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A distinctive histidine residue is essential for in vivo glycation-inactivation of human CD59 transgenically expressed in mice erythrocytes: Implications for human diabetes complications
Clinical and experimental evidences support a link between the complement system and the pathogenesis of diabetes complications. CD59, an extracellular cell membrane-anchored protein, inhibits formation of the membrane attack complex (MAC), the main effector of complement-mediated tissue damage. Thi...
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| Foilsithe in: | Am J Hematol |
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| Main Authors: | , , , |
| Formáid: | Artigo |
| Teanga: | Inglês |
| Foilsithe: |
2017
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| Ábhair: | |
| Rochtain Ar Líne: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5774238/ https://ncbi.nlm.nih.gov/pubmed/28815695 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1002/ajh.24886 |
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