Ask about this productRelated genes to: EFNA2 antibody
- Gene:
- EFNA2 NIH gene
- Name:
- ephrin A2
- Previous symbol:
- EPLG6
- Synonyms:
- ELF-1, LERK6
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-10
- Date modifiied:
- 2016-10-05
Related products to: EFNA2 antibody
Related articles to: EFNA2 antibody
- Bladder cancer (BC) is one of the most deadly diseases in the USA, with 84,530 new cases and 17,870 estimated deaths in 2026. The growth factor progranulin is involved in several human pathologies, including frontotemporal dementia (FTD), immune response, and cancer. We showed that in BC, progranulin and its signaling receptor, EphA2, drive tumor cell motility, invasion, and in vivo tumor formation, making it a critical pathway in tumor establishment. However, the molecular mechanisms of progranulin/EphA2 action are still poorly defined. - Source: PubMed
Publication date: 2026/08/11
Satasiya VrundaMartinelli CanioPascal GabrielDucci GiacomoVentura ElisaWilliams Stephen JBurk Sharon RaffaellaTchamou Manuela NanaShani ShendiKlain MicheleSacco ElenaVanoni MarcoBelfiore AntoninoIozzo Renato VGiordano AntonioMorrione Andrea - Prostate cancer is a prevalent disease with diverse tumor characteristics that complicate treatment. The integration of spatial patterns from prostate-specific membrane antigen (PSMA) positron emission tomography/computed tomography (PET/CT), pathology and expanding genomic data represents a groundbreaking advancement in histo-imaging genomics. The aim of this study was to elucidate the internetwork mapping between genetic biomarkers and PSMA PET/CT imaging in prostate cancer patients. - Source: PubMed
Publication date: 2026/07/04
Qu LiliLi KaiyueWang MuwenXiao YadiJin XinZhou HangYuan LujieLi YuekaiWang ShiweiLi RuiHacker MarcusLi XinLi Xiang - Schwann cell precursors (SCPs) migrate with peripheral sensory axons from DRGs to target regions. SCP migration involves adhesions to substrata to stabilize advancing cell margins, and contractile forces that pull a SCP forward and break rear adhesions. Ncadherin on axons provides adhesion for SCPs, and ephrin-A2 signaling from axons stimulates SCP contractions to complete SCP translocation. Modulation of these adhesive and contractile forces regulates SCP migratioin during development of peripheral nerves. - Source: PubMed
Publication date: 2026/06/10
Roche Florence KLetourneau Paul C - The development of resistance to anticancer therapies in cancer cell is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), a common malignant tumor. Erythropoietin-producing hepatocellular A2 (EphA2) affects several cancers, and this study examined its role in enhancing OSCC. Following screening, EphA2 and SRY-Box transcription factor 8 (SOX8) knocked down and overexpression cell lines were constructed, followed by treatment with Cetuximab. Quantitative real-time polymerase chain reaction, western blot, cell counting kit-8, wound healing, and transwell assay were used to detect the relevant indicators. Co-immunoprecipitation was used to detect the interaction between EphA2 and SH2 domain-containing protein-tyrosine phosphatase-2 (SHP2). Double luciferase reporter gene experiment and chromatin immunoprecipitation experiment were performed to verify the regulatory mechanism of EphA2 and SOX8. The mouse tumor model was established, and the tumor development was observed after plasmid transfection and Cetuximab treatment. EphA2 was highly expressed in OSCC cells, and overexpression of EphA2 up-regulated SOX8. EphA2 regulated SOX8 and associated protein expression to increase OSCC cell migration and invasion. EphA2 knockdown made OSCC cells more sensitive to Cetuximab, whereas SOX8 overexpression reduced this sensitivity. We found SHP2 bound to SOX8. Down-regulation of EphA2 decreased tumor growth in mice, increased Cetuximab sensitivity, and overexpression of SOX8/SHP2 decreased Cetuximab sensitivity. OSCC had elevated EphA2 levels, which enhanced cell migration and invasion via SHP2/SOX8 and impaired Cetuximab sensitivity. Down-regulation of EphA2 decreased tumor growth and enhanced Cetuximab sensitivity, suggesting new OSCC targets and potential treatments. - Source: PubMed
Publication date: 2026/05/26
Yan DayongGuo LelePei FeiZhong Ketao - Traumatic brain injury (TBI) remains a formidable clinical, neuropathological, and forensic challenge, constituting a leading cause of death as well a neuroscientific research target worldwide. A deeper understanding of the molecular signatures underlying vascular and extracellular matrix remodeling in TBI seems to be critical both for the development of diagnostic biomarkers in post-mortem neuropathology and for identifying potential therapeutic targets in the acute injury setting. Despite the individual exploration of HIF-1α, MMP-9/14, and EPHA2 in neurological injury, few studies have offered a comprehensive, integrative examination of these biomarkers within the human TBI brain, especially in post-mortem forensic contexts. The study concerned a total of 40 individuals, cases with head injuries (n = 20) suspected to be the cause of death, and atraumatic control cases of sudden death (n = 20) due to cardiopulmonary reasons. Brain tissue was obtained during forensic autopsies and subjected to immunohistochemical staining. Cerebrospinal fluid (CSF) and serum were collected approximately 24 h post-mortem and analyzed through ELISA testing. We observed the elevated concentration level of HIF-1α, MMP-9 and MMP-14 in CSF. In the frontal cortex, anti-EPHA2 immunohistostaining revealed a generalized homogenization of the reaction was observed both within the neuronal bodies (including nuclear area) and their axons among the study group. Rather than relying solely on macroscopic signs of trauma, the present study proposes a layered biomarker architecture wherein HIF-1α reflects hypoxic load, MMP-9/14 denotes matrix remodeling and barrier disruption, and EPHA2 signals cellular stress and neurovascular dysregulation. Such a composite signature provides a biological foundation that may ultimately be translated into post-mortem diagnostic algorithms or pilot machine-learning-based forensic stratification tools following validation in larger, multicenter cohorts. - Source: PubMed
Publication date: 2026/03/19
Poniatowski Łukasz AOlczak MieszkoAcewicz AlbertKwiatkowska MagdalenaSiwińska Agnieszka