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  CYP27A1 is the only mitochondrial 25-hydroxylase. It was to begin with identified as
  a sterol 27-hydroxylase involved in bile acid synthesis.
  
  In addition, when it is deleted in the mouse, blood degrees of 25OHD really
  increase (Zhu et al., 2013), and inactivating mutations in individuals lead to cerebrotendinous xanthomatosis with abnormal
  bile and cholesterol metabolism, but not rickets (Moghadasian, 2004).
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  Elevated calcium suppresses CYP27B1 generally by using suppression of PTH
  elevated phosphate suppresses CYP27B1 principally by stimulating FGF23, despite the fact that these ions can have direct
  results on renal CYP27B1 on their individual (Bikle and Rasmussen,
  1975 Bikle et al., 1975). The stimulation by PTH
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  are found in the proximal promoter of the CYP27B1 gene.
  The kidney and other tissues metabolize 25OHD
  to the active metabolite 1,25(OH)2D3 or the first move
  in the catabolic procedure 24,25(OH)2D3. The enzymes dependable, CYP27B1 and CYP24A1,
  respectively, are tightly controlled. The regulation of this move is modest at ideal.
  Finally, the 50 percent phase returns us to
  D (1 octave increased).