Recombinant Human PEA15
- Known as:
- Recombinant Human PEA15
- Catalog number:
- CF65
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human PEA15
Related genes to: Recombinant Human PEA15
- Gene:
- PEA15 NIH gene
- Name:
- proliferation and apoptosis adaptor protein 15
- Previous symbol:
- -
- Synonyms:
- HMAT1, MAT1, PED, PEA-15, MAT1H, HUMMAT1H, PED-PEA15, PED/PEA15
- Chromosome:
- 1q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-06
- Date modifiied:
- 2017-08-10
Related products to: Recombinant Human PEA15
Related articles to: Recombinant Human PEA15
- Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths globally. Although the hypoxia-inducible factor 1A (HIF1A) pathway is crucial in HCC progression, its regulatory mechanisms remain unclear as mutations in its primary regulator, von Hippel-Lindau tumor suppressor (), are rare in HCC. We aimed to elucidate the role of proliferation and apoptosis adaptor protein 15 (PEA15), identified through proteomic analysis, as a regulator of the VHL/HIF1A pathway and a therapeutic target in HCC. Proteomic and genomic analyses of over 1,000 HCC samples were conducted, identifying amplification. Functional validation involved in vitro and in vivo assays, including gene knockdown, ectopic expression, and antisense oligonucleotide (ASO) therapy in xenograft models. Protein interactions were assessed using immunoprecipitation and ubiquitination assays. We identified 3 clinically distinct HCC subtypes and found that was selectively amplified and highly expressed in the mesenchymal (MES) subtype, which exhibited the poorest prognosis. acted as a regulator of the VHL/HIF1A pathway and a key oncogene in HCC. The amplification of was significantly associated with the poor survival of HCC patients. Moreover, by interacting with the β-domain of VHL, PEA15 promoted HCC cell proliferation and migration by inhibiting VHL's interaction with the VHL/elongin C (ELOC)/elongin B (ELOB)/cullin 2 (CUL2) E3 ligase complex, destabilizing the complex and consequently activating HIF1A. Importantly, pharmacologically inhibiting PEA15 using ASO drugs attenuated tumor burden and restored VHL function in a xenograft mouse model. This study identified as a potential oncogene in HCC, regulating the VHL/HIF1A axis and driving tumor progression. Targeting using ASOs offers a promising therapeutic strategy for HCC, particularly in the MES subtype. These findings provide a basis for further exploration of -targeted therapies to improve HCC outcomes. - Source: PubMed
Publication date: 2026/04/08
Jeong Yun SeongShin Ji-HyunKim Soo MiSohn Bo HwaYim Sun YoungKim Ji HoonShim Jae JunLee Sung HwanChun Yun ShinLee Sunyoung SDai HuiKaseb AhmedKang Koo JeongEltzschig Holger KMacLeod A RobertLuo XiaolinRevenko AlexeyKim YoungsooLee Ju-Seog - Sepsis, a life-threatening condition with high mortality, is closely linked to energy metabolism (EM) and immune-inflammatory responses. However, the precise mechanisms remain incompletely understood. This research aims to identity EM-related genes (EMRGs) in sepsis and examine the diagnostic potential and molecular mechanisms through machine learning and single-cell RNA sequencing (scRNA-seq). - Source: PubMed
Publication date: 2026/02/03
Yu XiaoLiu CongruiJia LibinWan BingjieFeng JunWu YonghongTang JinJia YachunLiu HongweiLuo SiyuLi QiaoKong GuangyaoLi Ping - In colorectal cancer, approximately 50% to 70% of metastases go into the liver; however, their molecular signature remains unknown. We aimed to investigate the transcriptome and miRNome profiles of metachronous colorectal liver metastasis (mCLM) within the hepatic microenvironment and to identify key deregulated genes, microRNAs (miRNAs), pathways, and their clinical relevance. We performed differential expression analysis on 36 mCLM and adjacent nonmalignant liver tissue pairs using RNA sequencing. Gene set enrichment analysis and consensus molecular subtype (CMS) classification helped to explore pathways. Tumor samples were stratified based on their KRAS mutation status. miRNA-mRNA interactions were investigated through coexpression and correlation analysis, with prognostic relevance assessed using survival analysis. Validation of key interactions was accomplished using multiMiR. We identified 1809 upregulated and 1639 downregulated genes and 108 upregulated and 92 downregulated miRNAs in mCLM compared with the adjacent nonmalignant liver. Upregulated genes were associated with epithelial-to-mesenchymal transition, G2M checkpoints, and E2F targets. About 47% of samples belonged to CMS2 and 22% to mesenchymal CMS4, with distinct mutational patterns. mRNA coexpression identified 4 clusters (associated with metabolism, cell cycle, DNA metabolism, and oncogenic signaling pathways), and miRNA coexpression identified 6 clusters. The hub miRNAs hsa-let-7c, hsa-miR-21-5p, hsa-miR-106a-5p, hsa-miR-139-5p, hsa-miR-101-3p, and hsa-miR-20b-5p were among the inversely correlated miRNA-mRNA clusters. An integrative analysis highlighted PEA15 interaction with hsa-miR-320b/c, TEX2/CTSO with hsa-miR-103a-3p, and PHLDA3 with hsa-miR-1304, and prognostic relevance for ZNF441, CTSO, TEX2, EID1, CMC1, hsa-miR-4634, hsa-miR-3184-5p, has-miR-320b, hsa-miR-1304-3p, hsa-miR-7-1-3p, hsa-miR-144-3p, hsa-miR-1303, and hsa-miR-660-3p. The miRNA-mRNA interactions were validated using real-time PCR in independent patient cohorts. This study revealed a complex molecular landscape of mCLM within the hepatic microenvironment and novel miRNA-mRNA interactions with potential prognostic and therapeutic implications. - Source: PubMed
Publication date: 2025/12/19
Rao Bhavana HemanthaBoušková VeronikaHeczko LucieHolý PetrŠeborová KarolínaLiška VáclavVyčítal OndřejFiala OndřejSouček PavelHlaváč Viktor - Ulcerative colitis (UC) is a chronic inflammatory bowel disease of unknown etiology characterized by abnormal mucosal immune responses and persistent intestinal inflammation. UC significantly reduces quality of life and imposes a substantial economic burden. Early diagnosis and personalized treatment are crucial for improving outcomes; however, significant challenges remain. This study aimed to identify novel molecular targets for UC treatment. Gene expression data related to UC were obtained from the Gene Expression Omnibus, and differentially expressed genes (DEGs) were identified based on the criteria < 0.05 and |logFC| > 0.5. The DEGs were intersected with autophagy-related genes (ARGs) to explore the relationship between UC pathogenesis and autophagy. LASSO regression, random forest regression, and support vector machine-recursive feature elimination were employed to screen for differentially expressed ARGs. The robustness and generalizability of the intersected genes were validated in external datasets and mouse models, and immune infiltration was analyzed to assess the interaction between UC and the immune system. was identified as a potential UC diagnostic marker, and the diagnostic value of ,, and was reconfirmed. Our findings provide new insights into the pathogenesis of UC, facilitating early diagnosis and the development of personalized therapeutic strategies. - Source: PubMed
Publication date: 2025/12/20
Chen Xinyi XueMin ShichenShen ZhaofengZhang MengyuanHuang LejuanSu MengranShen HongZhu Lei - Osteosarcoma (OS), a primary malignant bone tumor, is characterized by resistance to chemotherapeutic agents such as cisplatin (DDP), posing a major obstacle to effective treatment. Tumor cells often exploit autophagy to survive chemotherapeutic stress, which contributes to this resistance. Using weighted gene co-expression network analysis (WGCNA), this study screened for autophagy-related genes associated with OS prognosis and identified PEA15 as a key indicator of poor outcomes. Through gene knockdown and overexpression experiments in OS cell lines and xenograft models, we found that PEA15 promotes tumor progression. Mechanistically, RNA sequencing revealed that PEA15 inhibits autophagy and apoptosis by modulating the downstream target FABP3 and the associated TNF signaling pathway. Notably, silencing PEA15 in resistant OS cells enhanced their sensitivity to cisplatin by activating autophagy. These findings identify the PEA15-FABP3-TNF signaling axis as a key pathway regulating chemoresistance in OS, suggesting that targeting PEA15 could be a promising therapeutic strategy to improve patient outcomes. - Source: PubMed
Publication date: 2025/10/04
Peng YuanxiangCai FengLiu LangGuo ChongZhang GuohuaShen FengLi Xiaofeng