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Artykuły w czasopismach na temat „Nucleotides binding/release”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 9 lutego 2022

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1

MISSIAEN, Ludwig, Jan B. PARYS, Humbert DE SMEDT, Ilse SIENAERT, Henk SIPMA, Sara VANLINGEN, Karlien MAES, and Rik CASTEELS. "Effect of adenine nucleotides on myo-inositol-1,4,5-trisphosphate-induced calcium release." Biochemical Journal 325, no. 3 (August 1, 1997): 661–66. http://dx.doi.org/10.1042/bj3250661.

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The effects of a whole series of adenine nucleotides on Ins(1,4,5)P3-induced Ca2+ release were characterized in permeabilized A7r5 smooth-muscle cells. Several adenine nucleotides activated the Ins(1,4,5)P3 receptor. It was observed that 3′-phosphoadenosine 5′-phosphosulphate, CoA, di(adenosine-5′)tetraphosphate (Ap4A) and di(adenosine-5′)pentaphosphate (Ap5A) were more effective than ATP. Ap4A and Ap5A also interacted with a lower EC50 than ATP. In order to find out how these adenine nucleotides affected Ins(1,4,5)P3-induced Ca2+ release, we have measured their effect on the response of perme

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2

Volkán-Kacsó, Sándor, and Rudolph A. Marcus. "Theory of single-molecule controlled rotation experiments, predictions, tests, and comparison with stalling experiments in F1-ATPase." Proceedings of the National Academy of Sciences 113, no. 43 (October 10, 2016): 12029–34. http://dx.doi.org/10.1073/pnas.1611601113.

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A recently proposed chemomechanical group transfer theory of rotary biomolecular motors is applied to treat single-molecule controlled rotation experiments. In these experiments, single-molecule fluorescence is used to measure the binding and release rate constants of nucleotides by monitoring the occupancy of binding sites. It is shown how missed events of nucleotide binding and release in these experiments can be corrected using theory, with F1-ATP synthase as an example. The missed events are significant when the reverse rate is very fast. Using the theory the actual rate constants in the c

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3

Beslin, A., M. P. Vié, J. P. Blondeau, and J. Francon. "Identification by photoaffinity labelling of a pyridine nucleotide-dependent tri-iodothyronine-binding protein in the cytosol of cultured astroglial cells." Biochemical Journal 305, no. 3 (February 1, 1995): 729–37. http://dx.doi.org/10.1042/bj3050729.

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High-affinity 3,3′,5-tri-iodo-L-thyronine (T3) binding (Kd approximately 0.3 nM) to the cytosol of cultured rat astroglial cells was strongly activated in the presence of pyridine nucleotides. A 35 kDa pyridine nucleotide-dependent T3-binding polypeptide (35K-TBP) was photoaffinity labelled using underivatized [125I]T3 in the presence of pyridine nucleotides and the free-radical scavenger dithiothreitol. Maximum activations of T3 binding and 35K-TBP photolabelling were obtained at approx. 1 x 10(-7) M NADP+ or NADPH, or 1 x 10(-4) M NADH. NAD+ and other nucleotides were without effect. NADPH i

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4

Dawicki, D. D., J. McGowan-Jordan, S. Bullard, S. Pond, and S. Rounds. "Extracellular nucleotides stimulate leukocyte adherence to cultured pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 4 (April 1, 1995): L666—L673. http://dx.doi.org/10.1152/ajplung.1995.268.4.l666.

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Adenosine, ATP, and various nucleotides were examined for their effects on the adherence of leukocytes to bovine pulmonary artery endothelial cells. Extracellular ATP enhanced adherence of HL-60 cells and human neutrophils to endothelial cells in a dose-dependent fashion. Maximal adherence occurred after 15 min coincubation of ATP and HL-60 cells or neutrophils with endothelial cells. ATP stimulation was mediated by direct effects on both HL-60 cells and endothelial cells. The potency profile of various nucleotides was ATP = 2-MeSATP > beta,gamma-CH2ATP, indicative of a P2y receptor. Intere

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5

Jackson, A. P., and C. R. Bagshaw. "Transient-kinetic studies of the adenosine triphosphatase activity of scallop heavy meromyosin." Biochemical Journal 251, no. 2 (April 15, 1988): 515–26. http://dx.doi.org/10.1042/bj2510515.

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Fluorescence stopped-flow experiments were performed to elucidate the elementary steps of the ATPase mechanism of scallop heavy meromyosin in the presence and in the absence of Ca2+. ATP binding and hydrolysis, as monitored by the change in tryptophan fluorescence, appear to be Ca2+-insensitive, whereas both Pi release and ADP release are markedly suppressed in the absence of Ca2+. Rate constants for Pi release are 0.2 s-1 and 0.002 s-1 and for ADP release are 6 s-1 and 0.01 s-1 in the presence and in the absence of Ca2+ respectively. Ca2+ binding to the specific site of the regulatory domain

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6

Batasheva, Svetlana, Marina Kryuchkova, Ramil Fakhrullin, Giuseppe Cavallaro, Giuseppe Lazzara, Farida Akhatova, Läysän Nigamatzyanova, Vladimir Evtugyn, Elvira Rozhina, and Rawil Fakhrullin. "Facile Fabrication of Natural Polyelectrolyte-Nanoclay Composites: Halloysite Nanotubes, Nucleotides and DNA Study." Molecules 25, no. 15 (August 4, 2020): 3557. http://dx.doi.org/10.3390/molecules25153557.

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Complexation of biopolymers with halloysite nanotubes (HNTs) can greatly affect their applicability as materials building blocks. Here we have performed a systematic investigation of fabrication of halloysite nanotubes complexes with nucleotides and genomic DNA. The binding of DNA and various nucleotide species (polyAU, UMP Na2, ADP Na3, dATP Na, AMP, uridine, ATP Mg) by halloysite nanotubes was tested using UV-spectroscopy. The study revealed that binding of different nucleotides to the nanoclay varied but was low both in the presence and absence of MgCl2, while MgCl2 facilitated significantl

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7

MISSIAEN, Ludwig, B. Jan PARYS, Humbert DE SMEDT, Ilse SIENAERT, Henk SIPMA, Sara VANLINGEN, Karlien MAES, Karl KUNZELMANN, and Rik CASTEELS. "Inhibition of inositol trisphosphate-induced calcium release by cyclicADP-ribose in A7r5 smooth-muscle cells and in 16HBE14o- bronchial mucosal cells." Biochemical Journal 329, no. 3 (February 1, 1998): 489–95. http://dx.doi.org/10.1042/bj3290489.

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Ca2+ release from intracellular stores occurs via two families of intracellular channels, each with their own specific agonist: Ins(1,4,5)P3 for the Ins(1,4,5)P3 receptor and cyclic ADP-ribose (cADPR) for the ryanodine receptor. We now report that cADPR inhibited Ins(1,4,5)P3-induced Ca2+ release in permeabilized A7r5 cells with an IC50 of 20 μM, and in permeabilized 16HBE14o- bronchial mucosal cells with an IC50 of 35 μM. This inhibition was accompanied by an increase in specific [3H]Ins(1,4,5)P3 binding. 8-Amino-cADPR, but not 8-bromo-cADPR, antagonized this effect of cADPR. The inhibition w

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8

Bokoch, G. M., and L. A. Quilliam. "Guanine nucleotide binding properties of rap1 purified from human neutrophils." Biochemical Journal 267, no. 2 (April 15, 1990): 407–11. http://dx.doi.org/10.1042/bj2670407.

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The guanine nucleotide binding properties of rap1 protein purified from human neutrophils were examined using both the protein kinase A-phosphorylated and the non-phosphorylated forms of the protein. Binding of GTP[S] (guanosine 5′-[gamma-thio]triphosphate) or GDP was found to be slow in the presence of free Mg2+, but very rapid in the absence of Mg2+. The binding of guanine nucleotides was found to correlate with the loss of endogenous nucleotide from the rap1 protein, which was rapid in the absence of Mg2+. The relative affinities of GTP and GDP for the binding site on rap1 were modulated by

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9

Milligan, G., та C. G. Unson. "Persistent activation of the α subunit of Gs promotes its removal from the plasma membrane". Biochemical Journal 260, № 3 (15 червня 1989): 837–41. http://dx.doi.org/10.1042/bj2600837.

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As assessed both by cholera-toxin-catalysed ADP-ribosylation and by immunoblotting with an anti-peptide antiserum raised against the C-terminal decapeptide of forms of Gs alpha (the alpha subunit of the stimulatory guanine nucleotide-binding protein), rat glioma C6 BU1 cells express two forms of Gs alpha: a major 44 kDa form and a much less prevalent 42 kDa form. We examined the effects of guanine nucleotides on the interaction of the 44 kDa form with the plasma membrane. Incubation of membranes of C6 BU1 cells with poorly hydrolysed analogues of GTP, but not with analogues of either ATP or GD

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10

Yao, Jia, and Sandra M. Bajjalieh. "Synaptic Vesicle Protein 2 (SV2) does not hydrolyze ATP." F1000Research 2 (October 9, 2013): 209. http://dx.doi.org/10.12688/f1000research.2-209.v1.

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Synaptic vesicle protein 2 (SV2) is a transporter-like protein specifically expressed in endocrine cells and neurons, where it is localized to vesicles that undergo regulated secretion and plays an essential role in regulating neurotransmitter release. SV2 binds adenine nucleotides including ATP. Analysis of ATP transport revealed that SV2 is not an ATP transporter, nor does it affect ATP transport. As a further step toward understanding how ATP binding contributes to SV2 function, we investigated whether SV2 is an ATPase using an in vitro measure of ATPase activity. The study reported here in

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11

Sprenger, Hans-Georg, Thomas MacVicar, Amir Bahat, Kai Uwe Fiedler, Steffen Hermans, Denise Ehrentraut, Katharina Ried, et al. "Cellular pyrimidine imbalance triggers mitochondrial DNA–dependent innate immunity." Nature Metabolism 3, no. 5 (April 26, 2021): 636–50. http://dx.doi.org/10.1038/s42255-021-00385-9.

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AbstractCytosolic mitochondrial DNA (mtDNA) elicits a type I interferon response, but signals triggering the release of mtDNA from mitochondria remain enigmatic. Here, we show that mtDNA-dependent immune signalling via the cyclic GMP–AMP synthase‒stimulator of interferon genes‒TANK-binding kinase 1 (cGAS–STING–TBK1) pathway is under metabolic control and is induced by cellular pyrimidine deficiency. The mitochondrial protease YME1L preserves pyrimidine pools by supporting de novo nucleotide synthesis and by proteolysis of the pyrimidine nucleotide carrier SLC25A33. Deficiency of YME1L causes i

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12

Jackson, A. P., and C. R. Bagshaw. "Kinetic trapping of intermediates of the scallop heavy meromyosin adenosine triphosphatase reaction revealed by formycin nucleotides." Biochemical Journal 251, no. 2 (April 15, 1988): 527–40. http://dx.doi.org/10.1042/bj2510527.

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The kinetics of interaction of formycin nucleotides with scallop myosin subfragments were investigated by exploiting the fluorescence signal of the ligand. Formycin triphosphate gives a 5-fold enhancement of the emission intensity on binding to heavy meromyosin, and the profile indicates that the kinetics of binding are Ca2+-insensitive. In contrast, the subsequent product-release steps show a marked degree of regulation by Ca2+. In the absence of Ca2+ formycin triphosphate turnover by the unregulated and the regulated heavy meromyosin fractions are clearly resolved, the latter showing a fluor

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13

Arenz, Stefan, Fabian Nguyen, Roland Beckmann, and Daniel N. Wilson. "Cryo-EM structure of the tetracycline resistance protein TetM in complex with a translating ribosome at 3.9-Å resolution." Proceedings of the National Academy of Sciences 112, no. 17 (April 13, 2015): 5401–6. http://dx.doi.org/10.1073/pnas.1501775112.

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Ribosome protection proteins (RPPs) confer resistance to tetracycline by binding to the ribosome and chasing the drug from its binding site. Current models for RPP action are derived from 7.2- to 16-Å resolution structures of RPPs bound to vacant or nontranslating ribosomes. Here we present a cryo-electron microscopy reconstruction of the RPP TetM in complex with a translating ribosome at 3.9-Å resolution. The structure reveals the contacts of TetM with the ribosome, including interaction between the conserved and functionally critical C-terminal extension of TetM with a unique splayed conform

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14

Holmes, K. C., D. R. Trentham, R. Simmons, Y. Takagi, H. Shuman, and Y. E. Goldman. "Coupling between phosphate release and force generation in muscle actomyosin." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1452 (December 29, 2004): 1913–20. http://dx.doi.org/10.1098/rstb.2004.1561.

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Energetic, kinetic and oxygen exchange experiments in the mid–1980s and early 1990s suggested that phosphate (P i ) release from actomyosin–adenosine diphosphate P i (AM·ADP·P i ) in muscle fibres is linked to force generation and that P i release is reversible. The transition leading to the force–generating state and subsequent P i release were hypothesized to be separate, but closely linked steps. P i shortens single force–generating actomyosin interactions in an isometric optical clamp only if the conditions enable them to last 20–40 ms, enough time for P i to dissociate. Until 2003, the av

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15

Balog, Edward M., Bradley R. Fruen, Patricia K. Kane, and Charles F. Louis. "Mechanisms of Pi regulation of the skeletal muscle SR Ca2+ release channel." American Journal of Physiology-Cell Physiology 278, no. 3 (March 1, 2000): C601—C611. http://dx.doi.org/10.1152/ajpcell.2000.278.3.c601.

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Inorganic phosphate (Pi) accumulates in the fibers of actively working muscle where it acts at various sites to modulate contraction. To characterize the role of Pi as a regulator of the sarcoplasmic reticulum (SR) calcium (Ca2+) release channel, we examined the action of Pi on purified SR Ca2+ release channels, isolated SR vesicles, and skinned skeletal muscle fibers. In single channel studies, addition of Pi to the cis chamber increased single channel open probability ( P o; 0.079 ± 0.020 in 0 Pi, 0.157 ± 0.034 in 20 mM Pi) by decreasing mean channel closed time; mean channel open times were

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16

Wang, Zhiming, Wenxin Hu, and Hongjin Zheng. "Pathogenic siderophore ABC importer YbtPQ adopts a surprising fold of exporter." Science Advances 6, no. 6 (February 2020): eaay7997. http://dx.doi.org/10.1126/sciadv.aay7997.

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To fight for essential metal ions, human pathogens secrete virulence-associated siderophores and retake the metal-chelated siderophores through a subfamily of adenosine triphosphate (ATP)–binding cassette (ABC) importer, whose molecular mechanisms are completely unknown. We have determined multiple structures of the yersiniabactin importer YbtPQ from uropathogenic Escherichia coli (UPEC) at inward-open conformation in both apo and substrate-bound states by cryo–electron microscopy. YbtPQ does not adopt any known fold of ABC importers but surprisingly adopts the fold of type IV ABC exporters. T

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17

Cattaneo, M., MT Canciani, A. Lecchi, RL Kinlough-Rathbone, MA Packham, PM Mannucci, and JF Mustard. "Released adenosine diphosphate stabilizes thrombin-induced human platelet aggregates." Blood 75, no. 5 (March 1, 1990): 1081–86. http://dx.doi.org/10.1182/blood.v75.5.1081.1081.

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Abstract Normal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, chymotrypsin, and prostaglandin E1 (PGE1). In contrast, thrombin-induced aggregates of platelets from patients with delta-storage pool deficiency (delta-SPD), which lack releasable nucleotides, are readily deaggregated by the same combination of inhibitors. The ease with which delta-SPD platelets are deaggregated is caused by the lack of stabilizing effects of released ADP, since: (1) exogenous adenosine diphosphate (ADP) (10 mumol/L), b

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Cattaneo, M., MT Canciani, A. Lecchi, RL Kinlough-Rathbone, MA Packham, PM Mannucci, and JF Mustard. "Released adenosine diphosphate stabilizes thrombin-induced human platelet aggregates." Blood 75, no. 5 (March 1, 1990): 1081–86. http://dx.doi.org/10.1182/blood.v75.5.1081.bloodjournal7551081.

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Normal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, chymotrypsin, and prostaglandin E1 (PGE1). In contrast, thrombin-induced aggregates of platelets from patients with delta-storage pool deficiency (delta-SPD), which lack releasable nucleotides, are readily deaggregated by the same combination of inhibitors. The ease with which delta-SPD platelets are deaggregated is caused by the lack of stabilizing effects of released ADP, since: (1) exogenous adenosine diphosphate (ADP) (10 mumol/L), but not se

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19

Raimbault, Cyrille, Catherine Perraut, Olivier Marcillat, Rene Buchet, and Christian Vial. "Nucleotide Binding Sites in Wild-Type Creatine Kinase and in W227Y Mutant Probed by Photochemical Release of Nucleotides and inFrared Difference Spectroscopy." European Journal of Biochemistry 250, no. 3 (December 1997): 773–82. http://dx.doi.org/10.1111/j.1432-1033.1997.00773.x.

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Dutta, Amal K., Kangmee Woo, R. Brian Doctor, J. Gregory Fitz, and Andrew P. Feranchak. "Extracellular nucleotides stimulate Cl− currents in biliary epithelia through receptor-mediated IP3 and Ca2+ release." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 5 (November 2008): G1004—G1015. http://dx.doi.org/10.1152/ajpgi.90382.2008.

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Extracellular ATP regulates bile formation by binding to P2 receptors on cholangiocytes and stimulating transepithelial Cl− secretion. However, the specific signaling pathways linking receptor binding to Cl− channel activation are not known. Consequently, the aim of these studies in human Mz-Cha-1 biliary cells and normal rat cholangiocyte monolayers was to assess the intracellular pathways responsible for ATP-stimulated increases in intracellular Ca2+ concentration ([Ca2+]i) and membrane Cl− permeability. Exposure of cells to ATP resulted in a rapid increase in [Ca2+]i and activation of membr

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21

TUGANOVA, Alina, and Kirill M. POPOV. "Role of protein–protein interactions in the regulation of pyruvate dehydrogenase kinase activity." Biochemical Journal 387, no. 1 (March 22, 2005): 147–53. http://dx.doi.org/10.1042/bj20040805.

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The transacetylase component (E2) of PDC (pyruvate dehydrogenase complex) plays a critical role in the regulation of PDHK (pyruvate dehydrogenase kinase) activity. The present study was undertaken to investigate further the molecular mechanism by which E2 modulates the activity of PDHK. In agreement with the earlier results, it was found that the inner L2 (lipoyl-bearing domain 2) of E2 expressed with or without the C-terminal hinge region had little, if any, effect on the kinase activity, indicating a lack of direct allosteric effect of L2 on PDHK. In marked contrast, significant activation o

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22

Carney-Anderson, L., L. V. Thompson, D. A. Huetteman, and S. K. Donaldson. "GTP gammaS removal of D-600 block of skeletal muscle excitation-contraction coupling." American Journal of Physiology-Cell Physiology 272, no. 2 (February 1, 1997): C572—C581. http://dx.doi.org/10.1152/ajpcell.1997.272.2.c572.

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G proteins interacting with dihydropyridine receptors (DHPR) in transverse tubules (TT) of skeletal muscle may have a role in skeletal excitation-contraction (EC) coupling. The aim of this study was to determine the effects of G protein-specific nucleotides [guanosine 5'-O-(3-thiotriphosphate) (GTP gammaS) and guanosine 5'-O-(2-thiodiphosphate) (GDP betaS)] on the EC coupling mechanism in the presence of D-600, an agent that blocks EC coupling by immobilizing the voltage-sensing subunit of the DHPR in its inactivated state. By use of the mechanically peeled single-fiber preparation from rabbit

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23

Rousseau, Eric, Janet Pinkos, and Diane Savaria. "Functional sensitivity of the native skeletal Ca2+-release channel to divalent cations and the Mg–ATP complex." Canadian Journal of Physiology and Pharmacology 70, no. 3 (March 1, 1992): 394–402. http://dx.doi.org/10.1139/y92-049.

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Sarcoplasmic reticulum (SR) vesicles, prepared from rabbit skeletal muscle, were characterized by functional and binding assays and incorporated into planar lipid bilayers. Single-channel activity was recorded in an asymmetric calcium buffer system and studied under voltage clamp conditions. Under these experimental conditions, a large conductance (100 pS in 50 mM Ca2+trans) divalent cation selective channel displaying high ruthenium red and low Ca2+ sensitivity was identified. This pathway has been previously described as the Ca2+-release channel of the SR of skeletal muscle. We now report th

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Howe, P. H., та E. B. Leof. "Transforming growth factor β1 treatment of AKR-2B cells is coupled through a pertussis-toxin-sensitive G-protein(s)". Biochemical Journal 261, № 3 (1 серпня 1989): 879–86. http://dx.doi.org/10.1042/bj2610879.

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Transforming growth factor beta (TGF beta 1) is a potent regulator of DNA synthesis and cellular proliferation. In this study, we investigated whether the growth stimulatory signal of TGF beta 1 is transduced intracellularly by guanine nucleotide regulatory proteins (G-proteins). In plasma membranes from AKR-2B cells, TGF beta 1 increased binding of the radiolabelled, non-hydrolysable GTP analogue, guanosine 5′-[gamma-[35S]thio]triphosphate (GTP[35S]), in a dose-dependent manner. Maximal effects occurred between 0.4 and 1.0 nM-TGF beta 1. Specific binding of GTP[35S] occurred with a Kd of 3.2

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Mihályi, Csaba, Iordan Iordanov, Beáta Töröcsik, and László Csanády. "Simple binding of protein kinase A prior to phosphorylation allows CFTR anion channels to be opened by nucleotides." Proceedings of the National Academy of Sciences 117, no. 35 (August 17, 2020): 21740–46. http://dx.doi.org/10.1073/pnas.2007910117.

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The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) anion channel is essential for epithelial salt–water balance. CFTR mutations cause cystic fibrosis, a lethal incurable disease. In cells CFTR is activated through the cAMP signaling pathway, overstimulation of which during cholera leads to CFTR-mediated intestinal salt–water loss. Channel activation is achieved by phosphorylation of its regulatory (R) domain by cAMP-dependent protein kinase catalytic subunit (PKA). Here we show using two independent approaches––an ATP analog that can drive CFTR channel gating but is unsuitable for

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Chada, Nagaraju, Kanokporn Chattrakun, Brendan P. Marsh, Chunfeng Mao, Priya Bariya, and Gavin M. King. "Single-molecule observation of nucleotide induced conformational changes in basal SecA-ATP hydrolysis." Science Advances 4, no. 10 (October 2018): eaat8797. http://dx.doi.org/10.1126/sciadv.aat8797.

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SecA is the critical adenosine triphosphatase that drives preprotein transport through the translocon, SecYEG, in Escherichia coli. This process is thought to be regulated by conformational changes of specific domains of SecA, but real-time, real-space measurement of these changes is lacking. We use single-molecule atomic force microscopy (AFM) to visualize nucleotide-dependent conformations and conformational dynamics of SecA. Distinct topographical populations were observed in the presence of specific nucleotides. AFM investigations during basal adenosine triphosphate (ATP) hydrolysis reveal

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Chou, Steven Z., and Thomas D. Pollard. "Mechanism of actin polymerization revealed by cryo-EM structures of actin filaments with three different bound nucleotides." Proceedings of the National Academy of Sciences 116, no. 10 (February 13, 2019): 4265–74. http://dx.doi.org/10.1073/pnas.1807028115.

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We used cryo-electron microscopy (cryo-EM) to reconstruct actin filaments with bound AMPPNP (β,γ-imidoadenosine 5′-triphosphate, an ATP analog, resolution 3.1 Å), ADP-Pi(ADP with inorganic phosphate, resolution 3.1 Å), or ADP (resolution 3.6 Å). Subunits in the three filaments have similar backbone conformations, so assembly rather than ATP hydrolysis or phosphate dissociation is responsible for their flattened conformation in filaments. Polymerization increases the rate of ATP hydrolysis by changing the positions of the side chains of Q137 and H161 in the active site. Flattening during assemb

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Breitwieser, G. E., and G. Szabo. "Mechanism of muscarinic receptor-induced K+ channel activation as revealed by hydrolysis-resistant GTP analogues." Journal of General Physiology 91, no. 4 (April 1, 1988): 469–93. http://dx.doi.org/10.1085/jgp.91.4.469.

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The role of a guanine nucleotide-binding protein (Gk) in the coupling between muscarinic receptor activation and opening of an inwardly rectifying K+ channel [IK(M)] was examined in cardiac atrial myocytes, using hydrolysis-resistant GTP analogues. In the absence of muscarinic agonist, GTP analogues produced a membrane current characteristic of IK(M). The initial rate of appearance of this receptor-independent IK(M) was measured for the various analogues in order to explore the kinetic properties of IK(M) activation. We found that IK(M) activation is controlled solely by the intracellular anal

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Vaandrager, A. B., M. C. Ploemacher, and H. R. De Jonge. "Phosphoinositide metabolism in intestinal brush borders: stimulation of IP3 formation by guanine nucleotides and Ca2+." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 3 (September 1, 1990): G410—G419. http://dx.doi.org/10.1152/ajpgi.1990.259.3.g410.

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The potential role of polyphosphoinositide (PPI) metabolism as a signal-transduction mechanism in apical membranes of polarized epithelial cells was evaluated by examining the formation and breakdown of PPI in rat intestinal brush-border membranes (BBM) prelabeled by intraluminal injection of [3H]inositol in vivo or by [gamma-32P]ATP in vitro. Freshly isolated BBM prelabeled with [3H]inositol contained higher amounts of [3H]phosphatidylinositol 4,5-diphosphate compared with a basolateral membrane (BLM) preparation (approximately 14 and 6.8% of total [3H]PPIs, respectively) and were enriched in

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ZCHUT, Sigalit, Wei FENG, and Varda SHOSHAN-BARMATZ. "Ryanodine receptor/calcium release channel conformations as reflected in the different effects of propranolol on its ryanodine binding and channel activity." Biochemical Journal 315, no. 2 (April 15, 1996): 377–83. http://dx.doi.org/10.1042/bj3150377.

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1. Propranolol, a β-blocker, inhibited or stimulated ryanodine binding to both the membrane-bound and purified ryanodine receptor (RyR) depending on the assay conditions. At high NaCl concentrations, propranolol increased the number of ryanodine-binding sites (Bmax) with no effect on the binding affinity. In the presence of 0.2 M NaCl, ryanodine binding was inhibited by propranolol. Half-maximal inhibition was obtained at 1.2 mM and complete inhibition at 2 mM propranolol. The inhibitory effect of propranolol obtained at low NaCl concentration was not restored by increasing the NaCl concentrat

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31

Afzal, Saira, Sumera Zaib, Behzad Jafari, Peter Langer, Joanna Lecka, Jean Sévigny, and Jamshed Iqbal. "Highly Potent and Selective Ectonucleoside Triphosphate Diphosphohydrolase (ENTPDase1, 2, 3 and 8) Inhibitors Having 2-substituted-7- trifluoromethyl-thiadiazolopyrimidones Scaffold." Medicinal Chemistry 16, no. 5 (August 7, 2020): 689–702. http://dx.doi.org/10.2174/1573406415666190614095821.

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Background: The ecto-nucleoside triphosphate diphosphohydrolases (NTPDases) terminate nucleotide signaling via the hydrolysis of extracellular nucleoside-5'-triphosphate and nucleoside- 5'-diphosphate, to nucleoside-5'-monophosphate and composed of eight Ca2+/Mg2+ dependent ectonucleotidases (NTPDase1-8). Extracellular nucleotides are involved in a variety of physiological mechanisms. However, they are rapidly inactivated by ectonucleotidases that are involved in the sequential removal of phosphate group from nucleotides with the release of inorganic phosphate and their respective nucleoside.

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PARK, Jae-Bong, Jun-Sub KIM, Jae-Yong LEE, Jaebong KIM, Ji-Yeon SEO, and Ah-Ram KIM. "GTP binds to Rab3A in a complex with Ca2+/calmodulin." Biochemical Journal 362, no. 3 (March 8, 2002): 651–57. http://dx.doi.org/10.1042/bj3620651.

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Ras-like small GTP-binding proteins of the Rab family regulate trafficking of the secretory or endocytic pathways. Rab3 proteins within the Rab family are expressed at high levels in neurons and endocrine cells, where they regulate release of dense-core granules and synaptic vesicles (SVs). Rab3A is present as either the soluble or the SV membrane-bound form in neurons that are dependent on the GDP- or GTP-bound states respectively. GDP dissociation inhibitor (GDI) is known to induce the dissociation of Rab3A from synaptic membranes when GTP is depleted. In an earlier study, Ca2+/calmodulin (C

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33

Volkán-Kacsó, Sándor, and Rudolph A. Marcus. "Theory of long binding events in single-molecule–controlled rotation experiments on F1-ATPase." Proceedings of the National Academy of Sciences 114, no. 28 (June 26, 2017): 7272–77. http://dx.doi.org/10.1073/pnas.1705960114.

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The theory of elastic group transfer for the binding and release rate constants for nucleotides in F1-ATPase as a function of the rotor angle is further extended in several respects. (i) A method is described for predicting the experimentally observed lifetime distribution of long binding events in the controlled rotation experiments by taking into account the hydrolysis and synthesis reactions occurring during these events. (ii) A method is also given for treating the long binding events in the experiments and obtaining the rate constants for the hydrolysis and synthesis reactions occurring d

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34

Larburu, Natacha, Christopher J. Adams, Chao-Sheng Chen, Piotr R. Nowak, and Maruf M. U. Ali. "Mechanism of Hsp70 specialized interactions in protein translocation and the unfolded protein response." Open Biology 10, no. 8 (August 2020): 200089. http://dx.doi.org/10.1098/rsob.200089.

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Hsp70 chaperones interact with substrate proteins in a coordinated fashion that is regulated by nucleotides and enhanced by assisting cochaperones. There are numerous homologues and isoforms of Hsp70 that participate in a wide variety of cellular functions. This diversity can facilitate adaption or specialization based on particular biological activity and location within the cell. In this review, we highlight two specialized binding partner proteins, Tim44 and IRE1, that interact with Hsp70 at the membrane in order to serve their respective roles in protein translocation and unfolded protein

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35

Kalambakas, SA, FM Robertson, SM O'Connell, S. Sinha, K. Vishnupad, and GI Karp. "Adenosine diphosphate stimulation of cultured hematopoietic cell lines." Blood 81, no. 10 (May 15, 1993): 2652–57. http://dx.doi.org/10.1182/blood.v81.10.2652.2652.

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Abstract Adenosine diphosphate (ADP) plays a critical role in platelet activation both by exogenous stimulation and the release of endogenous intracellular stores. As the platelet ADP receptor is not well defined, we have chosen to identify and characterize several cell lines that possess functional receptors for this nucleotide. Rat promegakaryoblasts (RPM), human erythroleukemia cells (HEL), U937, and K562 leukemia cells responded to ADP, as measured by a rapid increase in intracellular calcium. In the case of RPM cells, ADP was the only naturally occurring platelet agonist capable of elicit

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36

Kalambakas, SA, FM Robertson, SM O'Connell, S. Sinha, K. Vishnupad, and GI Karp. "Adenosine diphosphate stimulation of cultured hematopoietic cell lines." Blood 81, no. 10 (May 15, 1993): 2652–57. http://dx.doi.org/10.1182/blood.v81.10.2652.bloodjournal81102652.

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Adenosine diphosphate (ADP) plays a critical role in platelet activation both by exogenous stimulation and the release of endogenous intracellular stores. As the platelet ADP receptor is not well defined, we have chosen to identify and characterize several cell lines that possess functional receptors for this nucleotide. Rat promegakaryoblasts (RPM), human erythroleukemia cells (HEL), U937, and K562 leukemia cells responded to ADP, as measured by a rapid increase in intracellular calcium. In the case of RPM cells, ADP was the only naturally occurring platelet agonist capable of eliciting this

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37

Esue, Osigwe, Denis Wirtz, and Yiider Tseng. "GTPase Activity, Structure, and Mechanical Properties of Filaments Assembled from Bacterial Cytoskeleton Protein MreB." Journal of Bacteriology 188, no. 3 (February 1, 2006): 968–76. http://dx.doi.org/10.1128/jb.188.3.968-976.2006.

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ABSTRACT MreB, a major component of the recently discovered bacterial cytoskeleton, displays a structure homologous to its eukaryotic counterpart actin. Here, we study the assembly and mechanical properties of Thermotoga maritima MreB in the presence of different nucleotides in vitro. We found that GTP, not ADP or GDP, can mediate MreB assembly into filamentous structures as effectively as ATP. Upon MreB assembly, both GTP and ATP release the gamma phosphate at similar rates. Therefore, MreB is an equally effective ATPase and GTPase. Electron microscopy and quantitative rheology suggest that t

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38

Therrien, S., and P. H. Naccache. "Guanine nucleotide-induced polymerization of actin in electropermeabilized human neutrophils." Journal of Cell Biology 109, no. 3 (September 1, 1989): 1125–32. http://dx.doi.org/10.1083/jcb.109.3.1125.

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The effects of exogenous guanine nucleotides on the polymerization of actin in human neutrophils were tested in an electropermeabilized cell preparation. Close to 40% permeabilization was achieved with a single electric discharge as measured by nucleic acid staining with ethidium bromide or propidium iodide with minimal (less than 2%) release of the cytoplasmic marker lactate dehydrogenase. In addition, electropermeabilized neutrophils retained their capacity to produce superoxide anions and to sustain a polymerization of actin in response to surface-receptor dependent stimuli such as chemotac

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39

Lim, Siew Pheng, та Alfredo Garzino-Demo. "The Human Immunodeficiency Virus Type 1 Tat Protein Up-Regulates the Promoter Activity of the Beta-Chemokine Monocyte Chemoattractant Protein 1 in the Human Astrocytoma Cell Line U-87 MG: Role of SP-1, AP-1, and NF-κB Consensus Sites". Journal of Virology 74, № 4 (15 лютого 2000): 1632–40. http://dx.doi.org/10.1128/jvi.74.4.1632-1640.2000.

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ABSTRACT It has been shown that the human immunodeficiency virus type 1 (HIV-1) Tat protein can specifically enhance expression and release of monocyte chemoattractant protein 1 (MCP-1) from human astrocytes. In this study, we show evidence that Tat-induced MCP-1 expression is mediated at the transcriptional level. Transient transfection of an expression construct encoding the full-length Tat into the human glioblastoma-astrocytoma cell line U-87 MG enhances reporter gene activity from cotransfected deletion constructs of the MCP-1 promoter. HIV-1 Tat exerts its effect through a minimal constr

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40

Liang, Xue-hai, and Maurille J. Fournier. "The Helicase Has1p Is Required for snoRNA Release from Pre-rRNA." Molecular and Cellular Biology 26, no. 20 (August 14, 2006): 7437–50. http://dx.doi.org/10.1128/mcb.00664-06.

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ABSTRACT Synthesis of rRNA in eukaryotes involves the action of a large population of snoRNA-protein complexes (snoRNPs), which create modified nucleotides and participate in cleavage of pre-rRNA. The snoRNPs mediate these functions through direct base pairing, in many cases through long complementary sequences. This feature suggests that RNA helicases may be involved in the binding and release of snoRNPs from pre-rRNA. In this study, we determined that the DEAD box helicase Has1p, a nucleolar protein required for the production of 18S rRNA, copurifies with the snR30/U17 processing snoRNP but

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41

Smolen, J. E., S. J. Stoehr, B. Kuczynski, E. K. Koh та G. M. Omann. "Dual effects of guanosine 5′-[γ-thio]triphosphate on secretion by electroporated human neutrophils". Biochemical Journal 279, № 3 (1 листопада 1991): 657–64. http://dx.doi.org/10.1042/bj2790657.

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It is generally believed that G-proteins play stimulatory roles on cell activation. In contrast, we found that guanosine 5′-[gamma-thio]triphosphate (GTP[S]) was a potent inhibitor of Ca(2+)-induced secretion from specific granules (as monitored by vitamin B-12-binding protein). GTP[S] inhibition of specific-granule release occurred in the presence or absence of adenine nucleotides, required Mg2+ (1-3 mM), and was half-maximal at 30 microM-GTP[S]. The dual stimulatory and inhibitory effects of GTP[S] could be readily observed and differentiated when degranulation was monitored over a range of

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42

Ransnäs, L. A., J. R. Jasper, D. Leiber та P. A. Insel. "β-adrenergic-receptor-mediated dissociation and membrane release of the Gs protein in S49 lymphoma-cell membranes. Dependence on Mg2+ and GTP". Biochemical Journal 283, № 2 (15 квітня 1992): 519–24. http://dx.doi.org/10.1042/bj2830519.

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We reported [Ransnäs, Svoboda, Jasper & Insel (1989) Proc. Natl. Acad. Sci. U.S.A. 86, 7900-7903] that in intact S49 lymphoma cells the beta-adrenergic-receptor agonist isoprenaline dissociates the stimulatory guanine-nucleotide-binding protein, Gs, into its alpha s and beta gamma subunits, leading to redistribution of alpha s from plasma membranes to the cytoplasm. In the present studies we investigated the kinetics of Gs dissociation and membrane release in plasma membranes from S49 lymphoma cells. We analysed cholate extracts of membranes for alpha s levels by a competitive e.l.i.s.a. w

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43

Hinkle, P. M., E. L. Hewlett, and M. C. Gershengorn. "Thyroliberin action in pituitary cells is not inhibited by pertussis toxin." Biochemical Journal 237, no. 1 (July 1, 1986): 181–86. http://dx.doi.org/10.1042/bj2370181.

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The effects of pertussis toxin on the responses of rat pituitary-tumour (GH) cells to thyrotropin-releasing hormone (thyroliberin, TRH) were examined. Treatment of cells with pertussis toxin did not alter the affinity or concentration of TRH receptors, or the sensitivity of the TRH receptor to inhibition by guanine nucleotides. TRH caused an increase in low-Km GTPase activity in membrane-containing fractions from both control and pertussis-toxin-treated cells. TRH stimulation of inositol phosphate formation was insensitive to pertussis toxin. TRH caused a biphasic increase in the concentration

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44

Piccardoni, Paola, Virgilio Evangelista, Antonio Piccoli, Giovanni de Gaetano, Alfred Walz, and Chiara Cerletti. "Thrombin-activated Human Platelets Release two NAP-2 Variants that Stimulate Polymorphonuclear Leukocytes." Thrombosis and Haemostasis 76, no. 05 (1996): 780–85. http://dx.doi.org/10.1055/s-0038-1650660.

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SummaryThrombin-activated human platelets release substance(s) of a prote-ic nature which induce an increase in the intracellular calcium concentration in polymorphonuclear leukocytes (PMN). Aim of this study was to characterize the platelet released product(s) responsible for PMN stimulation.PMN-stimulating activity was isolated from platelet supernatant by FPLC and HPLC. The N-terminal sequence analysis revealed that the purified fractions consisted in 90% of a peptide of 73 amino acids and in 10% of a peptide of 74 amino acids; both are truncated forms of the connective tissue-activating pe

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45

Prat, A. G., I. L. Reisin, D. A. Ausiello, and H. F. Cantiello. "Cellular ATP release by the cystic fibrosis transmembrane conductance regulator." American Journal of Physiology-Cell Physiology 270, no. 2 (February 1, 1996): C538—C545. http://dx.doi.org/10.1152/ajpcell.1996.270.2.c538.

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Recent studies from our laboratory indicate that members of the ATP-binding cassette (ABC) family of transporters, including P-glycoprotein and cystic fibrosis transmembrane conductance regulator (CFTR), are ATP-permeable channels. The physiological relevance of this novel transport mechanism is largely unknown. In the present study, intra- and extracellular ATP content, cellular ATP release, and O2 consumption before and after adenosine 3',5'-cyclic monophosphate (cAMP) stimulation were determined to assess the role of CFTR in the transport of ATP under physiological conditions. The functiona

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Miyazaki, S. "Inositol 1,4,5-trisphosphate-induced calcium release and guanine nucleotide-binding protein-mediated periodic calcium rises in golden hamster eggs." Journal of Cell Biology 106, no. 2 (February 1, 1988): 345–53. http://dx.doi.org/10.1083/jcb.106.2.345.

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Periodic increases in intracellular free calcium occur upon fertilization of golden hamster eggs (Miyazaki et al. 1986. Dev. Biol. 118:259-267). To investigate the underlying mechanism, inositol 1,4,5-trisphosphate (IP3) and guanine nucleotides were microinjected into the egg while Ca2+ transients were monitored by aequorin luminescence and/or hyperpolarization in the membrane potential, which indicates the exact timing and spatial distribution of the Ca2+ rise. Injection of IP3 induced an immediate Ca2+ transient of 13-18 s in the entire egg. The critical concentration of IP3 was 80 nM in the

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47

Shoshan-Barmatz, V. "Chemical modification of sarcoplasmic reticulum with methylbenzimidate. Stimulation of Ca2+ efflux." Biochemical Journal 243, no. 1 (April 1, 1987): 165–73. http://dx.doi.org/10.1042/bj2430165.

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Treatment of sarcoplasmic reticulum membranes with 12 mM-methylbenzimidate (MBI) for 5 min, in the presence of 5 mM-ATP at pH 8.5, resulted in a 2-3-fold stimulation of ATP hydrolysis and over 90% inhibition of Ca2+ accumulation. This phenomenon was strictly dependent upon the presence of nucleotides with the following order of effectiveness: adenosine 5′-[beta, gamma-imido]triphosphate greater than or equal to ATP greater than UTP greater than ADP greater than AMP. Divalent cations such as Ca2+, Mg2+ and Mn2+, when present during the MBI treatment, prevented both the stimulation of ATPase act

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Kristiansen, Søren, Jakob N. Nielsen, Sylvain Bourgoin, Amira Klip, Michel Franco, and Erik A. Richter. "GLUT-4 translocation in skeletal muscle studied with a cell-free assay: involvement of phospholipase D." American Journal of Physiology-Endocrinology and Metabolism 281, no. 3 (September 1, 2001): E608—E618. http://dx.doi.org/10.1152/ajpendo.2001.281.3.e608.

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GLUT-4-containing membranes immunoprecipitated from insulin-stimulated rat skeletal muscle produce the phospholipase D (PLD) product phosphatidic acid. In vitro stimulation of PLD in crude membrane with ammonium sulfate (5 mM) resulted in transfer of GLUT-4 (3.0-fold vs. control) as well as transferrin receptor proteins from large to small membrane structures. The in vitro GLUT-4 transfer could be blocked by neomycin (a PLD inhibitor), and neomycin also reduced insulin-stimulated glucose transport in intact incubated soleus muscles. Furthermore, protein kinase Bβ (PKBβ) was found to associate

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49

Wollheim, Claes B., Susanne Ullrich, Paolo Meda, and Lucia Vallar. "Regulation of exocytosis in electrically permeabilized insulin-secreting cells. Evidence for Ca2+ dependent and independent secretion." Bioscience Reports 7, no. 5 (May 1, 1987): 443–54. http://dx.doi.org/10.1007/bf01362507.

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The regulation of insulin secretion from RINm5F cells exposed to high voltage discharge has been investigated. Electron microscopy revealed that the overall structure of the cells was preserved after permeabilization. In this preparation insulin release was stimulated by Ca2+ (EC50=2.4 μM). The stable GTP analogue GTPγS enhanced secretion both at intermediate (nano- to micromolar) and vanishingly low (<10 pM) Ca2+ concentrations. At optimal Ca2+ (10 μM) the effect of GTPγS was greatly reduced. We investigated whether the secretory response to GTP analogues was mediated by any of three enzym

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Junge, W., S. Engelbrecht, C. Griwatz, and G. Groth. "THE CHLOROPLAST H+-ATPase: PARTIAL REACTIONS OF THE PROTON." Journal of Experimental Biology 172, no. 1 (November 1, 1992): 461–74. http://dx.doi.org/10.1242/jeb.172.1.461.

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This article reviews proton intake, charge transfer and proton release by F-ATPases, based in part on flash spectrophotometric studies on the chloroplast ATPase in thylakoid membranes, CF1Fo. The synthesis-coupled translocation of charges by CF1Fo (maximum rate &lt;1500 s-1) and the dissipative flow through its exposed channel portion, CFo (rate &gt;10 000 s-1), are extremely proton-specific (selectivity H+:K+&gt;10(7):1). The proton-specific filter is located in CFo. Proton flow through exposed CFo can be throttled by adding subunit (&dgr;) or subunit &bgr; of CF1. These s

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