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HYDIN encodes a protein that may be involved in cilia motility.
Hydin is identified as a novel pain gene in mouse model.
A domain with homology to caldesmon, an actin-binding protein, suggests an interaction with the cytoskeleton.
data provide the first evidence of Hydin's role within the trypanosome axoneme, and reveal central pair anomalies and thus impairment of ependymal ciliary motility as the likely cause of the hydrocephalus observed in the hy3 mouse
We conclude that hydrocephalus in hydin mutants is caused by a central pair defect impairing ciliary motility and fluid transport in the brain.
Hydin is most abundantly expressed in tissues rich in highly ciliated cells, such as olfactory sensory neurons, and is predicted to be important to cilia.
First demonstration that Chlamydomonas reinhardtii hydin is a central pair (CP) protein required for flagellar motility. Suggests that hydrocephalus caused by mutations in hydin likely involves the malfunctioning of cilia because of a defect in the CP.
The results suggest frequent and coordinated adaptive immune responses against HYDIN variants in patients with cancer.
We have found that the human HYDIN locus has been very recently duplicated, with a nearly identical 360-kb paralogous segment inserted on chromosome 1q21.1
This gene encodes a protein that may be involved in cilia motility. Mutations in this gene cause of autosomal recessive primary ciliary dyskinesia-5, a disorder characterized by the accumulation of cerebrospinal fluid within the ventricles of the brain. A duplicate copy of this gene has been found in humans on chromosome 1.
, hydrocephalus 3
, hydrocephalus-inducing protein
, protein Hy-3
, hydrocephalus-inducing protein homolog
, protein phosphatase 1, regulatory subunit 31