Item request has been placed! ×
Item request cannot be made. ×
loading  Processing Request

cGMP transport by vesicles from human and mouse erythrocytes.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
اقرأ على الانترنت اقرأ أكثر حفظ في قائمتي
  • معلومة اضافية
    • المصدر:
      Publisher: Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies Country of Publication: England NLM ID: 101229646 Publication Model: Print Cited Medium: Print ISSN: 1742-464X (Print) Linking ISSN: 1742464X NLM ISO Abbreviation: FEBS J Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: Oxford, UK : Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies, c2005-
    • الموضوع:
      Cyclic GMP/*metabolism ; Erythrocytes/*cytology; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; ATP-Binding Cassette Transporters/chemistry ; ATP-Binding Cassette Transporters/genetics ; Alprostadil/metabolism ; Animals ; Biological Transport ; Dose-Response Relationship, Drug ; Erythrocyte Membrane/metabolism ; Erythrocytes/metabolism ; Humans ; Mice ; Mice, Knockout ; Multidrug Resistance-Associated Proteins/genetics ; Neoplasm Proteins/genetics
    • نبذة مختصرة :
      cGMP secretion from cells can be mediated by ATP-binding cassette (ABC) transporters ABCC4, ABCC5, and ABCC11. Indirect evidence suggests that ABCC4 and ABCC5 contribute to cGMP transport by erythrocytes. We have re-investigated the issue using erythrocytes from wild-type and transporter knockout mice. Murine wild-type erythrocyte vesicles transported cGMP with an apparent Km that was 100-fold higher than their human counterparts, the apparent Vmax being similar. Whereas cGMP transport into human vesicles was efficiently inhibited by the ABCC4-specific substrate prostaglandin E1, cGMP transport into mouse vesicles was inhibited equally by Abcg2 and Abcc4 inhibitors/substrates. Similarly, cGMP transport into vesicles from Abcc4-/- and Abcg2-/- mice was 42% and 51% of that into wild-type mouse vesicles, respectively, whereas cGMP transport into vesicles from Abcc4(-/-)/Abcg2(-/-) mice was near background. The knockout mice were used to show that Abcg2-mediated cGMP transport occurred with lower affinity but higher Vmax than Abcc4-mediated transport. Involvement of Abcg2 in cGMP transport by Abcc4-/- erythrocyte vesicles was supported by higher transport at pH 5.5 than at pH 7.4, a characteristic of Abcg2-mediated transport. The relative contribution of ABCC4/Abcc4 and ABCG2/Abcg2 in cGMP transport was confirmed with a new inhibitor of ABCC4 transport, the protease inhibitor 4-(2-aminoethyl)benzenesulfonyl fluoride.
    • Grant Information:
      CA23099 United States CA NCI NIH HHS; ES058571 United States ES NIEHS NIH HHS; GM60904 United States GM NIGMS NIH HHS; P30 CA21745 United States CA NCI NIH HHS
    • الرقم المعرف:
      0 (ABCC11 protein, human)
      0 (ABCC4 protein, human)
      0 (ABCG2 protein, human)
      0 (ATP Binding Cassette Transporter, Subfamily G, Member 2)
      0 (ATP-Binding Cassette Transporters)
      0 (Abcc4 protein, mouse)
      0 (Abcg2 protein, mouse)
      0 (Multidrug Resistance-Associated Proteins)
      0 (Neoplasm Proteins)
      F5TD010360 (Alprostadil)
      H2D2X058MU (Cyclic GMP)
    • الموضوع:
      Date Created: 20070119 Date Completed: 20070309 Latest Revision: 20181201
    • الموضوع:
      20221213
    • الرقم المعرف:
      10.1111/j.1742-4658.2006.05591.x
    • الرقم المعرف:
      17229149