Use your antibodies-online credentials, if available.
findings suggest that IYD transcription is activated by TH receptors early during intestinal remodeling to ensure efficient iodine recycling at the climax of metamorphosis when high levels of TH are needed for proper transformations of different organs.
The rate-limiting processes that contribute to the ability of flavin to promote reductive dehalogenation in human IYD.
A switch between one- and two-electron chemistry of iodotyrosine deiodinase is controlled by substrate.
Iodotyrosine deiodinase defect identified via genome-wide approach.
high activity of human saliva peroxidase with iodide as a substrate may play a crucial role in the bioavailability and metabolism of biologically active iodide.
Mutations in DEHAL1 leads to hypothyroidism, goiter and mental retardation (Review)
molecular cloning and investigation of the localization and activity of DEHAL1
the cytoplasmic tail of DEHAL1 could play a role in the stability of the protein
Diffuse cytoplasmatic localisation or downregulation of DEHAL1 expression in thyroid cancers suggests alteration or loss of DEHAL1 function during thyroid cell dedifferentiation.
homozygous mutations in DEHAL1 appear to cause human iodotyrosine deiodinase deficiency, leading to hereditary hypothyroidism and goiter
This study describes a functional mutation within IYD, demonstrating the molecular basis of the iodine wasting form of congenital hypothyroidism
At least for Metazoa, IYD should provide a new marker for tracing the evolutionary development of iodinated amino acids as regulatory signals through the tree of life.
Data show that the structures provide a molecular basis for understanding thyroid disease based on mutations of IYD.
This gene encodes an enzyme that catalyzes the oxidative NADPH-dependent deiodination of mono- and diiodotyrosine, which are the halogenated byproducts of thyroid hormone production. The N-terminus of the protein functions as a membrane anchor. Mutations in this gene cause congenital hypothyroidism due to dyshormonogenesis type 4, which is also referred to as deiodinase deficiency, or iodotyrosine dehalogenase deficiency, or thyroid hormonogenesis type 4. Alternative splicing results in multiple transcript variants.
, iodotyrosine dehalogenase 1
, iodotyrosine dehalogenase 1 protein