anti-Ephrin A2 (EFNA2) Antibodies

Mouse (Murine) Ephrin A2 (EFNA2) interaction partners

1. Study showed that in comparison with wild-type mice revealed that ephrin-A2A5-/- mice had reduced accuracy and response rates, suggesting a goal-directed behavioral deficit, which was improved by low intensity repetitive transcranial magnetic stimulation.

2. The ephrin-A2/-A3 DKO mice have utility as a novel ASD model with an emphasis on sensory abnormalities and restricted, repetitive behavioral symptoms.

3. The results of this study suggested that majority of the changes observed ephrin-A2 and ephrin-A5 KO mice appear to be mediated by the effects on motor neurons and their muscle targets, rather than changes in auditory sensitivity.

4. Ephrin-A2 and -A3 are negative regulators of the proliferative and neurogenic potentials of Muller cells.

5. Ephrin-A2 and Ephrin-A5 are important for the functional development of cutaneous innervation.

6. At high frequencies, the ephrin-A2A5(-/-) mice exhibited thresholds that were significantly lower than in wild-type mice by approximately 20 dB, suggesting ephrin-A2 and ephrin-A5 may have frequency-specific effects on the auditory system.

7. In EphA4 mutant mice, as well as after ephrin A2 knockdown using in utero electroporation, we found delayed interneuron migration at embryonic stages.

8. ephrin-A2 regulates experience-dependent, NMDA receptor-mediated synaptic pruning through glial glutamate transport during maturation of the mouse cortex.

9. EphA2-mediated mesenchymal-amoeboid transition induced by endothelial progenitor cells enhances metastatic spread due to cancer-associated fibroblasts.

10. Implicate EphA2 as a novel proinflammatory mediator and potential regulator of atherosclerotic plaque development.

11. The results of this study suggested that the misexpression of ephrin-A2 may lead to abnormal connectivity in regions known for their involvement in reversal learning and perseverative behaviours.

12. Tiam1 is required for neurite outgrowth induced by both ephrin-B1-mediated reverse signaling and EphA2-mediated forward signaling

13. ephrin-A2 expression was observed in synapses during reactive synaptogenesis

14. identification of ephrin-A2 and EphA7 as negative regulators of progenitor cell proliferation reveals a novel mechanism to control cell numbers in the brain

15. In mice deficient for ephrin-A2, A3 and A5, eye-specific inputs segregated but shape and location of eye-specific layers were profoundly disrupted. Ephrin-As and neural activity act together to control patterning of eye-specific retinogeniculate layers.

16. Misalignment of ipsilateral and contralateral visual information in the superior colliculus results in inappropriate terminations in ephrin-A2/A5(-/-) double knock-out mice and suggests a role for ephrin-As in integrating convergent visual inputs.

17. Bidirectional ephrinA2-EphA2 signaling regulates bone remodeling at the initiation phase.

Human Ephrin A2 (EFNA2) interaction partners

1. Ephrin-A2 expression was correlated with Ki-67 expression in PCa patients, both at the gene scale and protein level. Our data indicate that Ephrin-A2 is a potential diagnostic and prognostic biomarker and a promising molecular therapeutic target to attenuate prostate cancer progression

2. these studies suggested that Kaposi's sarcoma-associated herpesvirus utilizes CIB1 as one of the key molecule(s) to coordinate and sustain the EphA2 mediated signaling involved in its entry

3. High EphA2 receptor expression in colorectal cancer was associated with a worse outcome in patients treated with cetuximab-based therapy

4. Implicate EphA2 as a novel proinflammatory mediator and potential regulator of atherosclerotic plaque development.

5. Optic nerve section in adult rat differentially regulates the expression of ephrin-A2 in the superior colliculus(SC).At 1 month, levels were upregulated across the contralateral SC giving rise to an increasing rostro-caudal gradient.

6. Different forms of Elf-1 are the products of posttranslational modifications that determine its subcellular localization, activity, and metabolic degradation.

7. Abnormal posttranslational mechanisms of the Elf-1 protein result in defective expression of the functional 98-kDa form of Elf-1, and consequently, the transcriptional defect of TCR zeta-chain in patients with systemic lupus erythematosus.

8. There is a significant loss of ELF-1 and reduced Smad4 expression in gastrointestinal neoplasms.

9. Elf-1 represents the first transcription factor identified to be involved in the transcriptional regulation of Fc receptor gamma

10. The crystal structures of an A-class complex between EphA2 and ephrin-A1 and of unbound EphA2, are presented.