profound therapeutic benefits. In a DNCB-induced murine model of AD, topical application of octaparin alleviated disease severity, suppressed both Th1- and Th2-type inflammatory responses, and restored expression of key epidermal barrier proteins such as filaggrin and loricrin. Metabolomic profiling further confirmed that octaparin treatment globally reversed disease-associated metabolic perturbations. Mechanistically, engagement of DC-SIGN on keratinocytes attenuated JAK-STAT signalling induced by key AD-associated cytokines, including IFN-γ and IL-4/IL-13. This attenuation led to reduced production of pro-inflammatory chemokines and cytokines, accompanied by increased expression of barrier-related genes. Critically, inhibition of DC-SIGN abolished the therapeutic effects of octaparin, establishing a causal requirement for this receptor. Our findings unveil a previously unrecognized role for keratinocyte DC-SIGN in coordinating immune and barrier responses and highlight it as a druggable target for novel therapeutic strategies in AD. - Source: PubMed
Publication date: 2026/04/25
Liu QiaozhenChen SimengLin WenyuYu NingFang RuiWang JinglongZhang JianfaXu Xi - Women often experience greater disability after ischemic stroke than men, but the biological mechanisms underlying these differences remain unclear. Proteomic analysis may identify sex-specific molecular pathways that contribute to stroke rehabilitation and recovery. - Source: PubMed
Publication date: 2026/04/19
McLouth Christopher JHazelwood Hunter SFrank Jacqueline AHarp Jordan PDornbos DavidFraser Justin FPennypacker Keith R - In vivo-generated monocyte-derived dendritic cells (moDCs) play a pivotal role in inducing effective immune responses against infections and cancer due to their exceptional cross-presentation capabilities. However, the in vivo generation of moDCs during immunotherapy is constrained by the absence of safe and efficient in vivo strategies. Here, we propose a chitosan oligosaccharide-based CaCO nanoparticle-loaded hydrogel (CCH) to facilitate effective in vivo monocyte-to-moDC conversion by leveraging its in-situ spatiotemporal regulation capabilities. The CCH promotes the secretion of chemokines to recruit monocytes and then targets a dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN)-pathway to facilitate the differentiation of monocytes into moDCs within a subcutaneous immune niche formed by CCH. After the removal of DC-SIGN cells in DC-SIGN-DTR mice, the proportion of CCH-induced moDCs significantly decreased, indicating the DC-SIGN-dependent conversion of moDCs. Accordingly, the tumor cell loaded-CCH (TCH)-induced moDCs facilitate cross-presentation to prime T cells and enhance robust antitumor T cell memory responses. Thus, subcutaneous injection of TCH effectively prevent the growth of primary liver cancer and patient-derived xenograft (PDX) colorectal cancer. Moreover, TCH inhibits postoperative tumor recurrence, providing promising advancements in immunotherapy. Our CCH-based strategy provided important insights on how to in vivo induce moDCs to harness cross-presentation for anti-tumor therapy. - Source: PubMed
Publication date: 2026/03/02
Lin JiakeLi BenkeWang XunZhou YueminSong JinyuanTang JianghuiZhang JunleiHao HaibinJi YongtaoLiu ZhenyuShen XingcanChen XiaoSheng JianpengTang RuikangWang Xiaoyu - Primary resistance to hypomethylating agents (HMAs) remains a major obstacle in the treatment of elderly patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). An altered integrity of the vascular wall is suspected to contribute to this resistance, yet the underlying molecular mechanisms remain unclear. Here, we show that small extracellular vesicles (sEVs) derived from leukemic cells resistant to decitabine (DAC-R), a commonly used HMA, promote vascular permeability by downregulating tight junction proteins, including ZO-1, occludin, and claudin5, in endothelial cell monolayers. This disruption of vascular integrity may facilitate vascular leakage and leukemic cell dissemination. Mechanistically, DAC-R cells exhibit increased expression of the fucosyltransferase FUT4, driven by the transcription factor TWIST1, leading to enhanced biosynthesis of non-sialylated Lewis X (LeX) structures. FUT4-mediated LeX modification stabilizes intercellular adhesion molecule 3 (ICAM3) on sEVs, and the delivery of LeX-modified ICAM3 to endothelial cells suppresses NF-κB signaling, impairing endothelial barrier function. Functionally, vascular remodeling driven by fucosylated sEVs promotes leukemic dissemination, suggesting that disruption of vascular homeostasis represents an additional layer of therapeutic resistance. These findings define a TWIST1-FUT4-LeX-ICAM3 axis and highlight glycosylation as a critical mediator of vascular microenvironment remodeling in MDS/AML. - Source: PubMed
Publication date: 2026/03/05
Feng JingjingWang KexinGou JunjieWang YiHu BowenWei WeiGe JunqiFeng YanliFeng ShuangSolary EricGuan FengLi Xiang