Anterograde trafficking of ciliary MAP kinase-like ICK/CILK1 by the intraflagellar transport machinery is required for intraciliary retrograde protein trafficking.

ICK (also known as CILK1) is a mitogen-activated protein kinase-like kinase localized at the ciliary tip. Its deficiency is known to result in the elongation of cilia and causes ciliopathies in humans. However, little is known about how ICK is transported to the ciliary tip.

C11ORF74 interacts with the IFT-A complex and participates in ciliary BBSome localization.

Cilia are organelles that serve as cellular antennae. Intraflagellar transport particles containing the IFT-A and IFT-B complexes mediate bidirectional trafficking of ciliary proteins. Particularly, in concert with the BBSome complex, IFT particles play an essential role in trafficking of ciliary G-protein-coupled receptors (GPCRs).

Ciliopathy-associated mutations of IFT122 impair ciliary protein trafficking but not ciliogenesis.

The intraflagellar transport (IFT) machinery containing the IFT-A and IFT-B complexes mediates ciliary protein trafficking. Mutations in the genes encoding the six subunits of the IFT-A complex (IFT43, IFT121, IFT122, IFT139, IFT140, and IFT144) are known to cause skeletal ciliopathies, including cranioectodermal dysplasia (CED). As the IFT122 subunit connects the core and peripheral subcomplexes of the IFT-A complex, it is expected to play a pivotal role in the complex.