Taeko Fukuda-Kamitani

TL;DR: Sendrinization of PML, in the context of the RING finger and the B1 box, regulates nuclear body formation and it is shown that sentrinized PML-RARα could be restored by overexpression of sentrin, but not by retinoic acid treatment.

TL;DR: Using a COS cell expression system, it is shown that PML is covalently modified by all three members of the sentrin family of ubiquitin-like proteins, which highlights the fine substrate specificity of the sendrinization pathway.

TL;DR: Results demonstrate that sentrin-2 is another protein modifier for the sentrinization pathway and could covalently modify RanGAP1, a Ran GTPase-activating protein critically involved in nuclear transport.

TL;DR: It is possible that the early-onset form of retinal degeneration seen in patients with Leber congenital amaurosis patients with AIPL1 mutations may be due to a defect in the regulation of cell cycle progression during photoreceptor maturation, and this data raise the possibility that AipL1 is important for appropriatePhotoreceptor formation during development and/or survival following differentiation.

TL;DR: Interestingly, sera from patients with Sjögren's syndrome showed heterogeneity in their reactivity to poly-ubiquitinated Ro52, probably because of their differing antigenic determinants, suggesting that Ro52 may be downregulated by the ubiquitin-proteasome pathway in vivo.