DDX48 antibody - middle region (ARP36422_T100)
- Known as:
- DDX48 (anti-) - middle region (ARP36422_T100)
- Catalog number:
- arp36422_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DDX48 antibody - middle region (ARP36422_T100)
Related genes to: DDX48 antibody - middle region (ARP36422_T100)
- Gene:
- EIF4A3 NIH gene
- Name:
- eukaryotic translation initiation factor 4A3
- Previous symbol:
- DDX48
- Synonyms:
- KIAA0111, EIF4AIII, Fal1
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2019-04-23
Related products to: DDX48 antibody - middle region (ARP36422_T100)
Related articles to: DDX48 antibody - middle region (ARP36422_T100)
- Bone metastasis remains a major cause of morbidity in estrogen receptor-positive breast cancer, with RANKL inhibitor resistance emerging as a critical clinical challenge. Nearly 40% of patients develop progressive skeletal lesions despite denosumab therapy, highlighting an urgent need to identify resistance mechanisms and alternative therapeutic strategies. We identified a RANKL-independent osteoclast activation pathway mediated by the CRKL/circCCDC50/NFATc1 axis. Mechanistically, CRKL promoted EIF4A3-dependent circCCDC50 biogenesis, which was packaged into large oncosomes and transferred to osteoclast precursors. Nuclear circCCDC50 recruited CARM1 to epigenetically activate NFATc1 transcription, establishing a self-reinforcing loop that sustained osteolysis despite RANKL blockade. Pharmacological inhibition of CARM1 (TP-064) effectively suppressed osteoclastogenesis and bone metastasis in denosumab-resistant models. These findings revealed a targetable resistance mechanism and provided a clinically actionable strategy to overcome microenvironment-driven metastasis through dual targeting of tumor and bone niches. - Source: PubMed
Publication date: 2026/05/15
Lin QunLuo JinpengDuan ZhuxiLuo JieerZhang WeiXia YuanZeng YinduoFang XiaolinLiang JiahuiChen JiayiLin QianchongQuan YilinHu RuiyuLiu HongcaiLiu QiangLi JunGong Chang - Vascular remodeling, a pathological hallmark of hypertensive target-organ damage, is critically modulated by autophagy. Given the emerging role of TWEAK (tumor necrosis factor-like weak inducer of apoptosis)/TWEAK receptor (TWEAKR) signaling in cardiovascular pathogenesis, this study investigates the relationship between TWEAK/TWEAKR and autophagy in hypertension-associated vascular remodeling. - Source: PubMed
Publication date: 2026/05/14
Lan QingsuHan WenqiangWang TianyuWang JinxiaoYao LinaDi MingxueDi Qin Selina HZhong JingquanHao Li - The invasion and metastasis of hepatocellular carcinoma (HCC) have been confirmed to be primarily associated with angiogenesis, and the underlying mechanisms remain elusive. In this study, we analyzed the GSE121714 database to identify circRNA_0023016, which is closely related to angiogenesis but has not been studied, as our target RNA for further investigation. The expression of circRNA_0023016 was identified to be downregulated in high invasion HCC cell lines and patients' tissues as well as serum exosomes. Inhibition of exosomal circRNA_0023016 downregulated eukaryotic translation initiation factor 4A3 (EIF4A3) and ring finger protein 113 A (RNF113A), while elevating C-X-C chemokine receptor type 4 (CXCR4) in human umbilical vein endothelial cells (HUVECs). EIF4A3 was found to be bound to circRNA_0023016 at RNA-protein level and to interact with RNF113A. The inhibition of RNF113A prevented the Cullin-RING E3 ligases (CRLs)-mediated K48-linked ubiquitination and proteasomal degradation of CXCR4. Furthermore, the RNA level of circRNA_0023016 and the protein expression of EIF4A3/RNF113A/CXCR4 axis in angiogenic endothelial cells, which were isolated from mouse HCC tissues via flow sorting, were detected to minimize potential interference from other cells. Overall, a new exosomal circRNA_0023016/EIF4A3/RNF113A/CXCR4 axis was identified in HCC. Exosomal circRNA_0023016 may serve as a potential therapeutic target, particularly for high invasion HCC. - Source: PubMed
Publication date: 2026/05/12
Wang TianqiLi WeiweiYu AnhaiDing MengfuLu CanliangYuan WenkangChen JialeZhang ShiweiJiang XinyuDu ZihaoLiu XiaoyingShen TingtingZhang ChaoZhang Chong - To explore new circRNA and underlying mechanisms through which they regulate breast cancer progression. In this study, high-throughput sequencing were used to reveal the different expression of circRNA among breast cancer tissues and para-carcinoma tissue. Fluorescence in situ hybridization (FISH) were used to analysis the expression and subcellular localization of circ-ABCA1 in both breast cancer tissues and cells line. The regulatory mechanism and targets were then investigated utilizing bioinformatics analyses, luciferase reporter assay, transwell migration, CCK8, and EdU analysis. The in vivo experiments was used to elucidate the roles of circ-ABCA1 in breast cancer tumor metastasis and growth. The result show that circ-ABCA1 expression was increased in both breast cancer tissues and cells line. Downregulation circ-ABCA1 inhibit cells proliferation and tumor growth. Luciferase report analysis confirmed both miR-33a-5p and EIF4A3 were the downstream target of circ-ABCA1. Overexpression of EIF4A3 or inhibit miR-33a-5p restored breast cancer cells proliferaion, migration and breast cancer cells stemness ability after silence circ-ABCA1. Overexpression of EIF4A3 restored breast cancer proliferaion, migration and breast cancer cells stemness ability after expression miR-33a-5p. Taken together, our study confirmed that circ-ABCA1 promotes breast cancer stem cell-mediated malignant progression by modulating miR-33a-5p/EIF4A3 axis. - Source: PubMed
Publication date: 2026/05/09
Wang BingGuo XuejunSui Yang - Myocardial infarction (MI) is the most severe clinical complication of coronary atherosclerotic heart disease (CHD), representing a leading cause of global morbidity and mortality. Qi-Blood Harmony Formula (QBHF), a traditional Chinese medicine, has shown clinical promise for managing MI; however, its underlying mechanisms remain to be fully elucidated. - Source: PubMed
Publication date: 2026/04/20
Huang MeiwenGuo HongaiChen JuanXin QiqiXie XuenaHu LantianMiao YuMa HuagenMa ShudongZhu YizhunYuan RongCong Weihong