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7 the collectin family of proteins, including pulmonary surfactant protein A (SP-A), we hypothesized t
9 otein C1q, mannose-binding lectin (MBL), and pulmonary surfactant protein A (SPA) are structurally si
13 e location and depth of each residue of lung pulmonary surfactant protein B (SP-B(1-25)) in a phospho
14 For identification of structural changes of pulmonary surfactant protein B (SP-B) due to the heterog
18 along with a peptide model for collagen and pulmonary surfactant protein C have been simulated very
19 human serum mannose-binding lectin (MBL) and pulmonary surfactant protein D (SP-D) have distinctive m
20 sed on our previous studies documenting that pulmonary surfactant protein D (SP-D) protects C. neofor
23 domains of a collagenous C-type lectin, rat pulmonary surfactant protein D (SP-D), are sufficient to
25 of viral infection, and, when combined with pulmonary surfactant protein D, their antiviral effects
28 the conformational organization of the lung pulmonary surfactant proteins in the environment that mi
29 rfactant protein A (SP-A), the most abundant pulmonary surfactant protein, is implicated in multiple
30 been suggested to mimic some aspects of the pulmonary surfactant protein SP-B and has been tested cl
31 5), which is a truncated version of the full pulmonary surfactant protein SP-B, with dipalmitoylphosp
32 n spectroscopy to in-situ IR spectroscopy of pulmonary surfactant proteins SP-B and SP-C in lipid-pro
36 We have also engineered MASP binding into a pulmonary surfactant protein (SP-A), which has the same
38 We hypothesized that collectins, such as pulmonary surfactant proteins (SPs) SP-A and SP-D and se
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