Published on : Oct 07, 2019
Albany, New York, October 7, 2019: Steroid 17 Alpha Hydroxylase17,20 Lyase actively synthesize steroid hormone with help of a single enzyme P450c17 whereas different isozymes of P450c17 mediate activities of Steroid 17 Alpha Hydroxylase17,20 Lyase in testis and adrenal glands.
Steroid 17 Alpha Hydroxylase17,20 Lyase deficiency rarely occurs and amounts to very few cases of congenital adrenal hyperplasia that exists with symptoms such as sexual infantilism and hypertension. The primary cause is CYP17A1 gene’s loss of function which is located in 10q24-q25 chromosome. 17,20 lyase contributes significantly in sex steroids production by converting 17?-hydroxypregnenolone and progesterone into dehydroepiandrosterone. Precursor products are converted into corticosterone.
An intelligence report titled, “Steroid 17 Alpha Hydroxylase17,20 Lyase-Pipeline Review, H2 2019” is the source of all the stated insights. This report is the latest addition to Market Research Hub’s ever growing repository
Increased corticosterone protect from insufficiency in cortisol as glucocorticoid receptors. Sex development disorders are congenital conditions encouraging atypical development of anatomical sex and chromosome. Androgen insensitivity syndrome, CAH and gonadal dysgenesis are the main factors that cause DSDs. Steroid 17 Alpha Hydroxylase17,20 Lyase deficiency is presumed to be very rare which delays its diagnosis.
Human gene mutation database has recorded 95 mutation for CYP17A1 gene that includes deletions, nonsense mutations, missense, splice site variants and insertions. Hypokalemia, hypertension and genital undervirilization compose the phenotic severity symptoms for the deficiency and these symptoms represent full or partial of of enzyme functionalities.
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