loss of BBS1 BBS4 or OFD1 led to decreased NF-kappaB activity and concomitant IkappaBbeta accumulation and that these defects were ameliorated with SFN treatment.
the present study identifies Ofd1 as a developmental disease gene that is critical for forebrain development and ciliogenesis in embryonic life and indicates that Ofd1 functions after docking and before elaboration of the axoneme in vivo.
Odontoblasts in vitro express OFD1. This hypothesis is enhanced by the huge defects observed on molars from Ofd1 knockout mice showing undifferentiated dentin-forming cells.
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