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Gene Review

Efna1  -  ephrin A1

Mus musculus

Synonyms: AI325262, B61, EFL-1, EPH-related receptor tyrosine kinase ligand 1, Efl1, ...
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Disease relevance of Efna1

  • Cortical neurons from the E14 mouse embryos and neuroblastoma cells significantly extend neurites when placed on surfaces coated with the extracellular domain of EphB2 or ephrin-A1, which were abolished by the forced expression of the dominant-negative mutant of ephrin-B1 or EphA2 [1].
  • The formation of one such map, defined by the connection of ganglion cells in the retina to their targets in the superior colliculus of the midbrain, is thought to depend upon an interaction between complementary gradients of retinal EphA receptors and collicular ephrin-A ligands [2].
  • Since EphA2 is required for ephrin-A1 ligand-induced vascular remodeling and is overexpressed in a variety of vascularized human adenocarcinomas, we assessed tumor angiogenesis and metastatic progression in EphA2-deficient host animals [3].
  • Interestingly, the expression of EphA2 and ephrin-A1 is mutually exclusive in a panel of 28 breast cancer cell lines [4].

High impact information on Efna1

  • In addition, expression of a mutant form of ephexin in primary neurons interferes with ephrin-A-induced growth cone collapse [5].
  • Its sequence is homologous with B61, a ligand for the Eck kinase, defining a family of related ligands [6].
  • Subsequently, supernatants from selected cell lines were fractionated directly by receptor affinity chromatography, resulting in the single-step purification of B61, a protein previously identified as the product of an early response gene induced by tumour necrosis factor-alpha [7].
  • Axon guidance assays showed that SRF was a key mediator of ephrin-A and semaphorin guidance cues; in SRF-deficient neurons, these resulted in the formation of F-actin-microtubule rings rather than complete growth cone collapse [8].
  • Notably, CT axons that mis-express EphA7 do not shift the relative positioning of their pathway within the subcortical telencephalon (ST), indicating that they do not depend upon EphA7/ephrin-A signaling in the ST for establishing this topography [9].

Biological context of Efna1

  • These results demonstrate that ephrin-A1 suppresses T cell activation and Th2 cytokine expression, while preventing activation-induced cell death [10].
  • Finally, the gene for B61 was localized to a specific position on mouse chromosome 3 by interspecific back-cross analysis [11].
  • Gene expression screening showed decreased ephrin-A1 expression in CD4+ T cells of asthma patients [10].
  • Analysis using EphA8 extracellular and intracellular domain mutants has revealed that enhanced cell adhesion is dependent on ephrin A binding to the extracellular domain and the juxtamembrane segment of the cytoplasmic domain of the receptor [12].
  • Molecular cloning and expression of rat and mouse B61 gene: implications on organogenesis [13].

Anatomical context of Efna1

  • In addition, ephrin-A1 and ephrin-A5 were seen in the forming blood vessels and alveolar bone, respectively [14].
  • Prior to birth, ephrin-A1, ephrin-A5, EphA2, and EphA4 transcripts were present in the cuspal area of the dental papilla including the preodontoblasts [14].
  • B61 was originally described as a novel secreted tumor necrosis factor-alpha-inducible gene product in endothelial cells (Holzman, L. B., Marks, R. M., and Dixit, V. M. (1990) Mol. Cell. Biol. 10, 5830-5838) [11].
  • This study demonstrates significantly reduced ephrin-A1 expression in T cells of asthma patients using real time-PCR [10].
  • Ephrin-A1 suppresses Th2 cell activation and provides a regulatory link to lung epithelial cells [10].

Associations of Efna1 with chemical compounds


Regulatory relationships of Efna1


Other interactions of Efna1


Analytical, diagnostic and therapeutic context of Efna1

  • In addition, the expression patterns of B61 and Eck during mouse ontogeny were determined by in situ hybridization [11].
  • By immunohistochemistry, the ephrin-A1 ligand and one of its receptors, EphA2, were detected throughout tumor vasculature [26].
  • Furthermore, EphA2 was tyrosine-phosphorylated in the xenograft tumors, indicating that it was activated, presumably by interacting with ephrin-A1 [26].
  • Sequence analysis has revealed that there is a considerable degree of identity among rat, mouse and human B61 (98.0% between rat and mouse, 86.3% between rat and human in amino acid level) [13].
  • We have developed a co-culture assay to observe the dynamic cytoskeletal rearrangements comprising retinal growth cone collapse stimulated by contact with an ephrin-A-expressing fibroblast [16].


  1. Tiam1 mediates neurite outgrowth induced by ephrin-B1 and EphA2. Tanaka, M., Ohashi, R., Nakamura, R., Shinmura, K., Kamo, T., Sakai, R., Sugimura, H. EMBO J. (2004) [Pubmed]
  2. Topographic mapping from the retina to the midbrain is controlled by relative but not absolute levels of EphA receptor signaling. Brown, A., Yates, P.A., Burrola, P., Ortuño, D., Vaidya, A., Jessell, T.M., Pfaff, S.L., O'Leary, D.D., Lemke, G. Cell (2000) [Pubmed]
  3. Impaired tumor microenvironment in EphA2-deficient mice inhibits tumor angiogenesis and metastatic progression. Brantley-Sieders, D.M., Fang, W.B., Hicks, D.J., Zhuang, G., Shyr, Y., Chen, J. FASEB J. (2005) [Pubmed]
  4. A conditional feedback loop regulates Ras activity through EphA2. Macrae, M., Neve, R.M., Rodriguez-Viciana, P., Haqq, C., Yeh, J., Chen, C., Gray, J.W., McCormick, F. Cancer Cell (2005) [Pubmed]
  5. EphA receptors regulate growth cone dynamics through the novel guanine nucleotide exchange factor ephexin. Shamah, S.M., Lin, M.Z., Goldberg, J.L., Estrach, S., Sahin, M., Hu, L., Bazalakova, M., Neve, R.L., Corfas, G., Debant, A., Greenberg, M.E. Cell (2001) [Pubmed]
  6. Identification and cloning of ELF-1, a developmentally expressed ligand for the Mek4 and Sek receptor tyrosine kinases. Cheng, H.J., Flanagan, J.G. Cell (1994) [Pubmed]
  7. B61 is a ligand for the ECK receptor protein-tyrosine kinase. Bartley, T.D., Hunt, R.W., Welcher, A.A., Boyle, W.J., Parker, V.P., Lindberg, R.A., Lu, H.S., Colombero, A.M., Elliott, R.L., Guthrie, B.A. Nature (1994) [Pubmed]
  8. Serum response factor controls neuronal circuit assembly in the hippocampus. Knöll, B., Kretz, O., Fiedler, C., Alberti, S., Schütz, G., Frotscher, M., Nordheim, A. Nat. Neurosci. (2006) [Pubmed]
  9. Dissociation of corticothalamic and thalamocortical axon targeting by an EphA7-mediated mechanism. Torii, M., Levitt, P. Neuron (2005) [Pubmed]
  10. Ephrin-A1 suppresses Th2 cell activation and provides a regulatory link to lung epithelial cells. Wohlfahrt, J.G., Karagiannidis, C., Kunzmann, S., Epstein, M.M., Kempf, W., Blaser, K., Schmidt-Weber, C.B. J. Immunol. (2004) [Pubmed]
  11. Characterization of B61, the ligand for the Eck receptor protein-tyrosine kinase. Shao, H., Pandey, A., O'Shea, K.S., Seldin, M., Dixit, V.M. J. Biol. Chem. (1995) [Pubmed]
  12. The EphA8 receptor regulates integrin activity through p110gamma phosphatidylinositol-3 kinase in a tyrosine kinase activity-independent manner. Gu, C., Park, S. Mol. Cell. Biol. (2001) [Pubmed]
  13. Molecular cloning and expression of rat and mouse B61 gene: implications on organogenesis. Takahashi, H., Ikeda, T. Oncogene (1995) [Pubmed]
  14. Expression of ephrin-A ligands and EphA receptors in the developing mouse tooth and its supporting tissues. Luukko, K., Løes, S., Kvinnsland, I.H., Kettunen, P. Cell Tissue Res. (2005) [Pubmed]
  15. Expression analysis of the Epha1 receptor tyrosine kinase and its high-affinity ligands Efna1 and Efna3 during early mouse development. Duffy, S.L., Steiner, K.A., Tam, P.P., Boyd, A.W. Gene Expr. Patterns (2006) [Pubmed]
  16. A key role for Abl family kinases in EphA receptor-mediated growth cone collapse. Harbott, L.K., Nobes, C.D. Mol. Cell. Neurosci. (2005) [Pubmed]
  17. Caveolar structure and protein sorting are maintained in NIH 3T3 cells independent of glycosphingolipid depletion. Shu, L., Lee, L., Chang, Y., Holzman, L.B., Edwards, C.A., Shelden, E., Shayman, J.A. Arch. Biochem. Biophys. (2000) [Pubmed]
  18. EphA receptors direct the differentiation of mammalian neural precursor cells through a mitogen-activated protein kinase-dependent pathway. Aoki, M., Yamashita, T., Tohyama, M. J. Biol. Chem. (2004) [Pubmed]
  19. Ephrin signalling controls brain size by regulating apoptosis of neural progenitors. Depaepe, V., Suarez-Gonzalez, N., Dufour, A., Passante, L., Gorski, J.A., Jones, K.R., Ledent, C., Vanderhaeghen, P. Nature (2005) [Pubmed]
  20. EphA2 receptor tyrosine kinase regulates endothelial cell migration and vascular assembly through phosphoinositide 3-kinase-mediated Rac1 GTPase activation. Brantley-Sieders, D.M., Caughron, J., Hicks, D., Pozzi, A., Ruiz, J.C., Chen, J. J. Cell. Sci. (2004) [Pubmed]
  21. {alpha}-Syntrophin regulates ARMS localization at the neuromuscular junction and enhances EphA4 signaling in an ARMS-dependent manner. Luo, S., Chen, Y., Lai, K.O., Arévalo, J.C., Froehner, S.C., Adams, M.E., Chao, M.V., Ip, N.Y. J. Cell Biol. (2005) [Pubmed]
  22. The Eek receptor, a member of the Eph family of tyrosine protein kinases, can be activated by three different Eph family ligands. Park, S., Sánchez, M.P. Oncogene (1997) [Pubmed]
  23. EphA4 is not required for Purkinje cell compartmentation. Karam, S.D., Dottori, M., Ogawa, K., Henderson, J.T., Boyd, A.W., Pasquale, E.B., Bothwell, M. Brain Res. Dev. Brain Res. (2002) [Pubmed]
  24. Identification of the Jak/Stat proteins as novel downstream targets of EphA4 signaling in muscle: implications in the regulation of acetylcholinesterase expression. Lai, K.O., Chen, Y., Po, H.M., Lok, K.C., Gong, K., Ip, N.Y. J. Biol. Chem. (2004) [Pubmed]
  25. Eph-ephrin A system regulates murine blastocyst attachment and spreading. Fujii, H., Tatsumi, K., Kosaka, K., Yoshioka, S., Fujiwara, H., Fujii, S. Dev. Dyn. (2006) [Pubmed]
  26. The ephrin-A1 ligand and its receptor, EphA2, are expressed during tumor neovascularization. Ogawa, K., Pasqualini, R., Lindberg, R.A., Kain, R., Freeman, A.L., Pasquale, E.B. Oncogene (2000) [Pubmed]
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