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The inverse relationship between serum albumin concentration and its half-life suggested to early workers that albumin would be protected from a catabolic fate by a receptor-mediated mechanism much like that proposed for IgG. We show here that albumin binds FcRn in a pH dependent fashion, that the lifespan of albumin is shortened in FcRn-deficient mice, and that the plasma albumin concentration of FcRn-deficient mice is less than half that of wild-type mice. These results affirm the hypothesis that the major histocompatibility complex-related Fc receptor protects albumin from degradation just as it does IgG, prolonging the half-lives of both.
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Chaity Chaudhury
Samina Mehnaz
John M. Robinson
The Journal of Experimental Medicine
The Ohio State University
Jackson Laboratory
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Chaudhury et al. (Mon,) studied this question.
www.synapsesocial.com/papers/69d8e464ade63f05b9bedc98 — DOI: https://doi.org/10.1084/jem.20021829