PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2544801-3 1989 Incubation with 10 microM 5-cholestene-3 beta,22(R)-diol or 10 microM 5-cholestene-3 beta,20 alpha-diol together with hCG (10 ng/ml, 2 h) reversed most of the inhibitory effect of IFN gamma, suggesting that IFN gamma inhibits P450scc activity, possibly by inhibiting the substrate (cholesterol) availability for P450scc. Cholesterol 282-293 hypertrichosis 2 (generalised, congenital) Homo sapiens 118-121 3958520-8 1986 The cholesterol content in a 10 day LPPS culture with hCG had a tendency to be lower than that in a 10 day LPPS culture, but there was no statistical difference (p less than 0.1). Cholesterol 4-15 hypertrichosis 2 (generalised, congenital) Homo sapiens 54-57 3036468-7 1987 This suggests that the transport of cholesterol to inner mitochondrial membranes from outer membranes is regulated by hCG. Cholesterol 36-47 hypertrichosis 2 (generalised, congenital) Homo sapiens 118-121 2855024-0 1988 Stimulation of cholesterol side-chain cleavage enzyme activity by cAMP and hCG in MA-10 Leydig tumor cells. Cholesterol 15-26 hypertrichosis 2 (generalised, congenital) Homo sapiens 75-78 3958520-11 1986 It was estimated from the results of the present study that hCG enhanced utilization of intracellular cholesterol. Cholesterol 102-113 hypertrichosis 2 (generalised, congenital) Homo sapiens 60-63 6224978-7 1983 Our findings are compatible with the concept that the main difference in the gonadotropin-stimulated steroidogenesis in man and rat is the magnitude of the rapid steroidogenic response to hCG, which is very small in man and indicates smaller supply or lesser metabolism of mitochondrial cholesterol in human testis. Cholesterol 287-298 hypertrichosis 2 (generalised, congenital) Homo sapiens 188-191 2994765-9 1985 In desensitized cells from hCG-treated mice (2 micrograms i.p., 48 h) cellular unesterified and esterified cholesterol were decreased by 21% and 81%, respectively, when compared to control cells. Cholesterol 107-118 hypertrichosis 2 (generalised, congenital) Homo sapiens 27-30 2994765-11 1985 In conclusion, our data indicate that the impaired steroidogenesis in mouse Leydig cells desensitized in vivo by a single injection of hCG is the result of a depletion in cellular cholesterol, rather than of an impaired conversion of cholesterol to testosterone. Cholesterol 180-191 hypertrichosis 2 (generalised, congenital) Homo sapiens 135-138 2985225-4 1985 Examination of the time course for the loss of lipoprotein response after hCG injection revealed that injection with 50 IU of hCG results in a loss of gonadotropin response as early as 1 h after injection, but exogenous cholesterol-carrying lipoprotein fractions, LDL and HDL, were capable of stimulating progesterone production up to 4 h after hormone injection. Cholesterol 220-231 hypertrichosis 2 (generalised, congenital) Homo sapiens 126-129 7106051-11 1982 When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls. Cholesterol 204-215 hypertrichosis 2 (generalised, congenital) Homo sapiens 10-13 6305195-1 1983 The results of the present investigation support the conclusion that low-density lipoprotein (LDL)-cholesterol facilitates androgen synthesis in human chorionic gonadotropin (hCG)-treated human fetal testicular tissue in vitro. Cholesterol 99-110 hypertrichosis 2 (generalised, congenital) Homo sapiens 175-178 6305195-2 1983 Moreover, the number of LDL receptors and the rate of de novo synthesis of cholesterol are high during the period of active fetal testicular steroidogenesis and fall with advancing gestational age, suggestive of regulation by hCG. Cholesterol 75-86 hypertrichosis 2 (generalised, congenital) Homo sapiens 226-229 6296852-3 1982 The results presented herein show that the hCG-induced loss of steroidogenic response to cAMP is due to the depletion of intracellular cholesterol and that this depletion can be prevented by the addition of low density lipoprotein. Cholesterol 135-146 hypertrichosis 2 (generalised, congenital) Homo sapiens 43-46 7106051-11 1982 When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls. Cholesterol 204-215 hypertrichosis 2 (generalised, congenital) Homo sapiens 55-58 7106051-11 1982 When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls. Cholesterol 204-215 hypertrichosis 2 (generalised, congenital) Homo sapiens 55-58 7106051-11 1982 When PMSG-hCG-primed animals received iv injections of hCG on day 8 post-hCG, ovarian sterol ester stores were markedly depleted within 2 h. The ovarian ACAT activity of hCG-treated rats measured without cholesterol was significantly lower than that of controls. Cholesterol 204-215 hypertrichosis 2 (generalised, congenital) Homo sapiens 55-58 7106051-12 1982 With cholesterol, ACAT activities of hCG-treated rats were similar to those in controls. Cholesterol 5-16 hypertrichosis 2 (generalised, congenital) Homo sapiens 37-40 29366778-6 2018 Basal and hCG-stimulated progesterone secretion was significantly decreased by the combined actions of the LXR agonist T0901317 and the SREBP inhibitor fatostatin, which was associated with reduced intracellular cholesterol storage. Cholesterol 212-223 hypertrichosis 2 (generalised, congenital) Homo sapiens 10-13 6271226-9 1981 Further, [3H]cholesterol from [3H]cholesteryl linoleate-LDL was incorporated into luteal cell progesterone and the extent of this incorporation was enhanced by hCG. Cholesterol 13-24 hypertrichosis 2 (generalised, congenital) Homo sapiens 160-163 16230783-0 2005 LH/hCG-stimulated androgen production and selective HDL-cholesterol transport are inhibited by a dominant-negative CREB construct in primary cultures of rat theca-interstitial cells. Cholesterol 56-67 hypertrichosis 2 (generalised, congenital) Homo sapiens 3-6 20926582-8 2010 These data suggest that an initial action of LH/CG on the primate preovulatory follicle is to rapidly reduce the expression of PPARG, resulting in reduced NR1H3 with the consequence shifting the balance from cholesterol efflux via ABCA1 and ABCG1 to cholesterol uptake (SCARB1) and metabolism (STAR, P450 side-chain cleavage A1, hydroxysteroid dehydrogenase 3B). Cholesterol 208-219 hypertrichosis 2 (generalised, congenital) Homo sapiens 48-50 20926582-8 2010 These data suggest that an initial action of LH/CG on the primate preovulatory follicle is to rapidly reduce the expression of PPARG, resulting in reduced NR1H3 with the consequence shifting the balance from cholesterol efflux via ABCA1 and ABCG1 to cholesterol uptake (SCARB1) and metabolism (STAR, P450 side-chain cleavage A1, hydroxysteroid dehydrogenase 3B). Cholesterol 250-261 hypertrichosis 2 (generalised, congenital) Homo sapiens 48-50 16230783-10 2005 The selective uptake of HDL-cholesterol was also enhanced by hCG but exposure to Ad A-CREB also abrogated this effect. Cholesterol 28-39 hypertrichosis 2 (generalised, congenital) Homo sapiens 61-64 9214555-2 1997 Although the long-term effect of trophic hormones on Leydig cell cholesterol uptake, storage, and deesterification has been well documented, the early effects of the human choriogonadotropin (hCG) on cell cholesterol/lipid distribution are not yet known. Cholesterol 205-216 hypertrichosis 2 (generalised, congenital) Homo sapiens 192-195 9561722-6 1997 The obtained results suggest that paracrine factor(s) presents in STM and acting in synergy with LH/hCG generate(s) the rearrangement of cytoskeletal structures which, in turn, facilitates the availability of cholesterol for the mitochondria and finally enhances the testosterone production in the rat Leydig cells. Cholesterol 209-220 hypertrichosis 2 (generalised, congenital) Homo sapiens 100-103 1783364-7 1991 2) The concentration of cholesterol in plasma membrane fraction decreased significantly by hCG stimulation. Cholesterol 24-35 hypertrichosis 2 (generalised, congenital) Homo sapiens 91-94 8243314-16 1993 Also, levels of the ovarian cholesterol side-chain cleavage enzyme (CYP 11A) mRNA (2 kilobases) were low in control animals, but increased 20.5- and 14.3-fold after surge doses of rcFSH and hCG, respectively. Cholesterol 28-39 hypertrichosis 2 (generalised, congenital) Homo sapiens 190-193 1783364-10 1991 These results indicate the increase of membrane fluidity of the GCs luteinization induced by hCG is due to a decrease of cholesterol/phospholipids ratio. Cholesterol 121-132 hypertrichosis 2 (generalised, congenital) Homo sapiens 93-96 2226298-4 1990 The total cholesterol content of cells stimulated for 4 h with hCG was significantly decreased compared with unstimulated cells (8.4 vs. 17.6 micrograms/mg protein); both free and esterified cholesterol decreased by about 50%. Cholesterol 10-21 hypertrichosis 2 (generalised, congenital) Homo sapiens 63-66 2226298-4 1990 The total cholesterol content of cells stimulated for 4 h with hCG was significantly decreased compared with unstimulated cells (8.4 vs. 17.6 micrograms/mg protein); both free and esterified cholesterol decreased by about 50%. Cholesterol 191-202 hypertrichosis 2 (generalised, congenital) Homo sapiens 63-66 2226298-9 1990 HMG-CoA reductase activity induced by hCG was blocked by aminoglutethimide, an inhibitor of the cholesterol side-chain cleavage enzyme. Cholesterol 96-107 hypertrichosis 2 (generalised, congenital) Homo sapiens 38-41 2167768-5 1990 The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone. Cholesterol 124-135 hypertrichosis 2 (generalised, congenital) Homo sapiens 48-51 2167768-5 1990 The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone. Cholesterol 248-259 hypertrichosis 2 (generalised, congenital) Homo sapiens 48-51 2167768-5 1990 The following conclusions are drawn: 1) chronic hCG treatment enhances the ability of rat Leydig cells to take-up exogenous cholesterol from circulating lipoproteins, and to store it in lipid droplets as a reserve material; 2) lipid-droplet stored cholesterol is employed only in the case of intense acute stimulation, since, under basal conditions, endogenous cholesterol synthesis is able to meet the requirements for testosterone production alone. Cholesterol 248-259 hypertrichosis 2 (generalised, congenital) Homo sapiens 48-51