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Most mutations causing 21-hydroxylase deficiency originate from microconversions between CYP21 pseudogenes and active genes. However, around 20% of the alleles in the nonclassical form (NC-21OHD) remain without identified mutations, suggesting the involvement of regulatory regions. The pseudogene promoter is 80% less active than the CYP21A2 due to the presence of -126C&gt;T, -113G&gt;A, -110T&gt;C, and -103A&gt;G mutations. Additionally, mutations in the steroidogenic factor-1 binding sites of the CYP21 distal regulatory region, located at 4676 bases upstream from the cap site of the CYP21A2 gene, decrease its transcription to 35%.

Microconversion betweenCYP21A2andCYP21A1PPromoter Regions Causes the Nonclassical Form of 21-Hydroxylase Deficiency