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223 results on '"Wecker L"'

7. Receptor subtypes — Molecular biology and pharmacology

Author

Elgoyhen, A. B., Johnson, D., Boulter, J., Vetter, P., Heinemann, S. F., Allen, R., Hartley, M., Heinemann, S., Mukerji, Jishnu, Dumont, Éric, Séguéla, Philippe, Yu, Z. I., Morgan, D. G., Wecker, L., Fornasari, D., Battaglioli, E., Clementi, F., Cohen, B., Figl, A., Quick, M. W., Labarca, C., Davidson, N., Lester, H. A., Luetje, C. W., Harvey, S. C., Maddox, F., de Fiebre, C. M., Papke, R. L., Meyer, E. M., Gordon, J., McCreedy, S., Machulskis, A., Blosser, J., Xie, Y., Chiara, D. C., Cohen, J. B., Lentz, T. L., Jansson, B., editor, Jörnvall, H., editor, Rydberg, U., editor, Terenius, L., editor, Vallee, B. L., editor, Clarke, Paul Brian Sydenham, editor, Quik, Maryka, editor, Thurau, Klaus, editor, and Adlkofer, Franz, editor

Published
1994
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8. Receptor regulation

Author

Dávila-Garciá, M. I., Oasba, S. S., Houghtling, R. A., Kellar, K. J., Komourian, J., Ouik, M., Zhang, X., Gong, Z-H., Nordberg, Agneta, Donnelly-Roberts, Diana L., Gopalakrishnan, Murali, Arneric, Stephen P., Sullivan, James P., Puchacz, Elzbieta, Eisenhour, Cynthia, Lucas, Ronald J., Lucero, Linda, Rowell, Peter P., Bencherif, Merouane, Fowler, Kathy, Lippiello, Patrick M., Hsu, Y. N., Amin, J., Weiss, D., Wecker, L., Sargent, P. B., Garrett, E. N., Wilson, H. L., Matthews, S. D., Clarke, P. B. S., El-Bizri, H., Stitzel, J. A., Farnham, D. A., Collins, A. C., Leonard, S., Adler, L. E., Bickford, P. C., Hall, M., Rollins, Y., Breese, C., Logel, J., Drebing, C., Byerley, W., Coon, H., Freedman, R., Bullock, A. E., Schneider, A. S., Codilnola, A., Tarroni, P., Cattaneo, M. G., Vicentini, L. M., Clementi, F., Sher, F., Jansson, B., editor, Jörnvall, H., editor, Rydberg, U., editor, Terenius, L., editor, Vallee, B. L., editor, Clarke, Paul Brian Sydenham, editor, Quik, Maryka, editor, Thurau, Klaus, editor, and Adlkofer, Franz, editor

Published
1994
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41. Cyclic AMP-dependent protein kinase (PKA) and protein kinase C phosphorylate sites in the amino acid sequence corresponding to the M3/M4 cytoplasmic domain of α4 neuronal nicotinic receptor subunits.

Author

Wecker, L., Guo, X., Rycerz, A.M., and Edwards, S.C.

Subjects
*NEURONS, *CYCLIC adenylic acid, *XENOPUS, *PROTEIN kinases, *CYTOLOGY
Abstract

To determine whether α4 subunits of α4β2 neuronal nicotinic receptors are phosphorylated within the M3/M4 intracellular region by cyclic AMP-dependent protein kinase A (PKA) or protein kinase C (PKC), immunoprecipitated receptors from Xenopus oocytes and a fusion protein corresponding to the M3/M4 cytoplasmic domain of α4 (α4[sub 336-597]) were incubated with ATP and either PKA or PKC. Both α4 and α4[sub 336-597] were phosphorylated by PKA and PKC, providing the first direct biochemical evidence that the M3/M4 cytoplasmic domain of neuronal nicotinic receptor α4 subunits is phosphorylated by both kinases. When the immunoprecipitated receptors and the α4[sub 336-597] fusion protein were phosphorylated and the labeled proteins subjected to phosphoamino acid analysis, results indicated that α4 and α4[sub 336-597] were phosphorylated on the same amino acid residues by each kinase. Furthermore, PKA phosphorylated serines exclusively, whereas PKC phosphorylated both serines and threonines. To determine whether Ser[sup 368] was a substrate for both kinases, a peptide corresponding to amino acids 356–371 was synthesized (α4[sub 356-371]) and incubated with ATP and the kinases. The phosphorylation of α4[sub 356-371] by both PKA and PKC was saturable with K[sub m]s of 15.3 ± 3.3 µm and 160.8 ± 26.8 µm, respectively, suggesting that Ser[sup 368] was a better substrate for PKA than PKC. [ABSTRACT FROM AUTHOR]

Published
2001
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50. Dietary choline intake modulates benzodiazepine receptor binding and gamma-aminobutyric acidA receptor function in mouse brain.

Author

Miller, L G, Greenblatt, D J, Roy, R B, Lopez, F, and Wecker, L

Abstract

Several lines of evidence suggest that dietary choline intake influences the metabolism of membrane phospholipids with possible effects on GABAergic neurotransmission. Based on these findings, the present experiments determined whether chronic choline supplementation or deficiency alters GABAergic function at the level of the gamma-aminobutyric acid (GABA)/benzodiazepine-chloride channel complex. To accomplish this, mice were fed diets containing 0% (deficient), 0.2% (basal) or 2.0% (supplemented) choline chloride for 28 days, and behavior, ligand binding at several sites in the complex and chloride uptake were determined in various brain regions. For both rotarod ataxia and open-field activity, mice receiving choline supplementation had a decreased response to clonazepam compared to those receiving basal and deficient diets. Choline supplementation significantly increased the in vivo binding of [3H]Ro15-1788 to cortex and cerebellum by 19% and 24%, respectively, and in vitro studies in cortical membranes indicated a significant 36% increase in the maximal number of [3H]flunitrazepam binding sites without a change in affinity, as compared to basal controls. In contrast, [3H]Ro15-1788 binding in vivo in all brain regions from mice fed the deficient diet decreased significantly to 20 to 58% of control values. Dietary choline intake did not alter GABA levels in brain, the binding of [35S]t-butylbicyclophosphorothionate to the chloride channel or the coupling between GABA and either the t-butylbicyclophosphorothionate site or the benzodiazepine site. However, the function of the GABAA receptor, determined by muscimol-stimulated chloride uptake into cortical synaptoneurosomes, was increased significantly in tissue from the supplemented group as compared to both control and deficient groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1989

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