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. 2019 Jun 13;294(31):11817–11828. doi: 10.1074/jbc.RA119.009050

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© 2019 Poulsen et al.

Author's Choice—Final version open access under the terms of the Creative Commons CC-BY license.

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Figure 7. — FAS1-4 mutations lead to aberrant proteolytic processing of TGFBIp in the human cornea. 2DE immunoblotting against TGFBIp in normal human tissue and LCD A546D and V624M corneal tissues is seen. Differential TGFBIp processing resulted in the detection of smaller amounts of degradation products by an antiserum recognizing the FAS1-4 domain of TGFBIp in LCD patient tissues. These data suggest an intensive turnover of mutated FAS1-4 in the cornea of LCD patients, possibly involving HtrA1 proteolysis. The pictures are representative of experimental replicates performed for each tissue. Normal 1 and 2 are biological replicates.