Ask about this productRelated genes to: EphA2 antibody
- 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: EphA2 antibody
Related articles to: EphA2 antibody
- Peters Anomaly (PA) is the leading cause for corneal transplants in pediatric patients. We investigated whether disruption of Eph-ephrin signaling leads to phenotypes associated with PA, including microphthalmia, cloudy cornea, coloboma, cataract, corneo-lenticular touch (CLT), irido-corneal adhesion (ICA), and persistent fetal vasculature (PFV). Freshly enucleated mouse eyes were imaged under a dissection microscope, and high-resolution confocal images were collected to compare mouse eyes with genetic disruption of EphA2 or ephrin-A5. In ephrin-A5 knockout (KO or ) eyes, we commonly found microphthalmia, cloudy cornea, coloboma, CLT, ICA, anterior subcapsular cataracts, and PFV; control and EphA2 eyes did not display these phenotypes with significant frequency. Defects in ephrin-A5 eyes were often unilateral, and bilateral defects were not always the same between contralateral eyes. We did not observe premature eye opening in ephrin-A5 mice, and eye defects were present in ephrin-A5 pups at birth, suggesting embryonic development abnormalities. Imaging of tissues from live ephrin-A5 eyes revealed abnormal corneal epithelial cells in deeper corneal layers, shallow anterior chamber, and anterior lens defects due to CLT. Immunostaining demonstrated nerve patterning and epithelial cell defects in ephrin-A5 corneas. This work reveals that Eph-ephrin signaling is needed for separation of the embryonic lens from the cornea during development and nerve patterning in the cornea. Although ephrin-A5 has not been directly linked to PA, this KO model can be utilized for detailed studies of the cellular defects for all clinical signs of PA and suggests that Eph-ephrin signaling is involved in PA. - Source: PubMed
Publication date: 2026/08/28
Cheng CatherineInnis Isaiah JVu Michael POkada Yuka - Herpesvirus infection triggers excessive inflammation, contributing to tissue injury and disease severity, but the underlying drivers remain unclear. Here we identify EphA2 as a critical mediator of pseudorabies virus (PRV)-induced inflammatory response. Genetic or pharmacological inhibition of EphA2 reduced TNF-α production in PRV-infected cells and mice, alleviated liver and lung damage, and improved mice survival. Mechanistically, PRV infection promoted EphA2 phosphorylation at Ser-897, which activated NF-κB and MAPK pathways to drive TNF-α production. The PRV tegument protein UL40 directly bound the EphA2 kinase domain (residues 697-901), a region that also interacts with Akt. Unexpectedly, Akt acted as a negative regulator of inflammation, as its knockdown exacerbated cytokine production. UL40 competitively disrupted the constitutive EphA2-Akt complex in a time-dependent manner, relieving Akt-mediated restraint on EphA2 S897 phosphorylation. Accordingly, a UL40-deficient PRV mutant failed to enhance S897 phosphorylation, elicited lower inflammatory responses, and showed attenuated virulence in mice. Collectively, our findings reveal a proviral strategy whereby PRV UL40 hijacks EphA2 to counteract an intrinsic Akt-dependent inhibitory pathway. This UL40-EphA2-Akt cascade is a critical determinant of virus-induced inflammation, and EphA2 S897 represents a potential therapeutic target for mitigating alphaherpesvirus immunopathology. - Source: PubMed
Publication date: 2026/08/25
Tian YutongYin HangFu JiaxiangYang QingqingYan RuLi YuqingYe ChaoFang Rendong - Adoptive cell therapies utilizing both gene-modified and unmodified immune cells have revolutionized treatments for cancer and infection. Seven Chimeric antigen receptor (CAR) T cell products have been approved as therapies, providing the momentum to expand their clinical benefit to several cancer types. Many novel receptor-expressing cell therapies remain in preclinical development and require robust clinical testing Translating these into early-phase clinical trials requires navigating manufacturing, quality, and regulatory systems that are often not documented explicitly for academic investigators. This manuscript provides a stage-by-stage roadmap for translating academic CAR T-cell research into an investigator-led Phase I clinical trial in the Australian public sector. It draws on the E2CAR program, the first clinical translation of an EphA2-directed CAR T-cell product into pediatric bone sarcoma, conducted at the Children's Hospital at Westmead. We present our experience across six stages: construct finalization and vector strategy, manufacturing process development, quality infrastructure, assay development and validation, multi-entity operational coordination, and CTA regulatory engagement and provide recommendations for researchers at each stage. We also present a consolidated program timeline, minimum personnel requirements, and indicative costs to support grant applications and institutional planning. While the operational framework described here was developed specifically for our Health Precinct some of the recommendations we provide are likely to benefit academic groups navigating constraints in comparable settings. - Source: PubMed
Publication date: 2026/08/10
Tan Rui Ping AmandaWalsh RobynMcCowage GeoffreyO'Neill Geraldine MGowrishankar Kavitha - Marco et al. (https://doi.org/10.1083/jcb.202507217) identify a tumor-selective endocytic route in which CD44 and EPHA2 co-traffic antisense oligonucleotides (ASOs) to nuclear-proximal, recycling-endosome-like compartments that become leaky through lipid peroxidation and show that stress granule-mediated repair of these compartments limits productive ASO escape. - Source: PubMed
Publication date: 2026/08/24
Liao Ya-ChengBussi Claudio - Vemurafenib (VEM) is a BRAF inhibitor that improves the prognosis of melanoma, but acquired resistance represents a key limitation to its clinical efficacy. This study investigated the potential of A11, an Annexin A1 (ANXA1)-derived peptide, to enhance VEM efficacy in both VEM-sensitive and VEM-resistant melanoma cells. We evaluated the effects of A11 in melanoma through in vitro assays (including MTT, clonogenic survival, apoptosis, and cell cycle analysis) and in vivo xenograft models in nude mice. Furthermore, we mechanistically interrogated A11-mediated suppression of EphA2 expression and the downstream pS897-EphA2/AKT/ERK signalling pathway in resistant and parental cell lines via Western blotting and immunohistochemistry (IHC). Critically, our study demonstrates that A11 inhibits melanoma cell proliferation and reverses VEM resistance through EphA2 downregulation, consequently ablating this oncogenic pathway. This research highlights the promising application value of A11 in improving the efficacy of VEM treatment in melanoma, particularly in VEM-resistant melanoma. - Source: PubMed
Feng JuanHuang Xiao-PuZhang MingHuang WeiLu Shan-ShanXiao Zhi-QiangXie Zhi-HaiYi Hong