Ask about this productRelated genes to: UBL4A antibody
- Gene:
- UBL4A NIH gene
- Name:
- ubiquitin like 4A
- Previous symbol:
- UBL4
- Synonyms:
- GDX, DXS254E, GET5, MDY2, TMA24
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-21
- Date modifiied:
- 2015-12-01
Related products to: UBL4A antibody
Related articles to: UBL4A antibody
- - Source: PubMed
Publication date: 2026/03/25
Chen HongzeLi LeHu JishengZhao ZhongjieJi LiangCheng ChundongZhang GuangquanZhang TaoLi YilongChen HuaPan ShanghaSun Bei - Intracerebral hemorrhage (ICH) is a primary non-traumatic parenchymal hemorrhage of the brain with a high mortality and disability rate. Acupuncture has been proved to alleviate neurological deficits after ICH. - Source: PubMed
Publication date: 2026/01/23
Ou YuyangChen ChenWang ZiyiZhu XiLuo YaoxingLi ShulinLi Dan - Head and neck cancer (HNC) continues to pose a significant global health challenge, highlighting the urgent need for discovering new therapeutic targets. Recent studies highlight the role of solute carrier (SLC) proteins in cancer progression. This study investigates the expression and potential role of SLC10A3 in HNC, aiming to determine its clinical significance and therapeutic relevance. Publicly available datasets, including The Cancer Genome Atlas (TCGA), Clinical Proteomics Tumor Analysis Consortium (CPTAC), and Gene Expression Omnibus (GEO), were analyzed to assess SLC10A3 expression in head and neck squamous cell carcinoma (HNSCC). The prognostic relevance of SLC10A3 was assessed using Kaplan-Meier (KM) survival and Receiver Operating Characteristic (ROC) curve analysis. Correlation analysis within TCGA, CPTAC, and GEO datasets identified genes associated with SLC10A3 expression. Protein-protein docking studies were performed to predict potential interactions between SLC10A3 and identified protein coding genes. SLC10A3 was found to be significantly upregulated in HNSCC tumor samples compared to normal tissues across TCGA and CPTAC datasets. Increased SLC10A3 expression correlated with poor survival outcomes in TCGA-HNSCC patients. Correlation analysis identified 26 genes positively associated with SLC10A3, where BCAP31, IRAK1, and UBL4A showed consistent correlation across TCGA, CPTAC, and GEO datasets. Computational protein interaction modeling using docking and AI/ML-based Evolutionary Scale Modelling (ESM) framework revealed significant binding affinities between SLC10A3 and identified protein-coding genes, suggesting potential functional interactions. These findings establish SLC10A3 as a promising therapeutic target in HNC. Its consistent upregulation, association with poor prognosis, and potential interactions with key regulatory proteins highlight its relevance for future therapeutic strategies. - Source: PubMed
Publication date: 2025/11/17
Bintee BinteeBanerjee RuchiraHegde MangalaManteghi NafisehBhuyan PlabitaLongkumar ImliwatiAhmed Gazi NaseemBaruah Munindra NarayanAhn Kwang SeokKunnumakkara Ajaikumar B - The monocyte adhesion to vascular endothelial cells constitutes a key step in atherosclerosis pathogenesis. We previously found that ROS-autophagy pathway participated in the monocyte-endothelial cell adhesion induced by angiotensin domain type 1 receptor-associated proteins (APJ) and its endogenous ligand apelin-13. In this study, we investigated what specific type of autophagy apelin-13 regulated in this process. By conducting full-scale transcriptomic analysis in apelin-13-treated human umbilical vein endothelial cells (HUVECs), we found that the transcription levels of ER-phagy receptor protein SEC62 were significantly elevated. Importantly, SEC62 was also upregulated in human atherosclerotic lesions. Thus, we investigated the effects of SEC62-dependent ER-phagy on apelin-13-induced monocyte-endothelial cell adhesion and atherosclerosis pathogenesis. We demonstrated that Apelin-13 (0.001-1 μM) dose-dependently upregulated SEC62 expression thereby inducing ER-phagy in HUVECs. This effect was reversed by autophagy inhibitor 3MA (10 mM) and endoplasmic reticulum stress inhibitor salubrinal (10 μM). The siRNA-Sec62, 3MA (10 mM), and salubrinal (10 μM) all inhibited apelin-13-induced monocyte-endothelial cells adhesion, whereas vascular endothelial cells specific SEC62 deletion alleviated atherosclerotic plaques area, intercellular adhesion molecules expression and lesional macrophages in apelin-13-treated APOE mice with high-fat and high-cholesterol diet. Moreover, we demonstrated that ubiquitin-like modification of ALDH1L1 was involved in SEC62-dependent ER-phagy in apelin-13-treated HUVECs: apelin-13 upregulated small ubiquitin-like protein UBL4A, which mediated the ubiquitination-like modification of ALDH1L1 at 812-lysine site. This, in turn, promoted insertion of ALDH1L1 into ER membrane and led to SEC62-dependent ER-phagy. We showed that siRNA-UBL4A, siRNA-ALDH1L1, siRNA-ASNA1, and the mutant of 812 lysine site of ALDH1L1 all decreased apelin-13-induced monocyte-endothelial cell adhesion. We conclude that apelin-13 induces SEC62-dependent ER-phagy to promote monocyte-endothelial cell adhesion and atherosclerosis. This study reveals new mechanisms underlying atherosclerosis and identifies a potential therapeutic target. - Source: PubMed
Publication date: 2025/02/10
Chen ZheCheng JunZhou QunWu Le-leChen Jia-WeiDuan Xiang-NingYan Jia-LongCao Jian-GangXia Xiao-DanLi Lan-FangChen Lin-Xi - Acupuncture has obvious therapeutic effect on intracerebral hemorrhage (ICH). miR-34a-5p regulated by acupuncture was found to attenuate neurological deficits in ICH. However, the underlying mechanisms are unclear. Ubiquitin-like 4A (UBL4A) has not been studied in ICH. SD rats were injected with autologous blood to induce ICH and treated with Baihui-penetrating-Qubin acupuncture. Acupuncture resulted in an increase in forelimb placing test scores, and a decrease in corner test scores and brain water content of ICH rats. Histopathological examination showed that acupuncture inhibited ICH-induced inflammation, decreased damaged neurons and increased UBL4A expression. UBL4A overexpression increased cell viability, inhibited apoptosis, reduced reactive oxygen species (ROS) level and increased manganese superoxide dismutase (MnSOD) activity, mitochondrial membrane potential and mtDNA level in rat embryonic primary cortical neurons. miR-34a-5p knockdown increased UBL4A expression, apoptosis rate and ROS level in hemin-treated neurons. Dual luciferase assays showed that miR-34a-5p bound to UBL4A. Apoptotic cells and ROS level were increased in hemin-treated neurons with UBL4A and miR-34a-5p knockdown. We firstly demonstrate the inhibitory effect of UBL4A on neuronal apoptosis, and the regulation relationship between UBL4A and miR-34a-5p. This study provides a new candidate target for ICH treatment and more basis for elucidating the molecular mechanism of acupuncture. In the future, we will conduct a deeper exploration of the effects of UBL4A on ICH. - Source: PubMed
Publication date: 2024/06/07
Li DanWang LeShi ShufengDeng XiaofengZeng XuehanLi YunongLi ShulinBai Peng