{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T16:10:09Z","timestamp":1791389409449,"version":"4.3.3"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2009,3,31]],"date-time":"2009-03-31T00:00:00Z","timestamp":1238457600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Hematol"],"published-print":{"date-parts":[[2009,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In red blood cells (RBCs) adducin heterotetramers localize to the spectrin\u2010actin junction of the peripheral membrane skeleton. We previously reported that deletion of \u03b2\u2010adducin results in osmotically fragile, microcytic RBCs and a phenotype of hereditary spherocytosis (HS). Notably, \u03b1\u2010adducin was significantly reduced, while \u03b3\u2010adducin, normally present in limited amounts, was increased \u223c5\u2010fold, suggesting that \u03b1\u2010adducin requires a heterologous binding partner for stability and function, and that \u03b3\u2010adducin can partially substitute for the absence of \u03b2\u2010adducin. To test these assumptions we generated \u03b3\u2010adducin null mice. \u03b3\u2010adducin null RBCs appear normal on Wright's stained peripheral blood smears and by scanning electron microscopy. All membrane skeleton proteins examined are present in normal amounts, and all hematological parameters measured are normal. Despite a loss of \u223c70% of \u03b1\u2010adducin in \u03b3\u2010adducin null platelets, no bleeding defect is observed and platelet structure appears normal. Moreover, systemic blood pressure and pulse are normal in \u03b3\u2010adducin null mice. \u03b3\u2010 and \u03b2\u2010adducin null mice were intercrossed to generate double null mice. Loss of \u03b3\u2010adducin does not exacerbate the \u03b2\u2010adducin null HS phenotype although the amount \u03b1\u2010adducin is reduced to barely detectable levels. The stability of \u03b1\u2010adducin in the absence of a heterologous binding partner varies considerably in various tissues. The amount of \u03b1\u2010adducin is modestly reduced (\u223c15%) in the kidney, while in the spleen and brain is reduced by \u223c50% with the loss of a heterologous \u03b2\u2010 or \u03b3\u2010adducin binding partner. These results suggest that the structural properties of adducin differ significantly between erythroid and various nonerythroid cell types. Am. J. 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