Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have isolated a cDNA clone from mouse, m56, that encodes a member of the Conserved ATPase-containing Domain (CAD) protein family. Sequence analysis revealed that m56 is identical to mouse mSug1/FZA-B and shares high homology with human Trip1, moth 18-56, and yeast Sug1. When examined, Sug1-like CAD proteins appear to function in the regulation of the 26S proteasome, as well as associate with members of the steroid/thyroid receptor superfamily and other transcriptional activators. m56 can complement the lethal phenotype of loss of SUG1 in yeast. We have examined the tissue distribution of m56 using Northern and Western blots, in addition to immunocytochemistry and in situ hybridization. While m56 was expressed in all tissues and cells examined, several classes of neurons, most notably in the hippocampus, olfactory bulb, and cerebellum, displayed elevated levels of m56 mRNA and protein. We also examined distribution of RNA polymerase II and 26S proteasome subunit 4 (S4) within the mouse brain by in situ hybridization. While all three genes had similar patterns of expression, there were significant differences among them. In moths, the expression of the Sug1 homolog 18-56 is dramatically up-regulated during programmed cell death. In addition, it has been previously demonstrated that the proteasome plays an essential role in the regulation of apoptosis in mammals. We examined the expression of m56 in mouse during natural and induced cell death in a variety of tissues and found no significant changes in expression. Taken together, the data presented here suggest that while m56 is a highly conserved gene that presumably plays essential but complex roles in basal and developmental processes, it may not represent a rate-limiting step in these processes.
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PMID:Identification of a phylogenetically conserved Sug1 CAD family member that is differentially expressed in the mouse nervous system. 940 11

Several studies have indicated that olfactory responses are impeded by amiloride. Therefore, it was of interest to see whether, and if so which, olfactory epithelial cellular compartments have amiloride-sensitive structures. Using ultrastructural methods that involved rapid freezing, freeze-substitution and low temperature embedding of olfactory epithelia, this study shows that, in the rat, this tissue is immunoreactive to antibodies against amiloride sensitive Na(+)-channels. However, microvilli of olfactory supporting cells, as opposed to receptor cilia, contained most of the immunoreactive sites. Apices from which the microvilli sprout and receptor cell dendritic knobs had much less if any of the amiloride-antibody binding sites. Using a direct ligand-binding cytochemical method, this study also confirms earlier ones that showed that olfactory receptor cell cilia have Na+, K(+)-ATPase. It is proposed that supporting cell microvilli and the receptor cilia themselves have mechanisms, different but likely complementary, that participate in regulating the salt concentration around the receptor cell cilia. In this way, both structures help to provide the ambient mucous environment for receptor cells to function properly. This regulation of the salt concentration of an ambient fluid environment is a function that the olfactory epithelium shares with cells of transporting epithelia, such as those of kidney.
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PMID:Ultrastructural localization of amiloride-sensitive sodium channels and Na+,K(+)-ATPase in the rat's olfactory epithelial surface. 958 62

Previous work on classical olfactory learning and memory in flies has suggested at least four distinct phases of memory consolidation. Similarly, our behavioral and pharmacological analyses also provided clear evidence for at least four pharmacologically distinct memory phases in flies after operant conditioning. Anesthesia-resistant memory (ARM) is present between about 20 and 120 min after training, and susceptible to disruption by the ATPase deactivating chemicals such as ouabain and ethacrynic acid (EA). Long-term memory (LTM) is activated at least 150 min after training, and can be disrupted by protein synthesis inhibitors such as cycloheximide (CXM). In addition, a very short-term memory (pre-STM) is demonstrated by feeding flies with potassium chloride (KCl), which has been shown to disrupt the short-term memory. These observations confirm our previous argument that memory formation in flies involves an intricate, multiple-phase pathway of consolidation.
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PMID:Multiple-phase model of memory consolidation confirmed by behavioral and pharmacological analyses of operant conditioning in Drosophila. 970 Sep 62

The temperature dependence of transmitter release associated with axonal conduction, evoked by ligand-gated mechanism and by reversed operation of plasma membrane transporter was studied in superfused slice preparation. When the temperature was reduced from 37-17 degrees C the release of [3H]noradrenaline ([3H]NA) and [3H]dopamine ([3H]DA) in response to field stimulation was significantly enhanced in slice preparations of the hippocampus and main olfactory bulbs. The release of [3H]dopamine evoked by a ligand-gated mechanism (nicotine receptor stimulation) was potentiated at low temperature (12 degrees C). In contrast, when transmitter release was evoked by ouabain, a drug inhibiting Na+/K+-activated ATPase and thereby increasing [Na+]i the release of [3H]GABA was enhanced. This release was very sensitive to cooling (Q10=3.5 between 37 degrees C and 27 degrees C), indicating that the release was induced by a reversed operation of the transporter. The excessive release of [3H]NA from the hippocampal slice in response to oxygen and glucose deprivation (simulation of ischemia) was also inhibited in a temperature-dependent manner. Because at low temperatures (17-12 degrees C) only one type of release mechanism (exocytosis) is operational and carrier-mediated uptake and release is inhibited, this temperature condition provides a method to study the mode of action of different drugs (e.g. amphetamine) and the effect(s) of certain conditions (e.g. ischemia) on the mechanisms of transmitter release, specifically whether they exert their transmitter releasing effect through an exocytotic process or through the reversed operation of plasma membrane transporter. This finding also suggests that it would be important to re-examine mechanistic conclusions based on results from electrophysiological, neurochemical and pharmacological studies that have been carried out at room temperature (approximately 20 degrees C). In particular because transmitter release associated with the action potential, diffusion, receptor kinetics, active transport in both directions (uptake and release) and the probability of transmitter release are all temperature dependent, it would seem important to carry out experiments involving these processes at physiological temperature (37 degrees C).
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PMID:Different temperature dependence of carrier-mediated (cytoplasmic) and stimulus-evoked (exocytotic) release of transmitter: a simple method to separate the two types of release. 984 Feb 27

To study the mechanism of LH-releasing hormone (LHRH) pulse generation, the olfactory pit/placode and the migratory pathway of LHRH neurons from monkey embryos at embryonic age 35-37 were dissected out, under the microscope, and cultured on plastic coverslips coated with collagen in a defined medium for 2-5 weeks. First, we examined whether cultured neurons release the decapeptide into media. It was found that LHRH cells release LHRH in a pulsatile manner at approximately 50-min intervals. Further, LHRH release was stimulated by depolarization with high K+ and the Na+ channel opener, veratridine. However, whereas the Na+ channel blocker, tetrodotoxin suppressed the effects of veratridine, tetrodotoxin did not alter the effects of high K+. Subsequently, the role of extracellular and intracellular Ca2+ in LHRH release was examined. The results are summarized as follows: 1) exposing the cells to a low Ca2+ (20 nM) buffer solution suppressed LHRH release, whereas exposure to a normal Ca2+ solution (1.25 mM) maintained pulsatile LHRH release; 2) LHRH release from cultured LHRH cells was stimulated by the voltage-sensitive L-type Ca2+ channel agonist, Bay K 8644 (10 microM), whereas it was suppressed by the L-type Ca2+ channel blocker, nifedipine (1 microM), but not by the N-type channel blocker, omega-conotoxin GVIA (1 microM); 3) the intracellular Ca2+ stimulant, ryanodine (1 microM), stimulated LHRH release, whereas the intracellular Ca2+ transporting adenosine triphosphatase antagonist, thapsigargin (1 and 10 microM), did not yield consistent results; and 4) carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (1 microM), a mitochondrial Ca2+ mobilizer, stimulated LHRH release, whereas ruthenium red, a mitochondrial Ca2+ uptake inhibitor, did not induce consistent results. These results indicate that: 1) the presence of extracellular Ca2+ is essential for LHRH neurosecretion; 2) Ca2+ enters the cell via L-type channels but not N-type channels; and 3) mobilization of intracellular Ca2+ from inositol 1,4,5-triphosphate-sensitive stores, as well as mitochondrial stores, seem to contribute to LHRH release in these cells.
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PMID:Pulsatile release of luteinizing hormone-releasing hormone (LHRH) in cultured LHRH neurons derived from the embryonic olfactory placode of the rhesus monkey. 1006 21

Immunohistochemical localization of Copper-transporting P-type ATPase (ATP7B), a gene product responsible for Wilson disease, was visualized in the brain tissues of the Long-Evans agouti rat in detail using tissue-blotting technique and confocal laser microscopy. The ATP7B was intensely detected in neuronal cells of the hippocampal formation, olfactory bulbs, cerebellum, cerebral cortex and nuclei in the brainstem in which high amounts of copper and cuproenzymes, dopamine beta hydroxylase and Cu,Zn-superoxide dismutase (Cu,Zn-SOD) were detected. The present results suggest that ATP7B plays key roles in neurotransmissions of catecholamine pathway and preventing brain tissues from injury by superoxide radicals to regulate the cellular Cu concentration and/or activities of cuproenzymes related to neurotransmissions and a free radical metabolism. Furthermore, it is reasonable to assume that neurotoxicity due to abnormal copper accumulation or irregular regulation of cuproenzymes in the critical brain regions by mutation of the ATP7B gene leads to neurological failures of Wilson disease.
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PMID:Immunohistochemical determination of the Wilson Copper-transporting P-type ATPase in the brain tissues of the rat. 1033 72

The aim of this short review was to collate the data involving the effects of lithium alone, or in combination, with antidepressant drugs in several animal models of depression. It has been shown that lithium administration reduced immobility in the mouse forced swimming test when given 30 min, but not 45 min, before testing. Further studies indicated that this activity was probably a result of an activity on serotonin (5-HT) 1A and 1B receptor subtypes. Lithium treatment has been shown to reverse helpless behaviour in the learned helplessness model of depression after chronic treatment (30 days), where lithium was administered in the drinking water. Further studies showed that acute (5 days) administration of lithium failed to reverse behavioural deficits. In the olfactory bulbectomised rat model of depression, several immunological and enzymatic functions have been shown to be altered and these changes are regularised by antidepressant treatment as well as lithium administration for 15 days. Hypokinesia (reduced locomotor activity) is a phenomenon observed following immobilisation stress in rats. This behavioural deficit was attenuated by lithium together with a wide range of antidepressant drugs used in the treatment of unipolar depression at non-stimulant doses. In addition, a single administration of lithium slightly inhibited midbrain raphe lesion-induced muricidal behaviour (25%); however, repeated treatment (5 days) significantly attenuated this behavioural deficit. Lithium treatment has also been shown to reverse behavioural and biochemical deficits induced by reserpine together with those induced by acute administration of single intracerebroventricular (i.c.v.) dose of the Na, K-ATPase-inhibiting compound, ouabain. Long-term studies of lithium augmentation have not been performed, so that no clear recommendations for the duration of this therapy can be made. The points raised in this short review endorse the commencement of such studies.
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PMID:The effect of lithium administration in animal models of depression: a short review. 1039 5

We identified two mammalian ULK1 (Unc-51-like kinase involved in neurite extension) binding proteins by yeast two-hybrid screening. Both proteins showed high structural similarity to microtubule-associated protein (MAP) light chain 3 (LC3). One is identical to the Golgi-associated ATPase Enhancer of 16 kDa (GATE-16), an essential factor for intra-Golgi transport [39]. The other is identical to the gamma 2-subunit of GABA-A receptor associated protein (GABARAP) which has a possible role in receptor transport [46]. Using the yeast two-hybrid system and the in vitro GST pull-down assay, we found that the N-terminal proline/serine rich (PS) domain of ULK1 (amino acid 287-416) is required for ULK1-GATE-16 and ULK1-GABARAP protein interactions. However, the kinase activity of ULK1 affected neither ULK1-GATE-16 nor ULK1-GABARAP interaction. Immunohistochemical analysis using ULK1 and GABARAP antibodies showed that the ULK1 and the GABARAP proteins co-localized to many kind of neurons such as pyramidal cells of the hippocampus, mitral cells of the olfactory bulb, and Purkinje cells of the cerebellum. In HeLa cells, endogenous ULK1 and tagged GABARAP showed punctate structures in the cytosol, and were colocalized. These results suggest that the interaction of ULK1 and GABARAP is important to vesicle transport and axonal elongation in mammalian neurons.
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PMID:Interaction of the Unc-51-like kinase and microtubule-associated protein light chain 3 related proteins in the brain: possible role of vesicular transport in axonal elongation. 1114 1

The mushroom bodies of the Drosophila brain are important for olfactory learning and memory. To investigate the requirement for mushroom body signaling during the different phases of memory processing, we transiently inactivated neurotransmission through this region of the brain by expressing a temperature-sensitive allele of the shibire dynamin guanosine triphosphatase, which is required for synaptic transmission. Inactivation of mushroom body signaling through alpha/beta neurons during different phases of memory processing revealed a requirement for mushroom body signaling during memory retrieval, but not during acquisition or consolidation.
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PMID:The role of Drosophila mushroom body signaling in olfactory memory. 1150 18

Systemic or topical application of glucocorticoid is the treatment of choice for olfactory disturbance. Recently, Na(+)/K(+) ATPase and glucocorticoid receptor immunoreactivity in the olfactory mucosa was reported. To elucidate a glucocorticoid action on Na(+)/K(+) ATPase production, an animal model was produced by an intra-nasal application of 5% ZnSO(4) solution to Wistar rats. Dexamethasone was injected i.p. (0.01 mg/100 g) for 14 days after the insult. Histologically, the regeneration process was completed on day 14 in both dexamethasone- and saline-injected control rats. We used a quantitative polymerase chain reaction (PCR) method to evaluate mRNA production of Na(+)/K(+) ATPase and glucocorticoid receptor. In dexamethasone-injected rats, up-regulation of glucocorticoid receptor mRNA (95% more than control rats, P = 0.00068, unpaired t-test) and of Na(+)/K(+) ATPase mRNA expression (76% more than control rats, P = 0.0042) was observed on day 14. The increased Na(+)/K(+) ATPase expression in the regenerated olfactory mucosa is thought to be beneficial for an active uptake of K(+), which is released during excitation, around olfactory neurons and for the transepithelial absorption of Na(+) from olfactory mucus. Dexamethasone may thus contribute to the recovery of function after the morphological regeneration in part, at least, through its receptor by regulation of the ionic concentration in the olfactory mucosal microenvironment.
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PMID:Glucocorticoid enhances Na(+)/K(+) ATPase mRNA expression in rat olfactory mucosa during regeneration: a possible mechanism for recovery from olfactory disturbance. 1175 63


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