Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measurement of the effect of drugs on the in vivo rates of synthesis of rabbit liver organelle bound proteins were measured following individual treatments with the inducers phenobarbital, 3-methylcholanthrene and PCB (a mixture of polychlorinated biphenyls) and the inhibitors, cycloheximide, aflatoxin B1, chloramphenicol and actinomycin D. Following their isolation from a homogenate containing the combined livers of 14C-leucine injected experimental animals and 3H-leucine injected control animals, purified fractions of the following proteins were prepared: microsomal cytochrome b5, cytochrome P-450, NADH-cytochrome b5 reductase, NADPH-cytochrome P-450 reductase and proteolipids, outer mitochondrial membrane cytochrome b5, NADH-cytochrome b5 reductase and proteolipids, inner mitochondrial membrane cytochrome c, NADH dehydrogenase and proteolipids, intermitochondrial membrane cytochrome b5 and circulating serum albumin. The effect of a drug was examined by measuring the 14C/3H ratio of leucine incorporation of each fraction; ratios which differed markedly from a control value of 1 represented actual changes in the relative rates of protein synthesis. Increased rates of synthesis of cytochrome P-450 and its reductase, intermitochondrial membrane cytochrome b5 and all three proteolipid fractions resulted from each inducer treatment. Treatments with 3-methylcholanthrene and PCB also increased the rate of synthesis of cytochrome b5 and its reductase in both the microsome and outer mitochondrial membrane. In addition, the PCB treatment increased the rates of synthesis of cytochrome c and NADH-dehydrogenase. The rates of synthesis of cytochromes, reductases and of circulating serum albumin were inhibited following treatments with cycloheximide, aflatoxin B1 and actinomycin D. Actinomycin D appeared to inhibit the release of newly synthesized albumin into the bloodstream while chloramphenicol treatment appeared to inhibit the incorporation of cytochrome c into the mitochondria. After 20 hours of treatment with inhibitors, the inhibitory effect of actinomycin D and cycloheximide were still apparent while the rates of protein synt;esis in chloramphenicol and aflatoxin B1 treated animals increased to levels above the controls. The incorporation of radioactively labeled leucine into the proteolipids of the microsomal, and the outer and inner mitochondrial membranes were inhibited following the treatment with actinomycin D and stimulated following the treatment with cycloheximide.
Mol Cell Biochem 1979 Dec 14
PMID:Effect of a single dose of inducers and inhibitors on the rate of synthesis of cytochromes and reductases in liver organelles. 11 59

Recent work from our laboratory suggests that a complex interaction exists between ovarian and adrenal steroids in the regulation of preovulatory gonadotropin secretion. Ovarian estradiol serves to set the neutral trigger for the preovulatory gonadotropin surge, while progesterone from both the adrenal and the ovary serves to (1) initiate, (2) synchronize, (3) potentiate and (4) limit the preovulatory LH surge to a single day. Administration of RU486 or the progesterone synthesis inhibitor, trilostane, on proestrous morning attenuated the preovulatory LH surge. Adrenal progesterone appears to play a role in potentiating the LH surge since RU486 still effectively decreased the LH surge even in animals ovariectomized at 0800 h on proestrus. The administration of ACTH to estrogen-primed ovariectomized (ovx) immature rats caused a LH and FSH surge 6 h later, demonstrating that upon proper stimulation, the adrenal can induce gonadotropin surges. The effect was specific for ACTH, required estrogen priming, and was blocked by adrenalectomy or RU486, but not by ovariectomy. Certain corticosteroids, most notably deoxycorticosterone and triamcinolone acetonide, were found to possess "progestin-like" activity in the induction of LH and FSH surges in estrogen-primed ovx rats. In contrast, corticosterone and dexamethasone caused a preferential release of FSH, but not LH. Progesterone-induced surges of LH and FSH appear to require an intact N-methyl-D-aspartate (NMDA) neurotransmission line, since administration of the NMDA receptor antagonist, MK801, blocked the ability of progesterone to induce LH and FSH surges. Similarly, NMDA neurotransmission appears to be a critical component in the expression of the preovulatory gonadotropin surge since administration of MK801 during the critical period significantly diminished the LH and PRL surge in the cycling adult rat. FSH levels were lowered by MK801 treatment, but the effect was not statistically significant. The progesterone-induced gonadotropin surge appears to also involve mediation through NPY and catecholamine systems. Immediately preceding the onset of the LH and FSH surge in progesterone-treated estrogen-primed ovx. rats, there was a significant elevation of MBH and POA GnRH and NPY levels, which was followed by a significant fall at the onset of the LH surge. The effect of progesterone on inducing LH and FSH surges also appears to involve alpha 1 and alpha 2 adrenergic neuron activation since prazosin and yohimbine (alpha 1 and 2 blockers, respectively) but not propranolol (a beta-blocker) abolished the ability of progesterone to induce LH and FSH surges. Progesterone also caused a dose-dependent decrease in occupied nuclear estradiol receptors in the pituitary.(ABSTRACT TRUNCATED AT 400 WORDS)
J Steroid Biochem Mol Biol 1992 Mar
PMID:Interaction between ovarian and adrenal steroids in the regulation of gonadotropin secretion. 156 21

Metaplastic pancreatic cells have been infrequently observed in fish liver tumors induced by chemical carcinogens. An investigation with nitrosamine-exposed trout was undertaken to characterize the relationships of metaplastic pancreatic cells with other cell types. Eight-week-old rainbow trout (Salmo gairdneri) were fed a control diet or diets containing 500 ppm beta-naphthoflavone (BNF), 2000 ppm indole-3-carbinol (13C), or 100 ppm Aroclor 1254 (PCB) for 6 weeks. The fish were then exposed to 250 ppm diethylnitrosamine for 24 hr in an aqueous aquarium bath and reared on control diet for 39 weeks postexposure. Livers were excised, processed to paraffin sections, and stained with hematoxylin and eosin for histological evaluation. Metaplastic pancreatic cells were found only in tumors. Of the tumors with metaplastic pancreatic cells, 100/105 (95.2%) contained neoplastic cholangiolar components. Only 5/105 (4.76%) were hepatocellular carcinomas. 13C pretreatment inhibited the incidence of cholangiolar tumors (cholangioma 3.6% vs 31.3%, cholangiocarcinoma 3.6% vs 13.0%) and metaplastic pancreatic cells (5.1% vs 19.1%), whereas BNF and PCB had no effect. A hepatocellular origin for metaplastic pancreatic cells is supported. Cholangiolar neoplasia is associated with the expression, growth, or survival of metaplastic pancreatic cells in liver tumors. Hepatocarcinogenicity should not be described entirely by hepatocellular events since cholangiolar and metaplastic pancreatic cells can respond associatively to carcinogens and dietary modulators.
Exp Mol Pathol 1989 Feb
PMID:Metaplastic pancreatic cells in liver tumors induced by diethylnitrosamine. 253 49

The present results indicate that during sexual maturation the APOA-MBH from rats of 30 days of age released significantly higher quantities of GnRH than the tissue from 16-day-old rats (P < 0.01). The addition of NMDA, an agonist of the excitatory amino acids system (EAAs), to the medium after 30 min of incubation significantly increased (P < 0.01) the GnRH release in normal rats of both ages and this increase was significantly (P < 0.01) higher in 30-day-old rats (to 661%) than in rats of 16 days of age (to 273%). The administration of estrogen-progesterone (EP) to rats of 16 days of age did not modify the GnRH release response to NMDA. On the contrary, at 30 days of age EP administration significantly potentiated the GnRH release response to NMDA since while in the control group NMDA increased the GnRH release to 630%, in the EP-pretreated group this was to around 4700% (P < 0.01). EP pretreatment of prepubertal rats decreases the hypothalamic release of aspartate and glutamate, the excitatory amino acids involved in NMDA neurotransmission and glycine but increases EAAs release in peripubertal rats. On the basis of these results it is proposed that the increase in EAAs release by the hypothalamus is directly connected with the onset of puberty and that the maturation of the positive feedback effect of ovarian hormones on gonadotropin secretion is related to the maturation of the capacity of EP to increase hypothalamic EAAs. Before this maturational event EP inhibits EAAs release as well as gonadotropin release (prepubertal rats). NMDA receptor stimulation leads to a positive mechanism which increases the release of Asp and Glu from APOA-MBH both in prepubertal and peripubertal rats, but EP potentiates this mechanism only in peripubertal rats. This could be an additional neuroendocrine mechanism involved in the increase of gonadotropin during sexual maturation which induces the onset of puberty and the preovulatory discharge of these pituitary hormones.
J Steroid Biochem Mol Biol 1995 Jun
PMID:Hypothalamic excitatory amino acid system during sexual maturation in female rats. 762 77

Neuropeptides from the X-organ-sinus gland complex in the eyestalk have important roles in the regulation of growth and maturation in crustaceans. A complementary DNA encoding a molt-inhibiting hormone-like (MIH-like) neuropeptide from the eyestalk of Penaeus vannamei has been isolated and cloned in this laboratory. Using the reverse transcription-polymerase chain reaction (RT-PCR) method, the gene encoding the MIH-like neuropeptide was shown to be expressed in the brain as well as in the eyestalk. Subsequent cloning and sequencing of the PCR products showed that the MIH-like gene transcript of the brain shares 98% sequence identity with that of the eyestalk. In situ hybridization experiments showed that the MIH-like messenger RNA is exclusively localized in the X-organ complex in the medulla terminalis of the eyestalk, whereas in the brain the MIH-like gene transcript was detected in three regions including the neurosecretory cells, giant cells, and lateral cell bodies. These data suggest that the MIH-like peptide could have a specific function in nervous system activity other than its classic molt-inhibiting function.
Mol Mar Biol Biotechnol 1995 Sep
PMID:Expression of the molt-inhibiting hormone-like gene in the eyestalk and brain of the white shrimp Penaeus vannamei. 767 Jun 2

The effects of PCBs (mixture of 2, 3, 4, 5-tetra; 2, 2', 4, 5, 5'-penta; 2, 2', 3, 3', 6, 6'-hexa and 2, 2', 3, 3', 4, 4', 5, 5'-octa congeners) on androgen production were investigated by suspension of Leydig cells from adult rat testis. hCG-stimulated androgen production was significantly inhibited by PCBs while progesterone level was not affected. Progesterone supported testosterone production was also decreased by PCBs, while conversion of androstenedione to testosterone was unchanged. These results suggest that the activity of microsomal enzyme C21 side-chain cleavage P450 was decreased by PCB treatment of Leydig cells in vitro.
J Steroid Biochem Mol Biol 1995 Jun
PMID:Effect of PCBs on androgen production by suspension of adult rat Leydig cells in vitro. 777 64

The X-organ of the eyestalk in crustaceans is a source of neurosecretory peptides. Total RNA was isolated from X-organs of the white shrimp Penaeus vannamei and used to clone a cDNA encoding a molt-inhibiting hormone-like (MIH-like) neuropeptide by the 3' and 5' rapid amplification of cDNA ends (RACE) method. Sequence analysis of the 470-bp cDNA reveals a 306-bp open reading frame and a 164-bp 3' untranslated region. The deduced polypeptide consists of a 72-amino acid mature peptide and a 30-amino acid region of propeptide. The mature peptide shares 49 and 29% amino acid identity to the MIH from the lobster Homarus americanus and the crab Carcinus maenas, respectively. Northern hybridization shows that the MIH-like mRNA has a molecular size of 2.0 kb and is present in the eyestalk.
Mol Mar Biol Biotechnol 1994 Feb
PMID:Molecular cloning and sequence analysis of a cDNA encoding a molt-inhibiting hormone-like neuropeptide from the white shrimp Penaeus vannamei. 805 60

Adult male Sprague-Dawley rats were treated with para-chlorophenylalanine (pCPA) or alpha-methyl tyrosine (alpha-MT) to study the effect of serotonin or catecholamine depletion on the expression of vasoactive intestinal peptide (VIP) messenger RNA in the anterior pituitary. Single injections of pCPA (300 mg/kg) for two consecutive days resulted on the third day in a dramatic depletion of serotonin in the medial basal hypothalamus, and a significant reduction in the pituitary content of VIP mRNA (1.0 and 1.7 kb). The effect of pCPA on VIP mRNA appeared to be relatively specific for the anterior pituitary since VIP message levels in the cerebral cortex did not decrease. alpha-MT treatment, (150 mg/kg) for 2 consecutive days, reduced dopamine concentrations in the MBH but had no significant effect on pituitary VIP levels. In a time-course study, hypothalamic serotonin and pituitary VIP mRNA levels were significantly depressed 1-3 days after initiation of pCPA treatment; however, 12 days after pCPA treatment, serotonin concentrations in the hypothalamus approached control values and pituitary VIP mRNA content increased an average of 2-fold over control levels in an apparent rebound effect. pCPA-treated rats injected i.p. twice a day with 5-hydroxytryptophan (5-HTP; 50 mg/kg) experienced a partial reversal in the decline in the 1.7 kb VIP mRNA seen 24 h after the first pCPA injection. However, at 72 h, supplementation with 5-HTP did not prevent the pCPA-induced decrease of pituitary VIP mRNA. These data indicate that serotonergic pathways have a major role in the control of VIP mRNA expression in the rat anterior pituitary.
Brain Res Mol Brain Res 1993 Jan
PMID:Para-chlorophenylalanine treatment inhibits the expression of vasoactive intestinal peptide messenger RNA in rat anterior pituitary. 838 7

Our knowledge concerning the primary structures of crustacean neuropeptides has been broadened considerably during the last few years and has greatly contributed to the successful application of molecular biological techniques to crustacean neuroendocrine research. In this review, we compare and discuss the preprohormones of the Red Pigment Concentrating Hormone (RPCH), the Pigment-Dispersing Hormone (PDH) and the different members of the Crustacean Hyperglycemic Hormone, Molt-Inhibiting and Gonad-Inhibiting Hormone family (CHH/MIH/GIH peptide family), recently elucidated by cloning and sequencing of the respective cDNAs. Expression studies, using in situ hybridization, Northern blots and RNase protection assays, have demonstrated that the mRNAs encoding some of the aforementioned preprohormones (for example, preproPDH and preproCHH) are not only expressed in the eyestalk but also in other parts of the central nervous system. The combination of molecular biological techniques with (bio)chemical and immunochemical methods provides elegant tools to study neuropeptides at the level of mRNA and peptide in individual animals during different physiological conditions. The fundamental knowledge obtained by such a combined approach will give detailed insight into how neuropeptides are involved in the adaptation of Crustacea to a broad spectrum of natural and aquacultural conditions.
Comp Biochem Physiol B Biochem Mol Biol 1995 Dec
PMID:Molecular biology of neurohormone precursors in the eyestalk of Crustacea. 859 Mar 72

Monkey Clara cell 10 kDa protein (CC10) was purified from monkey lung lavage. This protein showed an apparent molecular weight of about 10 kDa and 5 kDa under non-reducing and reducing conditions, respectively, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. From the amino acid sequence data, monkey CC10 protein consisted of two identical 70-amino-acid polypeptide chains joined by two cystine residues, and possessed sequence identities of 78.6%, 52.9%, 52.9%, and 44.3% with human CC10, rat CC10 (PCB binding protein), rabbit uteroglobin, and mouse CC10, respectively. When monkey CC10 was compared with rabbit uteroglobin (progesterone binding protein), two polar residues of Tyr-21 and Thr-60, important for progesterone binding specificity, were substituted for Phe-21 and Met-60, and thus monkey CC10 may not have a binding capacity with progesterone. Monkey CC10 also possessed a surface homology with lipocortin I (anti-inflammatory peptide), thus suggesting that monkey CC10 plays a role in the anti-inflammatory process at the air-liquid interface over the bronchio-bronchiolar epithelium.
Am J Respir Cell Mol Biol 1996 Sep
PMID:Monkey Clara cell 10 kDa protein (CC10): a characterization of the amino acid sequence with an evolutional comparison with humans, rabbits, rats, and mice. 881 Jun 40


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