from Wiktionary, Creative Commons Attribution/Share-Alike License

  • n. Any of a class of protein that is involved in cell signalling


Sorry, no etymologies found.


  • Dr. McDonald and his collaborators coated magnetic cobalt-iron oxide nanoparticles with a molecular mimic of the natural ligand for this protein, a molecule known as ephrin-A1, to serve as a trap for ovarian cancer cells floating in ascites fluid, the liquid found in the intestinal cavity. - latest science and technology news stories

  • Todd McLaughlin, Ph. D., a senior research associate in the lab and co-first author, says that insight came in a eureka moment: "We realized that what we were observing in these mice was similar to what would happen if you deleted a gene called ephrin-A from the retina."

    EurekAlert! - Breaking News

  • A post is available for a Post-doctoral Training Fellow to work in the Cell Communication Team (Team Leader Dr Claus Jørgensen) on a project designed to systematically analyze bidirectional Eph-ephrin signalling in cancer using quantitative phospho-proteomics and RNAi screening.

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  • In the experiments, ephrin-A1, which normally resides on the surface of unsuspecting target cells, was instead protruding from Groves's artificial cell surface.

    HHMI News

  • The researchers inserted ephrin-A1 ligands into the supported membrane and brought them into close contact with cancer cells presenting EphA2 receptors.

    HHMI News

  • For the current study, Groves and his cross-disciplinary colleagues rigged an experimental platform that allowed them to manipulate the interface between a high-affinity receptor on the surface of cancer cells -- EphA2 -- and the ligand that binds to it, ephrin-A1.

    HHMI News

  • Systems analysis of bidirectional Eph-ephrin signalling in Cancer

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  • We have previously shown that superparamagnetic nanoparticles conjugated to an ephrin-A1 mimetic peptide with a high affinity for the EphA2 receptor can be used to capture and remove cultured human ovarian cancer cells from the peritonea of experimental mice.


  • Additional experiments indicated that the loss of responsiveness to ephrin signals resulted from activation of a molecular pathway called mTOR, whose activity increased when neurons were deficient in TSC2.

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  • We also found that EphA receptor activation by ephrin-A ligands in neurons led to inhibition of extracellular signal-regulated kinase 1/2 (ERK1/2) activity and decreased inhibition of Tsc2 by ERK1/2.

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