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Gene Review

Erp1  -  erythrocyte protein 1

Mus musculus

Synonyms: Erp-1
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Disease relevance of Erp1


Psychiatry related information on Erp1


High impact information on Erp1

  • A model of hematopoietic development wherein multipotentiality is conserved until segregation of myeloid and lymphoid potential has recently been challenged, proposing that megakaryocyte/erythrocyte (MegE) potential is lost in Flk2/Flt3-expressing early progenitors [9].
  • Targeted mutagenesis in embryonic stem cells and mice has revealed roles for the X-linked gene Gata1 in erythrocyte and megakaryocyte differentiation [10].
  • Anion exchanger 1 (band 3) is required to prevent erythrocyte membrane surface loss but not to form the membrane skeleton [11].
  • The observed viral-induced shift in the erythrocyte composition is paralleled by a similar change in the mosaic composition of the CFU-E pool but not the primitive (d8) BFU-E pool [12].
  • Our results indicate that the primary effect of the nb mutation is a deficiency of another erythrocyte membrane skeletal protein, ankyrin [13].

Chemical compound and disease context of Erp1


Biological context of Erp1


Anatomical context of Erp1

  • Cloned NK and T killer cell lines possess granules that are able to lyse erythrocyte targets [24].
  • A significant increase in the percentage of sialic acid released was found when the O-acetyl group was cleaved by O-acetylesterase activity from certain substrates (bovine submandibular gland mucin, rat serum glycoproteins, human saliva glycoproteins, mouse erythrocyte stroma, chick embryonic brain gangliosides and bovine brain gangliosides) [25].
  • Erythrocyte ghosts containing a known number of molecules of purified fragment A of diphtheria toxin with a constant amount of FITC-BSA as a fluorescence marker were prepared by dialyzing a mixture of erythrocytes and these substances against hypotonic solution [19].
  • These networks are similar to the cytoskeletal network seen after erythrocyte membranes are extracted with detergent, and may represent the first in vitro assembly of a cytoskeletal complex resembling that of the native cell both biochemically and structurally [26].
  • The development of the mouse erythroblast to a mature erythrocyte is accompanied by changes in the composition and properties of the plasma membranes of these cells [27].

Associations of Erp1 with chemical compounds

  • The biosynthesis of the erythrocyte anion transport protein, Band III (molecular weight 100,000), is of interest, as its NH2-terminal half is hydrophilic and faces the cytoplasmic surface, and its COOH-terminal half spans the phospholipid bilayer several times [28].
  • Mouse strains AcB55 and AcB61 are resistant to malaria by virtue of a mutation in erythrocyte pyruvate kinase (Pklr(I90N)) [29].
  • An autosomal dominant gene regulates the extent of 9-O-acetylation of murine erythrocyte sialic acids. A probable explanation for the variation in capacity to activate the human alternate complement pathway [30].
  • Because the C4d fragment bears the labile binding site of C4 for cell membranes, it is likely that the erythrocyte alloantigen is acquired from serum as a result of the activation of C4 [31].
  • Inhibition of erythrocyte superoxide dismutase, depletion of glutathione, and lysis of the erythrocytes do not diminish this protection [32].

Physical interactions of Erp1

  • In contrast, erythrocyte-binding affinities only played a minor role in in vivo hemolytic activities of the IgG1 and IgG2a isotypes of 34-3C and 4C8 antibodies, where complement was not or only partially involved, respectively [33].
  • The liver/erythrocyte pyruvate kinase gene complex [Pk-1] in the mouse: regulatory gene mutations [34].
  • A 1-year follow-up of 12 treated animals showed a stable correction of anemia associated with improved RBC morphology, increased beta-minor globin synthesis, and decreased amounts of alpha-globin chains bound to erythrocyte membranes [35].
  • The suppressive mechanism is poorly understood, but it has been proposed that IgG/erythrocyte complexes bind to the inhibitory Fc receptor for IgG (FcgammaRIIB) on the B cell surface, thereby triggering negative signals that turn off the B cell [36].
  • Calmodulin-binding domain of recombinant erythrocyte beta-adducin [37].

Co-localisations of Erp1


Regulatory relationships of Erp1


Other interactions of Erp1


Analytical, diagnostic and therapeutic context of Erp1


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  10. Familial dyserythropoietic anaemia and thrombocytopenia due to an inherited mutation in GATA1. Nichols, K.E., Crispino, J.D., Poncz, M., White, J.G., Orkin, S.H., Maris, J.M., Weiss, M.J. Nat. Genet. (2000) [Pubmed]
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  14. Invasion of mouse erythrocytes by the human malaria parasite, Plasmodium falciparum. Klotz, F.W., Chulay, J.D., Daniel, W., Miller, L.H. J. Exp. Med. (1987) [Pubmed]
  15. Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency. Yachie, A., Niida, Y., Wada, T., Igarashi, N., Kaneda, H., Toma, T., Ohta, K., Kasahara, Y., Koizumi, S. J. Clin. Invest. (1999) [Pubmed]
  16. Treatment with oral clotrimazole blocks Ca(2+)-activated K+ transport and reverses erythrocyte dehydration in transgenic SAD mice. A model for therapy of sickle cell disease. De Franceschi, L., Saadane, N., Trudel, M., Alper, S.L., Brugnara, C., Beuzard, Y. J. Clin. Invest. (1994) [Pubmed]
  17. Modulation of erythrocyte potassium chloride cotransport, potassium content, and density by dietary magnesium intake in transgenic SAD mouse. De Franceschi, L., Beuzard, Y., Jouault, H., Brugnara, C. Blood (1996) [Pubmed]
  18. Formation of dense erythrocytes in SAD mice exposed to chronic hypoxia: evaluation of different therapeutic regimens and of a combination of oral clotrimazole and magnesium therapies. De Franceschi, L., Brugnara, C., Rouyer-Fessard, P., Jouault, H., Beuzard, Y. Blood (1999) [Pubmed]
  19. One molecule of diphtheria toxin fragment A introduced into a cell can kill the cell. Yamaizumi, M., Mekada, E., Uchida, T., Okada, Y. Cell (1978) [Pubmed]
  20. Primary structure and transmembrane orientation of the murine anion exchange protein. Kopito, R.R., Lodish, H.F. Nature (1985) [Pubmed]
  21. Erythropoietin retards DNA breakdown and prevents programmed death in erythroid progenitor cells. Koury, M.J., Bondurant, M.C. Science (1990) [Pubmed]
  22. Widespread failure of hematolymphoid differentiation caused by a recessive niche-filling allele of the Ikaros transcription factor. Papathanasiou, P., Perkins, A.C., Cobb, B.S., Ferrini, R., Sridharan, R., Hoyne, G.F., Nelms, K.A., Smale, S.T., Goodnow, C.C. Immunity (2003) [Pubmed]
  23. In vivo effects of monoclonal antibodies that functionally inhibit complement regulatory proteins in rats. Matsuo, S., Ichida, S., Takizawa, H., Okada, N., Baranyi, L., Iguchi, A., Morgan, B.P., Okada, H. J. Exp. Med. (1994) [Pubmed]
  24. High activity of N-alpha-benzyloxycarbonyl-L-lysine thiobenzyl ester serine esterase and cytolytic perforin in cloned cell lines is not demonstrable in in-vivo-induced cytotoxic effector cells. Dennert, G., Anderson, C.G., Prochazka, G. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  25. Increased influenza A virus sialidase activity with N-acetyl-9-O-acetylneuraminic acid-containing substrates resulting from influenza C virus O-acetylesterase action. Muñoz-Barroso, I., García-Sastre, A., Villar, E., Manuguerra, J.C., Hannoun, C., Cabezas, J.A. Virus Res. (1992) [Pubmed]
  26. Spectrin-actin associations studied by electron microscopy of shadowed preparations. Cohen, C.M., Tyler, J.M., Branton, D. Cell (1980) [Pubmed]
  27. Molecular changes in the membranes of mouse erythroid cells accompanying differentiation. Geiduschek, J.B., Singer, S.J. Cell (1979) [Pubmed]
  28. The erythrocyte anion transport protein is contranslationally inserted into microsomes. Braell, W.A., Lodish, H.F. Cell (1982) [Pubmed]
  29. Complex genetic control of susceptibility to malaria: positional cloning of the Char9 locus. Min-Oo, G., Fortin, A., Pitari, G., Tam, M., Stevenson, M.M., Gros, P. J. Exp. Med. (2007) [Pubmed]
  30. An autosomal dominant gene regulates the extent of 9-O-acetylation of murine erythrocyte sialic acids. A probable explanation for the variation in capacity to activate the human alternate complement pathway. Varki, A., Kornfeld, S. J. Exp. Med. (1980) [Pubmed]
  31. The murine H-2.7 specificity is an antigenic determinant of C4d, a fragment of the fourth component of the complement system. Ferreira, A., David, C.S., Nussenzweig, V. J. Exp. Med. (1980) [Pubmed]
  32. Erythrocyte catalase. A somatic oxidant defense? Agar, N.S., Sadrzadeh, S.M., Hallaway, P.E., Eaton, J.W. J. Clin. Invest. (1986) [Pubmed]
  33. Complement activation selectively potentiates the pathogenicity of the IgG2b and IgG3 isotypes of a high affinity anti-erythrocyte autoantibody. Azeredo da Silveira, S., Kikuchi, S., Fossati-Jimack, L., Moll, T., Saito, T., Verbeek, J.S., Botto, M., Walport, M.J., Carroll, M., Izui, S. J. Exp. Med. (2002) [Pubmed]
  34. The liver/erythrocyte pyruvate kinase gene complex [Pk-1] in the mouse: regulatory gene mutations. Fitton, L.A., Davidson, M., Moore, K.J., Charles, D.J., Pretsch, W., Elston, R.C., Bulfield, G. Genet. Res. (1991) [Pubmed]
  35. Improvement of erythropoiesis in beta-thalassemic mice by continuous erythropoietin delivery from muscle. Bohl, D., Bosch, A., Cardona, A., Salvetti, A., Heard, J.M. Blood (2000) [Pubmed]
  36. Efficient IgG-mediated suppression of primary antibody responses in Fcgamma receptor-deficient mice. Karlsson, M.C., Wernersson, S., Diaz de Ståhl, T., Gustavsson, S., Heyman, B. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  37. Calmodulin-binding domain of recombinant erythrocyte beta-adducin. Scaramuzzino, D.A., Morrow, J.S. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
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  46. Deficiency of Src family kinases Fgr and Hck results in activation of erythrocyte K/Cl cotransport. De Franceschi, L., Fumagalli, L., Olivieri, O., Corrocher, R., Lowell, C.A., Berton, G. J. Clin. Invest. (1997) [Pubmed]
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