Biochemical and Biophysical Research Communications
Adenyl cyclase in human hair follicles: Its inhibition by dihydrotestosterone
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Cited by (35)
17β-estradiol enhances vascular endothelial growth factor production and dihydrotestosterone antagonizes the enhancement via the regulation of adenylate cyclase in differentiated THP-1 cells
2002, Journal of Investigative DermatologyCitation Excerpt :It is reported that E2 enhanced AC activity in rat uterine cells or human breast cancer MCF-7 (Aronica et al, 1994) and also increased cAMP content in human coronary arteries (Mugge et al, 1993) or rat duodenal cells (Picotto et al, 1996). DHT also inhibited AC activity in rat prostate epithelia (Sutherland and Singhal, 1975) or human scalp hair follicles (Adachi and Kano, 1970). These previous studies support our results; however, the precise mechanism for E2- or DHT-induced up- or downregulation of AC activity is unknown.
Characterization of type I 5α-reductase activity in DU145 human prostatic adenocarcinoma cells
1996, Journal of Steroid Biochemistry and Molecular BiologyAndrogenetic alopecia: An autosomal dominant disorder
1995, The American Journal of MedicineAndrogenetic alopecia and hair growth promotion state of the art: Present and future
1988, Clinics in DermatologySerum elevation of dehydroepiandrosterone sulfate associated with male pattern baldness in young men
1987, Journal of the American Academy of Dermatology
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The following trivial names are used in this text: dihydrotestosterone = 5α-androstan-17β-ol-3-one; androstenedione = 4-androstene-3, 17-dione; DHA = dehydroepiandrosterone = 5 - androsten-3β-ol-17-one; estrone = 1, 3, 5 (10)-estratrien-3-ol-17-one; estradiol - 17β = 1, 3, 5 (10)-estratrien-3, 17β-diol; progesterone = 4 - pregnen-3, 20-dione; and pregnenolone = 5 - pregnen-3β-ol-20-one.