Phosphosite T674A mutation in kinesin family member 3A fails to reproduce tissue and ciliary defects characteristic of CILK1 loss of function.
Casey D GaileyEric J WangLi JinSean AhmadiDavid L BrautiganXudong LiWenhao XuMichael M ScottZheng FuPublished in: Developmental dynamics : an official publication of the American Association of Anatomists (2020)
These results indicate that eliminating Kif3a Thr674 phosphorylation by Cilk1 is insufficient to reproduce the severe developmental defects in ciliopathies caused by Cilk1 loss of function. This suggests KIF3A-Thr672 phosphorylation by CILK1 is not essential for tissue development and other substrates are involved in CILK1 ciliopathies.
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