ANGPT4
- Known as:
- ANGPT4
- Catalog number:
- 001567A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANGPT4
Related genes to: ANGPT4
- Gene:
- ANGPT4 NIH gene
- Name:
- angiopoietin 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-28
- Date modifiied:
- 2014-11-19
Related products to: ANGPT4
Related articles to: ANGPT4
- Although long noncoding RNAs (lncRNAs) have been implicated in the progression of prostate cancer (PCa), the functional roles of many of these molecules, especially in metastasis, remain poorly understood. To identify novel lncRNAs linked to PCa malignant phenotypes, we analyzed the differences in lncRNA expression between the highly metastatic PCa cell line (PC-3 M-1E8) and the poorly metastatic PCa cell line (PC-3 M-2B4) using transcriptome sequencing. This differential expression was confirmed by RT-qPCR, which showed that the lnc-ALX1-2 gene cluster (including lnc-ALX1-2:5, lnc-ALX1-2:7, lnc-ALX1-2:10) was significantly upregulated in PC-3 M-1E8 cells. Functional studies demonstrated that knockdown of the lnc-ALX1-2 gene cluster suppressed proliferation, migration, and invasion in PC-3 M-1E8 cells, with lnc-ALX1-2:10 showing the most prominent effect. Transcriptome analysis further revealed that lnc-ALX1-2:10 knockdown altered the expression of 194 genes related to both proliferation and migration. RT-qPCR and Western blot validated that lnc-ALX1-2:10 knockdown downregulated pro-tumorigenic factors (CCNE1, PDGFRA, ANGPT4) and EMT markers (N-cadherin, Snail, Vimentin), while upregulating ITGAL and E-cadherin. In vivo, lnc-ALX1-2:10 knockdown obviously decreased tumor volume but had no effect on mouse body weight, and molecular analysis of xenograft tumors confirmed consistent expression changes of key proteins as in vitro. Collectively, our findings identify lnc-ALX1-2:10 as a novel lncRNA that promotes aggressive phenotypes in PCa, highlighting its potential as a therapeutic target for metastatic disease. - Source: PubMed
Publication date: 2026/03/03
Wang XinjunZong QianBu YueZhou BinWang XuqiangLi ZhangqunLuo Guangcheng - Optimizing bile acids (BAs) inclusion in commercial diets and understanding its molecular mechanisms in Pacific white shrimp () are crucial for improving growth performance. The present study investigated the effect of dietary BAs on shrimp growth and metabolic mechanisms using multiomics approaches. A total of 1800 shrimp (0.16 ± 0.01 g) were fed six diets with BAs levels: 0 mg kg (control, BA0), 50 mg kg (BA1), 100 mg kg (BA2), 150 mg kg (BA3), 200 mg kg (BA4), and 250 mg kg (BA5). After 56 days, the growth performance of BA4 and BA5 groups was significantly higher than the BA0, BA1, and BA2 groups. Regression analysis indicated an optimal dietary BAs level of 216-218 mg kg. Biochemical analysis showed that the BA4 group significantly reduced crude lipid content, triglycerides, and nonesterified fatty acids, while increasing digestive enzyme activities. RNA-seq revealed reduced expression of lipid synthesis genes (, , , etc.), while enhancing the expression of genes related to lipid catabolism (, , , and ) and digestive enzymes ( and ). Metabolomic analysis showed taurine-conjugated BAs as predominant, with taurine content decreasing likely due to its conjugation with BAs and loss in feces. These results suggest that the optimal BAs level of 216-218 mg kg improved shrimp growth and lipid metabolism by enhancing nutrient digestion, promoting lipolysis, and inhibiting lipid synthesis, without altering the BAs pool balance. This study first revealed taurine's critical role in Pacific white shrimp BAs metabolism. - Source: PubMed
Publication date: 2025/11/10
Zhang LeiZhang JinzhiTan PengZhang JunZhu AijunDing ZhiliYan XiaojunShao Qingjun - Hypopharyngeal squamous cell carcinoma (HPSCC) is a lethal malignancy with limited treatment options and poor survival rates. Recent studies have revealed that mutations in the histone acetyltransferases EP300 and CREBBP drive tumor progression by disrupting the chromatin structure and impairing antitumor immunity. However, no targeted therapies are currently available to treat these epigenetic defects. Natural compounds with epigenetic regulatory potential offer a promising therapeutic avenue but remain largely unexplored in HPSCC. - Source: PubMed
Publication date: 2025/11/05
Mao WeiFeng ChenGao GangJiao BiwenZhu PeiyanChen YufanMen YongzhiDong PinWang Baoxin - Atherogenic dyslipidemia remains an essential predictor of cardiovascular disease. This study tested whether combined dapagliflozin and alirocumab therapy could exert a synergistic effect on reducing dyslipidemia by inhibiting CD36 expression. - Source: PubMed
Publication date: 2025/09/23
Yeh Jui-NingWang Yi-TingLan Xian-WuChen Yi-LingHuang Chi-RueiShao Pei-LinYip Hon-KanGuo Jun - Cervical cancer (CC) is a major cause of morbidity and mortality in women, with complex etiology and progression. Diacylglycerol kinases (DGKs) are pivotal in lipid metabolism. Although diacylglycerol kinase beta (DGKβ) is well-studied in neurology, its role in cancer, especially CC, remains underexplored. This study aimed to explore DGKβ's role and mechanism in CC. - Source: PubMed
Publication date: 2025/08/06
Li QingZhou ZhenyuLi XiaoyingLan Qiongyu