Cell
ArticleCloning and expression of steroid sulfatase cDNA and the frequent occurrence of deletions in STS deficiency: Implications for X-Y interchange
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The Past and Future of Rare Skin Disease Research and Therapy
2022, Journal of Investigative DermatologyCitation Excerpt :Those were indeed halcyon days for gene hunters. It was not until the ESDR was approaching its 18th birthday that the first genetic breakthrough for an inherited skin disease was made: microdeletions in STS were shown to underlie X-linked ichthyosis (Ballabio et al., 1987; Yen et al., 1987). Thereafter, during the 1990s, a plethora of genes for major genodermatoses were identified through genetic linkage studies, including keratin genes KRT5 and KRT14 for epidermolysis bullosa (EB) simplex (Bonifas et al., 1991; Coulombe et al., 1991; Lane et al., 1992) and TGM1 for autosomal recessive congenital ichthyosis (ARCI) (Huber et al., 1995).
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2018, Vitamins and HormonesUpdated survey of the steroid-converting enzymes in human adipose tissues
2015, Journal of Steroid Biochemistry and Molecular BiologyCitation Excerpt :Overall, the specific role of 3β-HSD activity in adipose tissue steroid homeostasis remains to be formally established. Steroid sulfatase (STS) converts DHEA-sulfate (DHEA-S) and estrone-sulfate (E1-S) into their free forms, DHEA and E1 [212]. While it is uncertain that adipose tissue generates de novo DHEA and E1 directly from cholesterol, the sulfated forms of these steroids are highly abundant in the circulation and may represent a significant source for these steroids in adipose tissue, provided that STS is indeed, active [213].
Assessment of steroidogenesis and steroidogenic enzyme functions
2013, Journal of Steroid Biochemistry and Molecular BiologyCitation Excerpt :Since STS possesses broad substrate specificity, it is able to convert CholS, DHEAS and E1S into cholesterol, DHEA and E1 respectively. The use of inhibitors of STS to lower the concentration of active oestrogen in oestrogen-sensitive diseases should take into account the possible side effects due to the inhibition of DHT biosynthesis from ADTS and DHEAS and the accumulation of CholS that causes ichthyosis similar to that found in patients having X-linked ichthyosis due to STS deficiency [62,63]. Cancer cells are cells that have their regulatory machinery altered making them grow and divide in an uncontrolled manner.