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MeSH Review

Complement Pathway, Classical

 
 
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Disease relevance of Complement Pathway, Classical

 

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High impact information on Complement Pathway, Classical

  • C1-Inh, belonging to the superfamily of serine proteinase inhibitors (serpins), is a major inhibitor of the classical complement pathway, the contact activation system, and the intrinsic pathway of coagulation, respectively [7].
  • Mannose-binding protein (MBP), C1q, the recognition component of the classical complement pathway, and pulmonary surfactant protein A (SP-A) are members of a family of molecules containing a collagen-like sequence contiguous with a noncollagen-like sequence, and usually having the properties of a lectin [8].
  • C3 deposition on promastigotes activated through the classical complement pathway reaches a 50% maximum after similar50 s, and represents >85% of total C3 bound [9].
  • The role of the classical complement pathway in humoral immune responses was investigated in gene-targeted C1q-deficient mice (C1qA-/-) [10].
  • Using a functional assay that measures the surface deposition of C3 activated via the classical complement pathway, we show that Crry/p65-expressing cells have a markedly decreased amount of C3 deposited on them as compared with control cells expressing the antisense construct or cells expressing MCR1 or MCR2 [11].
 

Chemical compound and disease context of Complement Pathway, Classical

 

Biological context of Complement Pathway, Classical

 

Anatomical context of Complement Pathway, Classical

 

Associations of Complement Pathway, Classical with chemical compounds

 

Gene context of Complement Pathway, Classical

 

Analytical, diagnostic and therapeutic context of Complement Pathway, Classical

References

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  22. Inhibition of activation of the classical pathway of complement by human neutrophil defensins. van den Berg, R.H., Faber-Krol, M.C., van Wetering, S., Hiemstra, P.S., Daha, M.R. Blood (1998) [Pubmed]
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