DDX48 Blocking Peptide
- Known as:
- DDX48 Blocking Peptide
- Catalog number:
- 33r-7488
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- DDX48 Blocking Peptide
Related genes to: DDX48 Blocking Peptide
- 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 Blocking Peptide
Related articles to: DDX48 Blocking Peptide
- To clarify the role of the ALKBH5/circ_0091685/EIF4A3 axis in rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) and to investigate whether a traditional Chinese medicine preparation Huangqin Qingre Chubi Capsules (HQC) regulates inflammation and proliferation of RA-FLS through this axis. - Source: PubMed
Publication date: 2026/06/08
Hu YuediLiu Jian - Long non-coding RNA Urothelial carcinoma-associated 1 (UCA1) is a pivotal regulator in the progression of endometriosis (EMs), yet its mechanistic role remains elusive. This study identified UCA1 as a factor promoting glycolysis through bioinformatic screening and functional validation. Ectopic endometrial lesions exhibited significant UCA1 upregulation compared to normal endometrial tissues. In ectopic endometrial stromal cells, UCA1 knockdown suppressed glycolytic activity, evidenced by diminished glucose uptake and lactate production, while rescue experiments demonstrated that overexpression of E2F Transcription Factor 1 (E2F1) reversed this metabolic suppression. Mechanistically, UCA1 recruited eukaryotic translation initiation factor 4A3 (EIF4A3) to stabilize E2F1 mRNA, establishing an RNA-protein complex confirmed by RNA immunoprecipitation, RNA pull-down, and fluorescence in situ hybridization assays. Further experiments have demonstrated that EIF4A3 directly targets the 3'-untranslated region (UTR) of E2F1. Chromatin immunoprecipitation assays demonstrated that E2F1 binds to the promoter of pyruvate kinase isozyme type M2 (PKM2), thereby activating its transcription and linking UCA1-mediated E2F1 regulation to glycolytic reprogramming. In vivo validation using a subcutaneous xenograft model indicated that silencing UCA1 significantly inhibited the growth of endometriotic lesions. These findings support a UCA1/EIF4A3/E2F1/PKM2 regulatory axis that drives EMs progression through metabolic alterations. This study provides evidence for UCA1 as both a disease-promoting effector and a valuable therapeutic target, with implications for developing diagnostic and treatment strategies that target lncRNA-mediated metabolic dysregulation in EMs. - Source: PubMed
Publication date: 2026/06/02
Cao YingyingWang HonglinGou YanlingZhang HuiyanLiu JinmingBai RuruLiang ZongwenZhao YuxinHan XuZhang Zongfeng - Despite virologic suppression with ART, pregnant people living with HIV (PLWH) experience a disparate risk of chronic non-AIDS-related morbidities (NAMs) during pregnancy compared to people without HIV infection including preterm labor and small for gestational age. Many studies postulate that NAMs reflect immunological dysfunction from underlying continuous inflammation. Extracellular vesicles (EV) are fundamental to both HIV immune pathogenesis and maternal-placental-fetal systemic intercellular networking. Circular RNAs (CircRNA) are enriched within EVs and are readily transmissible with disease-specific functional outcomes in recipient cell populations. However, there is limited research addressing the intersection of EV circRNA and HIV during pregnancy. - Source: PubMed
Publication date: 2026/06/02
Brena DaraSchuch VivianeHuang Ming-BoSheth AnandiTisdale TinaMehta ChristinaBadell Martina LFloyd RiaunDawning AmberBashi AlaijahChan AustinChakraborty RanaBond VincentJohnson Erica L - 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