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Query: DrugBank:APRD00627 (
MAP
)
15,705
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Maternal protein-energy restriction (25% of the ad libitum intake) during the first 10 days of pregnancy resulted in severely altered fetal growth rates. Fetal development was assessed by body weight, brain weight, brain
DNA
, and brain protein content on fetal days 16, 18, 20 and at term. The individual placentas were also examined (weight,
DNA
and protein content) on each of these fetal days.
Progesterone
was administered commencing with day 3 of pregnancy until the day Caesarian section was done, in an attempt to rehabilitate placental development. This treatment did not improve placental development on fetal days 16 or 18. However, fetal development was significantly improved on day 16 and day 20, as compared to the dietary-restricted group without progesterone.
...
PMID:The effect of progesterone on fetal and placental development in normal and protein-energy-restricted rats. 12 Nov 53
The relationship between the cellular uptake of glucocorticoid hormones, the binding of these hormones to specific in vitro receptors, and the induction of mouse mammary tumor viruses in an established mouse mammary tumor cell line was highly correlated. These results suggest that the induction of mouse mammary tumor virus by glucocorticoid hormones is a physiological process acting through a mechanism of high affinity, saturable steroid-receptors. A temperature-sensitive or salt-dependent step following glucocorticoid-receptor interaction was required for nuclear uptake of the steroid. Induction studies with different adrenocorticoids indicate that the synthetic glucocorticoid, dexamethasone (1,4-pregnadiene-9-fluor-16alpha-methyl-11beta,17alpha,21-triol-3,20-dione), is the most potent inducer of mouse mammary tumor viruses and all steroids which caused significant induction were glucocorticoids. Other glucocorticoids appear to stimulate murine mammary tumor virus production by a mechanism similar to that of dexamethasone; for example, corticosterone competes with dexamethasone for binding to the glucocorticoid receptor and blocks the uptake of dexamethasone into cells.
Progesterone
also blocks the cellular uptake of dexamethasone and can bind to the glucocorticoid receptor at low concentrations (10-7 to 10-8 M) but progesterone does not consistently induce virus at hormone concentrations even as high as 10-4 M. Thus, in this system, binding to a cytoplasmic receptor is necessary but not sufficient for induction by glucocorticoids. Estrogens and androgens interfere with receptor binding and cellular uptake of dexamethasone but only at much higher concentration (10-4 M) than progesterone, and do not induce mammary tumor virus production. Although there was a positive correlation between steroid structure, binding, and biologic induction, other factors clearly affect the physiological manifestations of steroid actions. Mouse cells with comparable cytoplasmic receptor levels and comparable nuclear uptake differed absolutely in their degree of murine mammary tumor virus induction following hormone treatment. Although all mouse cells examined contain comparable levels of murine mammary tumor virus
DNA
, only cells producing constitutive levels of murine mammary tumor virus RNA could be induced to higher levels by a variety of glucocorticoids.
...
PMID:Glucocorticoid-receptor interaction and induction of murine mammary tumor virus. 16 67
Medroxyprogesterone acetate
(
Provera
) was administered orally during 2-4 days to women undergoing endometrial curettage during the follicular phase of the menstrual cycle. Estradiol (E2) receptor levels were estimated from the amounts of 2H-E2 tightly bound in nuclei after incubation of endometrial tissue with an excess of the labeled hormone. An average value (9 subjects) of 1.5 pmole E2/mg
DNA
+/- 0.7 (mean +1- SD) was found. This value is significantly lower than the average E2 receptor levels in proliferative endometrium of untreated subjects (3.2 +/- 1.3, n = 33) and equals the level observed in the early secretory phase (1.5 +/- 0.5, n = 5). These results indicate that one of the progestin effects on human endometrium is the reduction of E2 receptor levels.
...
PMID:Effects of progestins on estradiol receptor levels in human endometrium. 16 81
Progesterone
causes in goblet cells of oviducts of estrogen hormone-stimulated immature quails selectively gene activation without affecting
DNA
synthesis. This biological model has been used to study the influence of poly ADP-ribosylation during the processes of
DNA
transcription. Administration of progesterone in vivo causes an increase of the activity of RNA polymerase I and II in isolated nuclei. This increase is accompanied by a marked decrease of the specific activity of poly (ADP-Rib) polymerase. After in vitro ADP-ribosylation of nuclear proteins the template capacity of chromatin for ""exogenous'' RNA synthesis (with E. coli
DNA
-dependent RNA polymerases) as well as for ""endogenous'' RNA synthesis with
DNA
dependent RNA polymerases II is not affected, whereas the data presented seem to indicate that the capacity for RNA synthesis mediated by ""endogenous'' DNA-dependent RNA polymerase I might be inhibited after ADP-ribosylation. Evidence is presented to show that a considerable amount of poly (ADP-Rib), synthesized by poly (ADP-Rib) polymerase in isolated nuclei, is linked with RNA polymerase I. The rate of synthesis of poly (ADP-Rib) is dependent on the incubation temperature (optimum at 25 degrees C) and it can be inhibited by the specific inhibitors of poly (ADP-Rib) polymerase nicotineamide, thymidine and formycin B. Poly (ADP-Rib) is probably associated with RNA polymerase I through a covalent linkage. ADP-ribosylated RNA polymerase I has been purified 550 fold with respect to the nuclear extract corresponding to a 4,000 fold purification from the whole cell homogenate. The ratio between poly (ADP-Rib), formed during preincubation of nuclei with NAD, and RNA polymerase I remains almost constant during the purification procedures. The extent of ADP-ribosylation of RNA polymerase I decreases during gene expression. Thus we conclude that poly ADP-ribosylation of this enzyme is one of the regulatory mechanisms by which specificity of
DNA
transcription is achieved.
...
PMID:Poly ADP-ribosylation of DNA-dependent RNA polymerase I from quail oviduct. Dependence on progesterone stimulation. 18 9
The types of methylases are found in the cellular extract of Escherichia coli B, infected with phage DDVI. One of them is a cellular enzyme, which methylates adenine to form 6-methylaminopurine (6-MAP) and is repressed in the infected cell in vivo. The second type, which is not found in the non-infected cells, is specific for phage DDVI and induces the formation of 7-methylguanine (7-MG). Both enzymes recognize various sites, which accounts for the ratio 6-
MAP
/7-MG to vary in heterological DNAs between 2.07 in phage Sd
DNA
and 0.40 in phage DDII
DNA
. During in vitro incubation with homologous methylases phage DDVI
DNA
and especially phage T2
DNA
are subjected to further methylation, which is probably indicative of their "undermethylation" in vivo. The DDVI-specific enzyme, similar to B-specific type, methylates
DNA
with a normal set of nitrogenous bases (phages Sd and DDII), as well as DNAs containing 5-oxymethylcytosine and glucose (phages T2 and DDVI). Both methylases under study use only native double-helical
DNA
as substrate and are strongly inhibited by S-adenosylhomocysteine. Phage DDVI Methylase is characterized by low stability.
...
PMID:[Some peculiarities of phage DDVI-specific methylases]. 32 98
Proliferating tumor cells obtained from ovarian, mammary, and endometrial tumors in tissue culture were tested for the influence of proteohormones and steroid hormones on cellular
DNA
synthesis and cell growth. The gonadotropic hormones stimulated
DNA
synthesis of ovarian tumor cells by single administration, or in combination with cortisol, up to the 11-fold of the comparable controls. The hormone sensitivity of the cell lines was variable, resulting in individual reaction patterns. There was no correlation to the histological diagnosis of the primary tumors with respect to the grade of differentiation. The results suggest that ovarian tumor cells in tissue culture can maintain sensitivity to organotropic hormones. Compared to the ovarian carcinoma lines, mammary or endometrial tumor cells did not respond to a similar extent.
Progesterone
decreased
DNA
synthesis of endometrial carcinoma cells.
...
PMID:Hormone sensitivity of gynecological tumor cells in tissue culture. 47 69
Hydrocortisone acetate injected into pseudopregnant rabbits induced casein synthesis and a parallel accumulation of casein mRNA. These effects were not accompanied by any enrichment of total RNA in the mammary cell. Hydrocortisone acetate did not favour the attachment of polysomes to endoplasmic reticulum. Casein mRNA concentration was enhanced in free and membrane-bound polysomes. After long treatments, the concentration of casein mRNA reached a plateau in membrane bound polysomes whereas it continued to be accumulated in free polysomes, suggesting that a substantial part of casein synthesis is then carried out by free polysomes.
Progesterone
injected with high doses of prolactin was unable to prevent the stimulatory action of prolactin on the synthesis of casein, the accumulation of casein mRNA and mammary gland growth, as judged by
DNA
content. By contrast, the increase in the total RNA content of mammary gland was still significantly reduced by progesterone. In addition, progesterone inhibited almost completely the formation of membrane-bound polysomes and the anchorage of casein mRNA to endoplasmic reticulum. From these data, it was concluded that the formation of the endoplasmic reticulum is not a prerequisite for the initiation of casein synthesis. Glucocorticoids do not play a major role in the formation of the endoplasmic reticulum and the Golai apparatus and in the binding of casein synthesizing polysomes to membranes. Progesteronne is capable of inhibiting preferentially and gradually the stimulation of cellular functions requiring the most potent prolactin stimulation.
...
PMID:Role of glucocorticoids and progesterone in the development of rough endoplasmic reticulum involved in casein biosynthesis. 48 76
Clinical studies were carried out with laboratory female rats to ascertain the effects of daily dosing with
MPA
(medroxyprogesterone acetate). Some of the rats received .8 mg
MPA
in 1.4 ml acqueous suspension. The others received 2 mg
MPA
in intramuscular injections. The doses used were those necessary for estrus synchronisation. Body weight was increased by
MPA
given by gastric intubation. Liver weight, dry matter, protein,
DNA
, and RNA were not significantly affected by daily
MPA
, either by intubation or by injection. Adrenocortical atrophy occurred as a result of the
MPA
administration. This response was dose-dependent. Histologically, the loss of adrenal weight was due almost entirely to the involution of cortical cells. The mechanism of adrenocortical atrophy involved extensive single cell deletion, due perhaps to the suppression of pituitary ACTH secretion. No changes in the liver were observed through biochemical determinations.
...
PMID:Adrenocortical involution in rats during oestrus synchronisation with medroxyprogesterone. 56 35
Uterine peroxidase enzyme activity has been studied as a marker for estrogen action in the uterus to help clarify the mechanism of estrogen action and its modulation by antiestrogens and progestins. Estrogen-induced increases in peroxidase were found to closely parallel increases in uterine weight and
DNA
content in the castrate rat. In the cycling female rat, uterine peroxidase levels were highest during proestrus and estrus and the lower levels of metestrous and diestrous uteri could be raised to estrous levels by administration of estrogen. However, the estrous levels were not further increased by estrogen treatment. The antiestrogen, CI628, while a very weak inducer of uterine peroxidase, is an effective antagonist of the estrogen induction of the enzyme. The prolonged duration of this CI628-effected inhibition corresponds to the prolonged depletion of cytoplasmic estrogen receptor seen with CI628 treatment.
Progesterone
, R5020 and norethindrone were also found to be effective antagonists of estrogen-induced uterine peroxidase. Medrogestone and clogestrone, less potent progestins in the rat, were also less effective antagonists of peroxidase induction. Since progesterone was found to inhibit peroxidase induction due to both estrone and diethylstilbestrol, as well as estradiol, it is considered unlikely that this antagonism relates to progestin-induced increases in uterine 17 beta-hydroxysteroid dehydrogenase. Rather, it is proposed that progestins, acting through progestin receptor, may have a more direct role, possibly acting at the level of the genome to repress the expression of estrogen-induced products.
...
PMID:Steroid hormone regulations of uterine peroxidase activity. 57 50
Pituitary retention of [3H] oestradiol in ovariectomized rats was measured following in vivo progesterone pre-treatment and found to be significantly increased after 48, 72, 96 and 120 h of pre-treatment. Increased [3H]-oestradiol retention was also observed for at least up to 72 h after removal of the progesterone pre-treatment source. This retention was measured as DPM per mg dry tissue weight. [3H] Oestradiol retention was also measured in the nuclear fraction of tissues incubated with [3H]-oestradiol in vitro. Following 72 h of in vivo progesterone pre-treatment, the nuclear fraction from the pituitary was found to retain significantly more [3H]oestradiol than corresponding fractions from non-treated animals. In contrast to ovariectomized females, no increase in [3H]oestradiol retention was found in the pituitary of orchidectomized males pre-treated with progesterone for 72 h. [3H]Oestradiol retention by pituitaries of ovariectomized rats injected on the day of birth with 200 mug oestradiol benzoate (OeB) or 500 mug testosterone propionate (TP) was significantly decreased in comparison to control animals. When the rats were pre-treated in vivo with oestradiol for 6 or 72 h and [3H]oestradiol retention was measured 6 or 24 h after this pre-treatment, the OeB and TP treated animals retained significantly less [3H]oestradiol under most treatment conditions.
Progesterone
pre-treatment for 24 or 72 h in vivo followed by measurement of [3H]oestradiol retention immediately or 6 or 24 h later resulted in a significant increase in [3H]oestradiol retention for the control animals. In contrast, the neonatally OeB or TP treated animals differed significantly by not showing increased retention. When [3H]oestradiol retention of the pituitary was measured in vitro following homogenization at 0 degrees C and incubation at 37 degrees C for 1 h, the nuclear fraction from both OeB and TP treated animals was found to retain less hormone per unit
DNA
; however, this decrease was significant only for the TP animals. Thus, males and androgen- or oestrogen-sterilized females have an altered and reduced augmentation of pituitary oestradiol retention in response to both oestrogen and progesterone pre-treatments.
...
PMID:Progesterone treatment increases pituitary oestradiol retention in the ovariectomized normal female rat but not in the male nor in the androgen- or oestrogen-sterilized female rat. 57 43
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