By Jean Lewis, George De Santis
Kid's fiction-Big Tell-a-Tale booklet.
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J Biol Chem 2003;278:38084–38093. 38 Cheng JB, Levine MA, Bell NH, Mangelsdorf DJ, Russell DW: Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase. Proc Natl Acad Sci USA 2004;101:7711–7715. 39 Holick MF: Vitamin D: a D-lightful health perspective. Nutr Rev 2008;66:S182–S194. 40 St Arnaud R, Messerlian S, Moir JM, Omdahl JL, Glorieux FH: The 25-hydroxyvitamin D 1-alphahydroxylase gene maps to the pseudovitamin D-deficiency rickets (PDDR) disease locus. J Bone Miner Res 1997;12:1552–1559.
Mutations within or deletion of the genes responsible for these factors result in congenital hypoparathyroidism that is associated with other conditions such as the hypoparathyroidism, deafness, renal anomalies (HDR) (#146255) syndrome and the 22q deletion complex, of which the DiGeorge syndrome (DGS) (#188400) is part. The homologue of drosophila glial cells missing 2 (GCM2) (*603716) is a highly conserved gene that is necessary for PT gland development. It has no other known function in man. Mutations in this gene cause autosomal recessive familial isolated hypoparathyroidism (FIH) (#146200).
Skeletal Development The evolutionary landmarks giving rise to the vertebrate skeleton are reflected in the developmental biology of bone tissue. Axial skeletal patterning, segmentation, growth and condensation are regulated by homeobox (hox) genes (reviewed in ), bone morphogenic proteins (BMPs) and other members of the transforming growth factor-β (TGF-β) superfamily (reviewed in ), fibroblast growth factors (FGFs) , hedgehog  and Wnt proteins . Many of these factors act not only in skeletal patterning and development but also in the recruitment and differentiation of osteoblasts during bone modelling and remodelling throughout life.