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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
17 e COVID-19 harbor IgA autoantibodies against pulmonary surfactant proteins B and C and that these aut
18 d Main Results: IgA autoantibodies targeting pulmonary surfactant proteins B and C were elevated in p
20 virus is, in significant part, dependent on pulmonary Surfactant Protein-B, which plays an unanticip
22 along with a peptide model for collagen and pulmonary surfactant protein C have been simulated very
23 human serum mannose-binding lectin (MBL) and pulmonary surfactant protein D (SP-D) have distinctive m
24 sed on our previous studies documenting that pulmonary surfactant protein D (SP-D) protects C. neofor
27 domains of a collagenous C-type lectin, rat pulmonary surfactant protein D (SP-D), are sufficient to
30 of viral infection, and, when combined with pulmonary surfactant protein D, their antiviral effects
33 the conformational organization of the lung pulmonary surfactant proteins in the environment that mi
34 rfactant protein A (SP-A), the most abundant pulmonary surfactant protein, is implicated in multiple
35 been suggested to mimic some aspects of the pulmonary surfactant protein SP-B and has been tested cl
36 5), which is a truncated version of the full pulmonary surfactant protein SP-B, with dipalmitoylphosp
37 n spectroscopy to in-situ IR spectroscopy of pulmonary surfactant proteins SP-B and SP-C in lipid-pro
41 We have also engineered MASP binding into a pulmonary surfactant protein (SP-A), which has the same
43 We hypothesized that collectins, such as pulmonary surfactant proteins (SPs) SP-A and SP-D and se