Mouse Anti Human EPH receptor A2 EPHA2
- Known as:
- Mouse Anti Human EPH receptor A2 EPHA2
- Catalog number:
- ant-425
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Mouse Anti Human EPH receptor A2 EPHA2
Related genes to: Mouse Anti Human EPH receptor A2 EPHA2
- Gene:
- EPHA2 NIH gene
- Name:
- EPH receptor A2
- Previous symbol:
- ECK
- Synonyms:
- -
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2016-10-05
Related products to: Mouse Anti Human EPH receptor A2 EPHA2
Related articles to: Mouse Anti Human EPH receptor A2 EPHA2
- Receptor tyrosine kinases are key regulators of various fundamental cellular processes, and dysregulation of their activities may lead to many human diseases including cancer. EphA2 is a member of the Eph subfamily of receptor tyrosine kinases that play an important role in regulating tissue patterning, homeostasis, and regeneration. Accumulating evidence indicates that EphA2 is a critical regulator of cancer development and progression and can function as both a tumor suppressor and an oncogenic driver. When acting as an oncogenic driver, EphA2 can promote tumor initiation, growth, invasion, metastasis, stemness, and angiogenesis by activating or enhancing the oncogenic signaling pathways. High expression of EphA2 in a wide range of human tumor tissues is closely associated with poor prognosis, thus it is a very promising target for cancer treatment. A number of studies on EphA2-targeted cancer treatment are currently at the clinical trial stage. In this review, we discuss the oncogenic roles and mechanisms of action of EphA2 in cancer development and progression, which could provide novel insights into EphA2-targeted cancer treatment. - Source: PubMed
Publication date: 2026/06/30
Song HanbingQin NingFeng XiaoheHan ChenLiu YunJia YunshaLu Peiyuan - EphA2 is highly expressed in colorectal cancer (CRC), and high EphA2 expression indicates a worse prognosis. We investigated EphA2 dynamics in a clinically relevant model: CRC patient-derived organoids (PDOs) treated with chemotherapy. - Source: PubMed
Publication date: 2026/06/12
Gatti VeronicaCapolupo Gabriella TeresaTaffon ChiaraMarra AndreaPerrone GiuseppeMasciana' GianlucaCaricato MarcoCioce MarioFazio Vito Michele - EphA2 is a receptor tyrosine kinase that suppresses tumor growth when bound by its ligand ephrin-A1 (EA1), but promotes tumor progression in the absence of ligand. In hepatocellular carcinoma (HCC) cells, EphA2 is proteolytically cleaved by membrane-type 1 matrix metalloproteinase (MT1-MMP), producing a C-terminal fragment (EphA2-CF) and an N-terminal fragment (EphA2-NF). The functional role of these cleavage fragments on HCC remains unclear. Herein, we investigated their roles in hepatocarcinogenesis and malignant progression. Western blotting and membrane biotinylation assays revealed that EphA2-CF was present in HCC cells co-expressing EphA2 and MT1-MMP. EphA2-CF-expressing cells were resistant to EA1-induced growth suppression, while MT1-MMP knockdown restored EA1 sensitivity. In Hep3B cells, stable EphA2-CF expression confirmed resistance to EA1-mediated inhibition of proliferation and survival. Mechanistically, EphA2-CF sustained oncogenic signaling through constitutive phosphorylation at EphA2-S, while failing to induce Y phosphorylation after EA1 stimulation. Mutation of EphA2-S abolished EphA2-CF-driven proliferation and survival. Reverse-phase protein array identified activation of the EGFR-AKT axis and inactivation of GSK3β as key downstream events. Both pharmacological inhibition of EGFR or AKT, and activation of GSK3β suppressed EphA2-CF-driven proliferation. Furthermore, enforced expression of a constitutively active GSK3β mutant (S9A) markedly suppressed EphA2-CF-driven tumorigenesis in mice, genetically validating GSK3β inactivation as a critical effector of EphA2-CF oncogenic signaling. In addition, soluble EphA2-NF functioned as a decoy receptor for EA1, blocking its tumor-suppressive activity. These findings demonstrate that MT1-MMP-mediated EphA2 processing promotes HCC malignancy via dual mechanisms: EphA2-CF drives ligand-independent EGFR/AKT/GSK3β signaling, while EphA2-NF inhibits EA1-mediated tumor suppression. - Source: PubMed
Publication date: 2026/06/29
Ikeda KazukiAsakura NobuhikoSengoku SoyogiTsukamoto EikiFunahashi NobuakiKoshikawa Naohiko - The epidermal growth factor receptor (EGFR) is a membrane protein that is essential to growth, differentiation, and survival in healthy cells. Misregulation of EGFR causes these pathways to function abnormally leading to tumorigenesis. There are several therapeutics targeting EGFR on the clinic. Unfortunately, EGFR-driven tumors often develop resistance to therapeutics, hampering long-term cancer treatment with EGFR inhibitors. Overexpression of the receptor EphA2 is a common mechanism of EGFR therapeutic resistance. Importantly, EGFR and EphA2 interact at the plasma membrane, but the factors that control this interaction are poorly understood. Here, we investigate how EGFR and EphA2 interact functionally and physically. Immuno-fluorescence and proximity ligation data indicate that EGFR-EphA2 interactions rapidly decrease after EGFR activation with EGF. Inhibition of endocytosis blocked the effect of EGF on co-localization between both receptors, indicating that endocytosis of EGFR impairs its ability to form hetero-complexes with EphA2. Pharmacological inhibition of EGFR with tyrosine kinase inhibitors were only partially able to block this effect. Our data indicate that endocytosis is an important negative regulatory factor that impacts the levels of EGFR-EphA2 complexes. This information has implications for EGFR drug resistance in cancer. - Source: PubMed
Publication date: 2026/06/27
Rybak Jennifer ABarrera Francisco N - Hepatocellular carcinoma (HCC) is the third leading cause of cancer death globally, often arising on a background of cirrhosis. Here, we aimed to establish genetic drivers of all-cause HCC across ancestries in a large meta-analysis. We included 15 cohorts comprising 17,697 HCC cases and 2,715,683 controls in this meta-analysis. We found 15 genome-wide significant (P < 5x10) germline loci, including in/near GCKR, MTTP, ADH5, 8q24.21 (nearest gene MYC), MAP3K9, and GABPB2, and a further two loci found on transcriptome- and regulome-wide association analyses. MAP3K9, TERT, and GABPB2 variants act independently of cirrhosis on both co-localisation analysis and sensitivity analyses. There was significant ancestral heterogeneity in 6 loci including variants in the HLA locus that had divergent effects on HCC risk between East Asian and European ancestries. Fine-mapping identified 11 potentially causal coding variants, including p.Leu446Pro in GCKR and p.Asp423Glu in MEN1. MEN1, 8q24.21 (nearest gene MYC), and TERT are all involved in the beta-catenin pathway transactivation complex. Transcriptome-wide analysis identified enrichment of germline-encoded DHRS1 in HCC. Regulome-wide analysis replicated the germline signal for EPHA2 and found a chromatin accessible region containing genes ZNF367 and HABP4. Finally, we demonstrated that population-level genetic architecture for HCC overlaps with steatotic and viral liver disease, and individuals with genetic risk for lower BMI have higher risk of HCC. Genetic risk for HCC is determined by germline susceptibility to beta-catenin pathway activation and cirrhosis. HCC is driven by both heterogenous and homogenous genetic factors across ancestries. - Source: PubMed
Publication date: 2026/06/25
Chinaka IfechukwuamakaSchofield AnnabelleAmos Christopher IRoberts Lewis RChen Vincent LHan YounghunHassan ManalShetty ShishirMann Jake P