Hydin axonemal central pair apparatus protein (HYDIN)

Hydin axonemal central pair apparatus protein (HYDIN) is a highly conserved structural protein essential for the assembly and function of the central pair apparatus in cilia and flagella. HYDIN localizes to the C2 microtubule within the central pair and is required for proper flagellar and ciliary motility; it participates in the regulation of dynein arm activity and bending of cilia/flagella. Loss-of-function mutations lead to structural defects in the central pair, impaired motility, and neurodevelopmental diseases such as hydrocephalus. HYDIN has multiple ASH (ASPM, SPD-2, Hydin) domains potentially involved in microtubule binding, and interacts with other central pair proteins including CPC1 and KLP1, anchoring components within the axoneme. Humans possess a duplicate, HYDIN2, expressed as alternatively spliced forms. HYDIN is not currently regarded as a therapeutic target, and no approved drugs or investigational agents act on HYDIN directly. While PPP1R31 is listed among aliases, there is no clear evidence that HYDIN acts as a classical regulatory subunit of protein phosphatase 1 in the context of human axonemal protein biology; the key roles, functional domains, and disease associations point to its principal structural function in cilia/flagella.

Other names

Hydrocephalus-inducing protein homologHYDIN1KIAA1864DKFZp434D0513PPP1R31CILD5Protein phosphatase 1, regulatory subunit 31HYDIN2

Not applicable; there are no drugs targeting HYDIN, so there is no mechanism of action to specify