Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We isolated cDNA clones that represent genes whose expression is enhanced when resting Swiss mouse 3T3 cells are stimulated to proliferate with serum. Two clones (designated pME1 and pMR6) were analyzed further. A partial sequence analysis of the pME1 insert DNA indicated that it contained a 104-base-pair stretch with extensive homology to the 3' untranslated region of gamma actin. Similar analysis of the insert DNA from the pMR6 clone indicated that it did not correspond to any previously reported gene sequence. We used the pME1 clone as a probe to determine the level of gamma actin-specific transcript in 3T3 cells under a variety of conditions. The level of gamma actin-specific mRNA began to increase in resting cells upon serum stimulation and reached a peak at 6 h. Thereafter its level declined, and by 24 h it was hardly detectable. In contrast, pMR6-specific transcript was detectable in resting cells but remained elevated even at 24 h poststimulation. The level of gamma-actin mRNA was elevated in resting cells by 12-O-tetradecanoylphorbol-13-acetate, calcium ionophore A23187, and bombesin and to a lesser extent by cholera toxin, fibroblast-derived growth factor, and dibutyryl cyclic AMP. However, insulin, vasopressin, or epidermal growth factor failed to enhance gamma-actin mRNA levels in resting cells. Inhibitors of transcription diminished the induction of gamma-actin mRNA. Gamma-actin gene was superinduced in serum-stimulated cells by cycloheximide, an inhibitor of translation. Analysis of proteins from serum-stimulated cells by two-dimensional gel electrophoresis indicated that enhanced transcription of gamma-actin mRNA resulted in a concomitant increase in the corresponding actin protein. The possible role of gamma actin, a component of the cytoskeleton, in the regulation of cell growth is discussed.
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PMID:Cell-cycle-specific and serum-dependent expression of gamma-actin mRNA in Swiss mouse 3T3 cells. 340 6

The characteristics of intracellular Ca2+ transient induced by vasopressin and bombesin in aortic smooth muscle cells were studied using flow cytometric analysis of indo-1 loaded cells. The two hormones induced a rapid and transient rise in [Ca2+]i. This Ca2+ transient was independent of the presence of extracellular Ca2+. Addition of bombesin to cells that have already been stimulated by vasopressin (or conversely the addition of vasopressin to bombesin-stimulated cells) results in a second Ca2+ transient that has a smaller amplitude. This transient is the same when the external Ca2+ concentration is lowered from 1.8 mM to 50 nM, suggesting that the agonist-sensitive pool reloaded using the Ca2+ that has been previously released into the cytoplasm. Intracellular Ca2+ pools that have been depleted by a prolonged incubation of the cells in a low Ca2+ medium can be refilled by shifting cells to a high Ca2+ medium. The reloading was analyzed in detail and found to be a slow process. It is hardly affected by Ni2+ or by (-)D888, a potent inhibitor of the voltage-dependent Ca2+ channels. It is accelerated when Ca2+ uptake by the Na+/Ca2+ exchange system is stimulated. The results suggest that Ca2+ homeostasis in aortic smooth muscle cells is achieved using mechanisms that are distinct from those operating in various acini and in striated muscles.
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PMID:The regulation of the cytoplasmic free Ca2+ concentration in aortic smooth muscle cells (A7r5 line) after stimulation by vasopressin and bombesin. 341 73

The mitogens phorbol 12,13-dibutyrate, bombesin and vasopressin stimulate the phosphorylation of an acidic Mr 80,000 cellular protein, a specific substrate of protein kinase C, in intact Swiss 3T3 cells. Phosphorylation of this substrate was rapidly reversed upon the removal of each of these agents. Dephosphorylation occurred with a similar half-life in each of the cases studied (2.2, 1.5 and 2 minutes for phorbol 12,13-dibutyrate, bombesin and vasopressin respectively) and agreed closely with the dissociation of the ligands from their specific high-affinity binding sites in Swiss 3T3 cells.
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PMID:Rapid dephosphorylation of a Mr 80,000 protein, a specific substrate of protein kinase C upon removal of phorbol esters, bombesin and vasopressin. 346 23

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

The effects of compounds affecting gastric acid secretion were studied on the formation of inositol phosphates after prelabelling with [3H]-inositol in enriched gastric parietal cells of the rat, prepared by isopycnic centrifugation with Percoll. In cell preparations with 60 to 70% parietal cells, carbachol (10(-6)-10(-2) M) enhanced the accumulation of [3H]-inositol monophosphate ([3H]-IP1), [3H]-inositol bisphosphate ([3H]-IP2) and [3H]-inositol trisphosphate ([3H]-IP3) in a concentration-dependent manner, an effect which was antagonized by 10(-8) M atropine. Li+ (0.5-30 mM) enhanced the basal and carbachol-induced accumulation of all three [3H]-inositol phosphates, the formation of [3H]-IP1 being more sensitive to Li+ than those of [3H]-IP2 and [3H]-IP3. The concentration of Ca2+ in the incubation medium did not affect the relative stimulation of the accumulation of [3H]-inositol phosphates by carbachol, although the basal formation was higher in the presence of Ca2+ in the medium. In the absence of added Ca2+, the incorporation of [3H]-inositol into phospholipids was increased--an effect which was further enhanced by the addition of EGTA to the medium. Gastrin and pentagastrin (10(-8)-10(-5) M) enhanced the formation of [3H]-inositol phosphates, although they were clearly less effective than carbachol. Histamine (10(-6)-10(-3) M) had no effect of its own, but slightly attenuated the effect of carbachol. Cholecystokinin octapeptide (10(-9)-10(-6) M) slightly increased the formation of [3H]-inositol phosphates. Indomethacin (10(-4) M) had no consistent effect on the basal and carbachol-induced accumulation of [3H]-inositol phosphates, nor did prostaglandin E2 (10(-5) M) modify it. Adrenaline (10(-3) M), 5-hydroxytryptamine (10(-3) M), forskolin (10(-5) M), vasopressin (10(-5) M), angiotensin II (10(-5) M) and bombesin (10(-9)-10(-6) M) were all without effect. We suggest that the hydrolysis of inositol phospholipids may be involved in the signal transduction mechanism by which the activation of the muscarinic and gastrin receptors on the parietal cells leads to Ca2+ mobilization and the stimulation of hydrogen ion secretion.
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PMID:Effect of gastric secretagogues on the formation of inositol phosphates in isolated gastric cells of the rat. 356 57

The distribution of vasoactive intestinal polypeptide (VIP), gastrin-releasing peptide (GRP)/bombesin, somatostatin, vasopressin, neuropeptide Y (NPY) and serotonin was examined immunohistochemically in the suprachiasmatic nucleus (SCN) of male rats genetically deficient for vasopressin (Brattleboro strain). VIP-containing neurons and their varicose fibers were preferentially distributed in large numbers in the ventromedial part of the SCN. GRP/bombesin-containing neurons and their fibers were also gathered in the ventral part of the SCN, particularly in the ventromedial region of the nucleus. Somatostatin-containing neurons and their fibers were prominent in the rostral and middle portions of the SCN, where the highest concentration of immunoreactivity was restricted in their ventromedial part. No vasopressin-immunoreactivity was found at all throughout the SCN. Profuse NPY-containing varicose fibers were observed in the ventrolateral part of the SCN, but no immunoreactive neurons were distributed in this nuclear region. Serotonergic fibers showed a topographic arrangement in the SCN: a serotonin-immunoreactive nerve plexus was predominantly distributed in the ventrolateral part. These findings indicate that the SCN of Brattleboro rats is composed of distinct subdivisions of immunoreactive cell bodies and fibers. The distribution of the five peptides and indoleamine within the SCN in the Brattleboro strain was compared with that in normal Long-Evans rats. Furthermore, both strains of rats were exogenously administered with arginine-vasopressin, but no conspicuous difference in the regional patterns of immunoreactivity was detected. The possible role of vasopressin in the SCN is discussed.
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PMID:Immunohistochemical studies on the distribution of neuropeptides and serotonin in the suprachiasmatic nucleus of the Brattleboro rat. 361 94

Normal cells require growth factors to multiply. One group of growth factors such as platelet-derived growth factor, bombesin and vasopressin in fibroblasts or antigen in lymphocytes uses a specific inositol lipid as part of a transduction mechanism for generating intracellular mitogenic signals. These growth factors stimulate the hydrolysis of phosphatidylinositol 4,5-bisphosphate to give diacylglycerol (DG) and inositol 1,4,5-trisphosphate (Ins1,4,5P3). The DG remains within the plane of the membrane to activate protein kinase C, one function of which is to increase intracellular pH by switching on a Na+/H+ exchanger. The other product, Ins1,4,5P3, functions as a second messenger to mobilize calcium from intracellular stores. These two ionic events, the increase in pH and calcium, contribute to the onset of DNA synthesis. The hydrolysis of an inositol lipid is a key event in this signal pathway which mediates the action of competence factors. A separate signal pathway, perhaps based on tyrosine phosphorylation, carries out the effects of progression growth factors such as epidermal growth factor (EGF) and insulin. It is argued that oncogenes may be arranged into groups associated with specific signal pathways. For example, the sis oncogene encodes platelet-derived growth factor which might use the src gene product as part of its transduction mechanism to generate the second messengers DG, Ins1,4,5P3 and calcium. These last then act to stimulate the transcription of myc and fos. On the other hand, the erbB gene encodes a protein which resembles the receptor for EGF. The function of the ras protein remains a major unsolved problem but there is indirect evidence for proposing that it may mediate the action of progression factors such as EGF or insulin.
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PMID:Growth factors, oncogenes and inositol lipids. 377 62

The effects of intracerebroventricular administration of bombesin on mean arterial pressure and heart rate were studied in conscious, freely moving rats. Injection of bombesin produced dose-dependent elevations of mean arterial pressure and reductions of heart rate. These effects were not caused by leakage of bombesin into the peripheral circulation. Adrenalectomy abolished the pressor action of bombesin but did not alter bombesin-induced bradycardia. Systemic phentolamine pretreatment prevented bombesin-induced changes of mean arterial pressure, whereas rats treated intravenously with captopril or a vasopressin antagonist still exhibited pressor responses to bombesin administration. Bombesin-induced bradycardia was partially antagonized by intravenous atropine methyl nitrate administration, whereas systemic injections of propranolol did not modify this response. It is concluded that bombesin acts within the central nervous system to elevate mean arterial pressure through an adrenal-dependent mechanism involving alpha-adrenergic receptors and to reduce heart rate through an adrenal-independent mechanism involving, at least in part, cardiac parasympathetic nervous activation.
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PMID:Central nervous system cardiovascular effects of bombesin in conscious rats. 388 56

Peptides and non-peptides acting as vasoconstrictors or vasodilators have been tested in dog isolated carotid arteries with and without endothelium and in the presence and absence of a variety of antagonists and inhibitors of endogenous substances. It has been found that substance P and several other tachykinins, bradykinin, neurotensin, bombesin and acetylcholine relax the isolated artery only when the endothelium is present, while VIP, isopropylnoradrenaline, adenosine, histamine, prostaglandins E1 and E2, glucagon and insulin relax and angiotensin, vasopressin, oxytocin, 5-HT and noradrenaline contract the isolated vessel, no matter whether the endothelium is present or not. Peptide and non-peptide antagonists have been used with success to show that vasoconstrictors and vasodilators act on specific receptors, since their effects are reduced in the presence of antagonists, specific for one or another of the various agents. Inhibitors of the arachidonic acid cascade only reduce the effect of acetylcholine, suggesting that at least two different mechanisms are involved in the endothelium-mediated relaxation of arterial smooth muscles to peptide and non-peptide agents. The results summarised in this paper suggest that the site of action of several vasodilators is the endothelium, while other vasodilators and all the vasoconstrictors influence the arterial vessels tone presumably by acting on the smooth muscle cells.
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PMID:Effects of peptides and non-peptides on isolated arterial smooth muscles: role of endothelium. 393 Feb 67

Three different antisera to the molluscan neuropeptide Phe-Met-Arg-Phe-amide (FMRFamide) and two different antisera to the fragment RFamide were used to stain sections or whole mounts of the hydrozoan medusa Polyorchis penicillatus. All antisera stained the same neuronal structures. Strong immunoreactivity was found in neurons of the ectodermal nerve nets of the manubrium and tentacles, in neurons of the sensory epithelium, and in neurons at the periphery of the sphincter muscle. Strong immunoreactivity was also present in processes and perikarya of the whole outer nerve ring, in the ocellar nerves, and in nerve cells lying at the periphery of the ocellus. The inner nerve ring contained a moderate number of immunoreactive processes and perikarya, which were distinct from the swimming motor neurons. In contrast to the situation in the hydrozoan polyp Hydra attenuata, no immunoreactivity was found with several antisera to oxytocin/vasopressin and bombesin/gastrin-releasing peptide. The morphology and location of most FMRFamide-immunoreactive neurons in Polyorchis coincides with two identified neuronal systems, which have been recently discovered from neurophysiological studies.
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PMID:FMRFamide immunoreactivity in the nervous system of the medusa Polyorchis penicillatus. 615 69


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