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    Ricin-resistant cells reveal cryptic ricin receptors and altered cell surface properties. Genetic control influences these receptors, impacting cell adhesion and glycoprotein expression.

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    Area of Science:

    • Cell Biology
    • Glycobiology
    • Molecular Biology

    Background:

    • Baby hamster kidney (BHK) cells selected for ricin resistance (RicR) display varied surface changes.
    • RicR cell lines are categorized by minimal versus extreme alterations in surface properties.

    Purpose of the Study:

    • To investigate the nature of ricin receptors in RicR BHK cells.
    • To understand the genetic control and surface property alterations associated with ricin resistance.

    Main Methods:

    • Analysis of glycopeptides from pronase-treated RicR cells.
    • Treatment with neuraminidase to expose ricin receptors.
    • Characterization of cell adhesion and aggregation properties.
    • Assessment of 250K glycoprotein expression in RicR cell lines.

    Main Results:

    • RicR cell lines with extreme surface changes show reduced sialic acid, galactose, and N-acetylglucosamine, with diminished ricin binding.
    • Neuraminidase treatment unmasks new ricin receptors, increasing cell sensitivity.
    • Altered surface property RicR cells exhibit poor adhesion and aggregation.
    • The 250K glycoprotein is absent in most extreme RicR lines.

    Conclusions:

    • BHK cells possess multiple classes of ricin receptors, including cryptic ones under independent genetic control.
    • Changes in surface glycoprotein organization, particularly the 250K glycoprotein, are linked to ricin-induced receptor alterations and affect cell adhesion.