CDH5 _ Cadherin_5 _ CD144 Protein
- Known as:
- CDH5 _ Cadherin_5 _ CD144 Protein
- Catalog number:
- 10433-H03H
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- CDH5 _ Cadherin_5 CD144 Protein
Related genes to: CDH5 _ Cadherin_5 _ CD144 Protein
- Gene:
- CDH5 NIH gene
- Name:
- cadherin 5
- Previous symbol:
- -
- Synonyms:
- 7B4, CD144
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2016-10-05
Related products to: CDH5 _ Cadherin_5 _ CD144 Protein
Related articles to: CDH5 _ Cadherin_5 _ CD144 Protein
- CD31EMCN (type H) vessels orchestrate the bone metabolic microenvironment, yet the epigenetic control of their endothelial identity remains unclear. N6-methyladenosine (m6A), catalyzed by Mettl3, is essential for mRNA fate and emerging as a regulator of skeletal homeostasis. After isolating and validating type H bone microvascular endothelial cells (H-BMECs) from mouse femora, we used lentiviral shRNA and endothelial-specific Cdh5-Cre;Mettl3 mice to silence Mettl3 in vitro and in vivo. m6A-seq and RNA-seq pinpointed downstream targets; qPCR, Western blot, MeRIP-qPCR, RNA stability, migration, and tube formation assays dissected mechanisms. Local platelet-derived growth factor-BB (PDGF-BB) administration was employed to rescue Mettl3-null phenotypes. Mettl3 expression and global m6A levels were reduced in ovariectomy-induced osteoporosis. Knock-down or genetic deletion of Mettl3 decreased m6A methylation within the 3'UTR of Pdgfrb, accelerated Pdgfrb mRNA decay, blunted PI3K/AKt signaling and impaired H-BMEC proliferation, migration and tube formation. Consequently, type H vessels and trabecular bone mass were markedly diminished. PDGF-BB ligand delivery restored Pdgfrb abundance, reactivated PI3K/AKt, and fully reversed vascular and skeletal defects in Mettl3-null mice. Mettl3-mediated m6A methylation preserves Pdgfrb mRNA stability in bone endothelial cells and is associated with the maintenance of type H vessels, thereby coupling angiogenesis to bone formation. Targeting the Mettl3-m6A-Pdgfrb/PI3K-AKt axis may represent a potential therapeutic strategy for estrogen-deficiency-induced bone loss. - Source: PubMed
Zhou ShijieZhu YihuaYun LiLi MuzheZhang TianchiWumiti TaxiZhou QinfengChen ShuangliuHu YueHan ZhitaoZhang ChunleiTong KaiZhang YafengMa YongGuo YangWang Lining - Myocardial ischemia-reperfusion (I/R) injury presents a significant clinical challenge characterized by a complex pathological mechanism. The role of protein ubiquitination in I/R injury has not been systematically investigated. Global ubiquitinome profiling was conducted to identify the potential key players in myocardial I/R injury. - Source: PubMed
Publication date: 2026/04/17
Shuolin LiuChuanyin LiZhu MinZhu TingfangLi Yiran ELiu YanlinXu ChenguoWang HongyanHu RongguiGe JunboZhang Yingmei - miR-142-3p is aberrantly expressed in preeclampsia placentas, but its regulatory mechanisms in trophoblasts remain incompletely understood. Given that miRNAs exert biological effects primarily by targeting the 3'UTR of downstream genes, we prioritized potential downstream regulators of miR-142-3p to elucidate its pathogenic mechanism in preeclampsia. This study aims to elucidate how miR-142-3p modulates trophoblast functions and its clinical significance in preeclampsia pathogenesis using integrated bioinformatics and experimental approaches. - Source: PubMed
Publication date: 2026/03/25
Shan LongLu KunZhang YuanTao XuejiaoMa YalanFen Shaomin - Cadherin-5 (CDH5), also known as vascular endothelial cadherin (VE-cadherin), plays crucial roles in endothelial cell adhesion, vascular barrier function, and signaling. CDH5 manages endothelial cell-cell junctions during vascular remodeling, which is vital for both vascular homeostasis and adaptive responses to pathological stimuli. Although anti-CDH5 monoclonal antibodies (mAbs) are used for specific applications such as flow cytometry, Western blotting, and immunohistochemistry (IHC), highly sensitive and versatile anti-CDH5 mAbs suitable for all these applications remain limited. Here, new anti-human CDH5 mAbs, called CaMabs, were developed through a flow cytometry-based high-throughput screening. Among them, clone CaMab-8 (mouse IgG, kappa) recognized CDH5-overexpressed Chinese hamster ovary-K1 (CHO/CDH5) cells in flow cytometry. Moreover, CaMab-8 also recognized endogenous CDH5-expressing human endothelial cell lines (HUVEC/TERT2 and HDMVEC/TERT164-B) and a cervical cancer cell line (HeLa). These reactivities exceeded those of a commercial anti-CDH5 mAb (clone BV9). The apparent dissociation constant of CaMab-8 for CHO/CDH5 was measured as 6.1 × 10 M. CaMab-8 can detect endogenous CDH5 in Western blotting. In addition, CaMab-8, but not BV9, can be used for IHC to detect endothelial cells in formalin-fixed paraffin-embedded tissues. These findings suggest that CaMab-8 is a versatile basic research tool in vascular biology and has potential for clinical applications including tumor diagnosis and therapy. - Source: PubMed
Publication date: 2026/04/09
Yamamoto HarutoSuzuki HiroyukiKaneko Mika KKato Yukinari - Atherosclerotic plaques form through lipid and immune cell accumulation beneath the arterial endothelium. CD8 T cells are abundant in lesions, and their activation correlates with cardiovascular disease severity. Although endothelial cells recruit CD8 T cells to low and disturbed flow regions, whether they regulate CD8 activation and persistence is unknown. These interactions may be mediated by posttranscriptional control of mRNA translation. - Source: PubMed
Publication date: 2026/04/09
Nicholas Sarah-Anne EHelming Stephen BMénoret AntoinePathoulas Christopher LXu Maria MHensel JessicaKimble Amy LHeineman BrentJellison Evan RReese BoZhou BeiyanRodriguez-Oquendo AnnabelleVella Anthony TMurphy Patrick A