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 - BACKGROUNDS: Neoadjuvant chemoradiation (nCRT) is a standard treatment for rectal carcinoma that reduces tumor size and local recurrence while improving the rate of sphincter preservation. However, many patients remain insensitive to nCRT, with some exhibiting tumor progression. To date, there is still a lack of clinically available prognostic models to differentiate the sensitivity of patients with rectal carcinoma to nCRT. This study aimed to develop a genetic predictive model that predicts the effectiveness of nCRT in patients with rectal carcinoma, offering guidance for future treatments and studies on the underlying mechanisms. METHODS: Based on the NCBI GEO database datasets, key hub genes affecting the efficacy of neoadjuvant chemoradiotherapy in rectal carcinoma were identified using WCGNA. Subsequently, a consistency analysis of 101 model combinations constructed using ten different machine learning algorithms was performed in two independent cohorts, and a prognostic model (chemoradiation resistance score, CRTR score) was developed and validated. Moreover, the clinical applicability of CRTR in immunotherapy and drug selection was investigated using multi-omics analysis and public databases. Finally, the effect of KIF14 on the radiosensitivity of rectal carcinoma cells was studied using in vitro experiments. RESULTS: The CRTR model was composed of 13 genes impacting nCRT sensitivity, whereas six genes (KIF4, DBF4, UBL4A, SLC10A3, PRRG4, and PAPSS2) acted as protective factors and seven (BMS1, DSC2, PROM2, MNAT1, PPID, SMPDL3B, and TNFRSF14) served as risk factors. The CRTR model showed a significant negative correlation with the prognosis of patients with rectal carcinoma undergoing nCRT. Furthermore, patients with higher CRTR values displayed an increased potential to benefit from immunotherapy. Drug sensitivity analysis indicated that aurora kinase inhibitors, telomerase inhibitors, JAK1 inhibitors, and others may enhance the efficacy of nCRT. Finally, we identified KIF14 as the gene that contributed the most to the model and performed preliminary validation. Radiation significantly upregulated the expression of KIF14, and overexpression of KIF14 increased the radiosensitivity of rectal carcinoma cells. CONCLUSION: The CRTR score, based on 13 genes, was able to predict the prognosis of patients with rectal carcinoma undergoing neoadjuvant chemoradiotherapy and demonstrated immense potential in providing personalized risk assessments and recommendations for targeted immunotherapy. The core gene, KIF14, in the CRTR model may serve as a potential predictive biomarker of radiosensitivity in rectal carcinioma. - Source: PubMed
Publication date: 2026/03/21
Gao ZhanhuaQiu MinghanYang ZhenFang XinyueYin GuoxingZhang QiaonanLiu JinpuLiu RuxueWang YayunLiu YuyaZhang MengZhang HaiyangZheng XiangqianWang HuiHao JieGao Ming - 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