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)

The nerve growth factor protein (NGF) favors polymerization of brain actin and induces its organization to form paracrystalline structures that activate myosin ATPase (ATP phosphohydrolase, EC 3.6.1.3) to an extent greater than actin alone. Binding studies show that the initial 1:1 stoichiometry of NGF-G-actin complexes decreases to 1:7-10 when polymerization is ended and paracrystalline structures are formed. The ratio becomes even lower when heavy meromyosin is added in the absence of ATP, suggesting that heavy meromyosin displaces NGF bound to actin microfilaments. This conclusion is supported by the finding that when heavy meromyosin is added to NGF-microfilament complexes, under conditions for "decorating" microfilaments, the usual paracrystalline structure of the complexes disappears. The NGF-mediated organization of actin and activation of myosin ATPase is visualized as a self-regulatory and self-propagating mechanism, because progressive displacement of the growth factor induced by heavy meromyosin binding to F actin as ATP consumption proceeds renders an increasingly higher amount of NGF free for new interactions. These findings are discussed in the light of the mechanism of action of NGF in the target cells.
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PMID:Nerve growth factor potentiates actomyosin adenosinetriphosphatase. 14 85

In the preceding paper it was shown that an isoform of serum albumin (ASA; active serum albumin) causes a rapid retraction of neurites and increases intracellular content of Ins1,4,5P3 in PC12 cells. Here we examined whether ASA's effects in nerve growth factor-differentiated PC12 cells were mediated through the Ins1,4,5P3/Ca2+ second messenger pathway by monitoring intracellular Ca2+ (Ca2+i) with Fura2. It was found that ASA caused a dose-dependent increase in Ca2+i. In Ca(2+)-free medium, the increase in Ca2+i elicited by ASA was smaller, but the rise in Ins1,4,5P3 content was not appreciably changed. The small Ca2+i increase seen in Ca(2+)-free medium was probably due to the release of Ca2+ from Ins1,4,5P3-sensitive intracellular stores. In Ca(2+)-containing medium the Ca2+ transient induced by ASA was not affected by organic Ca2+ channel blockers, but decreased when Co2+, Mn2+ or Zn2+ were present in the extracellular medium. The effect of other ligands, such as carbachol and bradykinin, whose receptors are coupled to the phosphoinositide system was also investigated. Carbachol at concentrations from 2 to 200 microM, and bradykinin at a concentration of 2 microM did not cause neurite retraction, whereas 200 microM bradykinin caused an approximately 40% decrease in neurite length. Thapsigargin, a Ca(2+)-ATPase inhibitor, caused a sustained elevation of Ca2+i and retraction of neurites, whereas depolarization of the cells by high K+ gave only a transient elevation of Ca2+i, and no neurite retraction. Therefore, a sustained elevation in Ca2+i might be a sufficient trigger to induce neurite retraction in differentiated PC12 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of active serum albumin on PC12 cells: II. Intracellular Ca2+ transients and their role in neurite retraction. 132 93

The biological activity of Ras proteins is thought to be controlled by the guanine nucleotide exchange factor and the guanosine triphosphatase activating protein (GAP). Treatment of rat pheochromocytoma PC-12 cells with nerve growth factor (NGF) increased the amount of active Ras guanosine triphosphate complex and stimulated the activities of both the guanine nucleotide exchange factor and GAP. In PC-12 cells that overexpressed the tyrosine kinase encoded by the trk proto-oncogene (a component of the high-affinity NGF receptor), the NGF-induced activation of the regulatory proteins was potentiated. These results suggest that the NGF receptor system enhances the activities of both the guanine nucleotide exchange factor and GAP and that the activation of Ras might be controlled by the balance in activity between these two regulatory proteins.
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PMID:Nerve growth factor stimulation of the Ras-guanine nucleotide exchange factor and GAP activities. 160 23

Bafilomycin A1, a selective inhibitor of vacuolar H(+)-ATPase, induced neurite outgrowth of PC12 cells dose- and time-dependently: more than 50% of the cells extended neurite-like spikes after 24 h treatment with 100 nM bafilomycin A1. Its dose-response ran roughly parallel to that of a bafilomycin A1-induced lysosomal pH increase. It was inhibited by LiCl, an inhibitor of the phosphorylation of microtubule-associated proteins and, like nerve growth factor (NGF)-induced neurite outgrowth, it was also inhibited by cycloheximide and actinomycin D. But, unlike the NGF-effect, it was not associated with rapid induction of c-fos.
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PMID:Induction of neurite outgrowth of PC12 cells by an inhibitor of vacuolar H(+)-ATPase, bafilomycin A1. 166 Apr 9

A linkage map determined from segregation analysis of 338 meiotic events in an interspecific mouse cross was utilized to help investigate genomic organization of a linkage group conserved between human chromosome 1p and mouse chromosome 3. Using pulsed-field gel electrophoresis, the genes encoding the lymphocyte adhesion molecule human CD2/murine Ly-37, the alpha 1-subunit of Na, K-ATPase, the beta-subunit of thyrotropin, the beta-subunit of nerve growth factor, and muscle adenylate deaminase were similarly positioned on long-range restriction maps in both species. These studies indicate that the development of detailed genetic maps using interspecific Mus crosses facilitates rapid analysis of murine genomic organization and may enable physical mapping of syntenic regions within the human genome. Moreover, the data suggest profound conservation of genomic organization during mammalian evolution.
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PMID:Long-range restriction site mapping of a syntenic segment conserved between human chromosome 1 and mouse chromosome 3. 197 Aug 2

The effects of nerve growth factor (NGF) on induction of Na+,K+-ATPase were examined in a rat pheochromocytoma cell line, PC12h. Na+,K+-ATPase activity in a crude particulate fraction from the cells increased from 0.37 +/- 0.02 (n = 19) to 0.55 +/- 0.02 (n = 20) (means +/- SEM, mumol Pi/min/mg of protein) when cultured with NGF for 5-11 days. The increase caused by NGF was prevented by addition of specific anti-NGF antibodies. Epidermal growth factor and insulin had only a small effect on induction of Na+,K+-ATPase. A concentration of basic fibroblast growth factor three times higher than that of NGF showed a similar potency to NGF. The molecular form of the enzyme was judged as only the alpha form in both the untreated and the NGF-treated cells by a simple pattern of low-affinity interaction with cardiotonic steroids: inhibition of enzyme activity by strophanthidin (Ki approximately 1 mM) and inhibition of Rb+ uptake by ouabain (Ki approximately 100 microM). As a consequence, during differentiation of PC12h cells to neuron-like cells, NGF increases the alpha form of Na+,K+-ATPase, but does not induce the alpha(+) form of the enzyme, which has a high sensitivity for cardiotonic steroid and is a characteristic form in neurons.
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PMID:Nerve growth factor induces Na+,K+-ATPase in a nerve cell line. 244 35

The mechanisms of cell proliferative activity regulation under the effect of growth factors, mitogens, virus transformation, etc. were analyzed. Changes in the location of cAMP-dependent protein kinase caused by these factors, the effect of the nerve growth factor on the activities of protein kinase and high-affinity ATPase, and the mechanism of antiproliferative action of staphylococcal enterotoxin A were specified. Data on receptor-independent intracellular penetration of protein factors hydrophobized by fatty acid residues are overviewed.
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PMID:[The main pathogenetic mechanisms of disorders of the detoxication function of the liver in endogenous toxemia of various etiologies]. 262 79

Effects of nerve growth factor (NGF) on the uptake of non-metabolizable alpha-aminoisobutyric acid (AIB) and on Na,K-ATPase activity in superior cervical sympathetic ganglia (SCG) excised from adult rats were examined during aerobic incubation in vitro. Active uptake of labelled AIB into isolated SCG during 1 to 5 hours incubation at 37 degrees C was significantly accelerated by the addition of NGF to the incubation medium in a dose-dependent manner. Although the Km value of the AIB uptake by the SCG did not change with the addition of NGF, Vmax was nearly doubled. The NGF-evoked increase in AIB uptake was antagonized by the further addition of its specific antiserum in a dose-dependent fashion, and was largely suppressed in a medium containing ouabain. In SCG, axotomized one week prior to the examination, from which most of the neurons had disappeared and reactive proliferation of satellite glial components was in progress, the NGF-induced acceleration of AIB uptake was completely absent. The ganglionic Na,K-ATPase activity was greatly stimulated in the presence of NGF, and the effect was completely eliminated in the axotomized SCG. These results strongly suggest that the NGF-induced acceleration of active AIB uptake by the isolated SCG occurs not in glial cells but exclusively in the neuronal components with the apparent coupling of an Na ion extrusion process.
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PMID:Stimulative effect of nerve growth factor on alpha-aminoisobutyric acid uptake and Na,K-ATPase activity in superior cervical sympathetic ganglia excised from adult rats. 299 47

Gangliosides are carbohydrate-rich complex lipids of large size and great complexity which are found in cell membranes, especially neuronal cell membranes. They are present in the external leaflet of the membrane. The hydrophobic moiety, consisting of sphingosine and fatty acid (stearic acid, 95%), is inserted into the membrane, while the hydrophilic moiety, consisting of sialic acid (NANA) and other carbohydrates, protrudes towards the extracellular fluid. Although gangliosides were discovered some 50 years ago, their potential role in neuronal functions has been appreciated only recently. During development, their composition and concentration change in a variety of animal species. Their role is indicated from studies which have shown that abnormalities in ganglioside metabolism can have a severe impairing effect on normal development. The mouse mutant weaver is characterized by cerebellar granule cell death, which is correlated by the lack of GM1 expression on the neuronal surface. On the other hand, inborn metabolic errors causing ganglioside accumulation in neurons (GM1 gangliosides) are correlated to an aberrant neurite outgrowth. A further appreciation of ganglioside action has been obtained either by adding gangliosides to neurons in culture or by treating animals during neuronal regeneration. It was found that these agents increased the rate and extent of sprouting of regenerating axons and enhanced neuronal differentiation and sprouting in vitro. Such effects were dependent upon the presence of the growth factor in the bathing medium; ganglioside incorporation, however, did not alter nerve growth factor (NGF) binding and internalization, indicating that some membrane events triggered by ganglioside incorporation may be relevant in neuronal differentiation and sprouting. More recently, we have obtained evidence showing that neurons from animals treated with gangliosides are more resistant to anoxia and ionic unbalances. It seems that ganglioside treatment prevents the decay of some key enzyme activity, such as Na+-K+-ATPase occurring after trauma. Indeed, the recent literature suggests that gangliosides may play an important role during development and, when injected into animals, enhance reparatory events in the central and peripheral nervous system.
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PMID:Ganglioside enhancement of neuronal differentiation, plasticity, and repair. 353 11

Thyroid hormones modulate energy metabolism and importantly influence growth and development. These effects are independently mediated. Thyroid calorigenesis is influenced predominantly via nuclear receptor mediated synthesis of mitochondrial respiratory assemblies and cell membrane sodium potassium ATPase. Accumulating evidence suggests that many of the thyroid hormone effects on development are mediated via growth factors, including somatomedins (SM), erythropoietin (EP), nerve growth factor (NGF) and epidermal growth factor (EGF). Thyroid hormone binding to nuclear receptors is known to stimulate growth hormone (GH) synthesis, and thyroid hormones probably potentiate GH stimulation of SM production as well as the anabolic effects of SM. The production of EP, NGF and EGF also are thyroid hormone responsive, and it seems likely that these growth factors mediate the thyroid hormone effects on erythrocyte production, autonomic and perhaps central nervous system maturation, and epidermal development, respectively.
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PMID:The thyroid hormone effects on growth and development may be mediated by growth factors. 621 63


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