Publications by authors named "Madoka Kitamura"
Article Synopsis
- * In mice with mutations in ciliary proteins, abnormal cranial neural crest-derived cells disrupt signaling pathways, leading to improper cell differentiation and subsequent tongue issues like ankyloglossia.
- * The research also indicates that these tongue deformities can be artificially triggered in normal mice, suggesting potential avenues for treatment approaches in ciliopathies.
The pre-spliceosomal complex involves interactions between U1 and U2 snRNPs, where a ubiquitin-like domain (ULD) of SF3A1, a component of U2 snRNP, binds to the stem-loop 4 (SL4; the UUCG tetraloop) of U1 snRNA in U1 snRNP. Here, we reported the 1.80 Å crystal structure of human SF3A1 ULD (ULDSF3A1) complexed with SL4.
View Article and Find Full Text PDFObjectives: The ciliopathies are a wide spectrum of human diseases, which are caused by perturbations in the function of primary cilia. Tooth enamel anomalies are often seen in ciliopathy patients; however, the role of primary cilia in enamel formation remains unclear.
Materials And Methods: We examined mice with epithelial conditional deletion of the ciliary protein, Ift88, (Ift88 ;K14Cre).