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On page 115, Ku and Omary add one more function to keratin's expanding repertoire. In addition to acting as a structural protein in liver cells, keratin 8 (K8) apparently absorbs excess phosphorylation during stress and thus reduces the likelihood of apoptosis.
Fas-induced death (top) is increased when mutated keratin 8 cannot absorb phosphorylations (bottom).
Humans who carry a G61C polymorphism in K8 are predisposed to liver disease when exposed to insults such as infection. Unlike keratin-associated disorders in skin, these K8 variants do not appear to cause disease directly by decreasing the mechanical strength of cells. In fact, Ku and Omary found that mouse hepatocytes expressing G61C had normal mechanical strength, suggesting that the G61C polymorphism was affecting another stress response process.
G61C interfered with phosphorylation at serine-73 (S73), which is one of two sites in K8 that are phosphorylated by stress-activated kinases during...
The Rockefeller University Press
2006
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