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This design allows for strong but “safe” binding of factor XII, limiting its ability to propagate the signal and generate thrombin while still maintaining overall hemostatic function
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Compared with smarca5 sibling embryos in which the circulating RBCs had normal organization in mitochondria (Figure 3A-B), we found that the smarca5 -deficient erythrocytes displayed disintegration of cristae in mitochondria while nuclear integrity was preserved in smarca5 zko1049a (Figure 3C-E)
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