ZMYND10

This gene encodes a protein containing a MYND-type zinc finger domain that likely functions in assembly of the dynein motor. Mutations in this gene can cause primary ciliary dyskinesia. This gene is also considered a tumor suppressor gene and is often mutated, deleted, or hypermethylated and silenced in cancer cells. Alternative splicing results in multiple transcript variants.

zinc finger, MYND-type containing 10

Plays a role in axonemal structure organization and motility (PubMed:23891469, PubMed:23891471).
Involved in axonemal pre-assembly of inner and outer dynein arms (IDA and ODA, respectively) for proper axoneme building for cilia motility (By similarity).
May act by indirectly regulating transcription of dynein proteins (By similarity).

Biological Process cilium movement Source:Ensembl
Biological Process inner dynein arm assembly Source:UniProtKB2 Publications
Biological Process motile cilium assembly Source:UniProtKB2 Publications
Biological Process outer dynein arm assembly Source:UniProtKB2 Publications
Biological Process positive regulation of motile cilium assembly Source:UniProtKB
Biological Process protein localization to cilium Source:Ensembl

Cytoplasm
Cytoplasm, cytoskeleton, microtubule organizing center, centrosome, centriolar satellite
Apical cell membrane
Dynein axonemal particle

Ciliary dyskinesia, primary, 22 (CILD22):
A disorder characterized by abnormalities of motile cilia. Respiratory infections leading to chronic inflammation and bronchiectasis are recurrent, due to defects in the respiratory cilia. Patients may exhibit randomization of left-right body asymmetry and situs inversus, due to dysfunction of monocilia at the embryonic node. Primary ciliary dyskinesia associated with situs inversus is referred to as Kartagener syndrome.