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Publication : The erythrocyte skeletons of beta-adducin deficient mice have altered levels of tropomyosin, tropomodulin and EcapZ.

First Author  Porro F Year  2004
Journal  FEBS Lett Volume  576
Issue  1-2 Pages  36-40
PubMed ID  15474006 Mgi Jnum  J:93294
Mgi Id  MGI:3056826 Doi  10.1016/j.febslet.2004.08.057
Citation  Porro F, et al. (2004) The erythrocyte skeletons of beta-adducin deficient mice have altered levels of tropomyosin, tropomodulin and EcapZ. FEBS Lett 576(1-2):36-40
abstractText  The erythrocyte membrane cytoskeleton is organized as a polygonal spectrin network linked to short actin filaments that are capped by adducin at the barbed ends. We have constructed a mouse strain deficient in beta-adducin having abnormal erythrocytes. We show here that the levels of several skeletal proteins from beta-adducin mutant erythrocytes are altered. In fact, CapZ, the main muscle actin-capping protein of the barbed ends that in the erythrocytes is cytoplasmic, is 9-fold upregulated in mutant skeletons of erythrocytes suggesting a compensatory mechanism. We also detected upregulation of tropomodulin and downregulation of alpha-tropomyosin and actin. In addition, purified adducin can be re-incorporated into adducin-deficient ghosts.
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