*Note: I'm using the nomenclature as suggested in Janeway's Immuno Biology where the smaller fragment of C2 gets the 'b'.
This may not be a direct answer to your question. But it may help to understand the role of C2b.
Perfect, thank you... It's amazing how often this fragment simply drifts off the page without any attention. I'll have to read it tomorrow, but I wanted to thank you as soon as I noticed your response.
There is no known function yet for C2b (the smaller fragment of complement C2). The larger fragment (C2a) is the serine protease attached non-covalently to C4b to form the C3 convertase of the classical pathway of complement.
The claim in the paper of Strang et al. from 1988 was not confirmed and in fact it is believed today that Bradykinin, a peptide generated in plasma in the absence of C1 Inhibitor, is the major factor causing HAE symptoms.
Thank you all... Svi, I noticed that numerous textbook references name C2b as a kinin precursor, yet I don't see it supported. One thing making things difficult is the mix in the nomenclature with some still using C2a. C2a as part of the C3 convertase is the standard now, right?
Peter, the link does not work for me... I get a 404 page not found.
Also, I found the structure for C2b solved, but it mentions CCP-domain assemblies, which I thought odd, but given how little I know of C2b, that doesn't mean much.
Yes, until further notice from the complement community C2a is the C2 fragment associated with C4b. The nomenclature is being discussed now and soon the conclusions will be published.
As Peter indicated, domains within the C2b region of C2 participate in the initial interaction of C2 with C4b. Whether or not the dissociated C2b has a function is till not clear.
BTW there are quite a few false claims in textbooks.
As Zvi indicated, CCP domains within the C2b region particpate in the initial interaction of uncleaved C2 with C4b; however, this interaction seems to be crucial since preventing this CCP interaction (blocking anti-C2b antibody or chimeric CCP C2 versions) suppresses C2 hemolytic activity. For refs see Oglesby et al. Journal of Immunolgy 1988; 141: p926 and Xu et al. 1Journal of Immunology 1997; 158: 5958.
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