The Experts below are selected from a list of 8508 Experts worldwide ranked by ideXlab platform
Leon Avery - One of the best experts on this subject based on the ideXlab platform.
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starvation activates map kinase through the muscarinic Acetylcholine Pathway in caenorhabditis elegans pharynx
Cell Metabolism, 2006Co-Authors: Youngjai You, Jeongho Kim, Melanie H Cobb, Leon AveryAbstract:Starvation activates MAPK in the pharyngeal muscles of C. elegans through a muscarinic Acetylcholine receptor, Gqα, and nPKC as shown by the following results: (1) Starvation causes phosphorylation of MAPK in pharyngeal muscle. (2) In a sensitized genetic background in which Gqα signaling cannot be downregulated, activation of the Pathway by a muscarinic agonist causes lethal changes in pharyngeal muscle function. Starvation has identical effects. (3) A muscarinic antagonist blocks the effects of starvation on sensitized muscle. (4) Mutations and drugs that block any step of signaling from the muscarinic receptor to MAPK also block the effects of starvation on sensitized muscle. (5) Overexpression of MAPK in wild-type pharyngeal muscle mimics the effects of muscarinic agonist and of starvation on sensitized muscle. We suggest that, during starvation, the muscarinic Pathway to MAPK is activated to change the pharyngeal muscle physiology to enhance ingestion of food when food becomes available.
Jeongho Kim - One of the best experts on this subject based on the ideXlab platform.
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starvation activates map kinase through the muscarinic Acetylcholine Pathway in caenorhabditis elegans pharynx
Cell Metabolism, 2006Co-Authors: Youngjai You, Jeongho Kim, Melanie H Cobb, Leon AveryAbstract:Starvation activates MAPK in the pharyngeal muscles of C. elegans through a muscarinic Acetylcholine receptor, Gqα, and nPKC as shown by the following results: (1) Starvation causes phosphorylation of MAPK in pharyngeal muscle. (2) In a sensitized genetic background in which Gqα signaling cannot be downregulated, activation of the Pathway by a muscarinic agonist causes lethal changes in pharyngeal muscle function. Starvation has identical effects. (3) A muscarinic antagonist blocks the effects of starvation on sensitized muscle. (4) Mutations and drugs that block any step of signaling from the muscarinic receptor to MAPK also block the effects of starvation on sensitized muscle. (5) Overexpression of MAPK in wild-type pharyngeal muscle mimics the effects of muscarinic agonist and of starvation on sensitized muscle. We suggest that, during starvation, the muscarinic Pathway to MAPK is activated to change the pharyngeal muscle physiology to enhance ingestion of food when food becomes available.
Youngjai You - One of the best experts on this subject based on the ideXlab platform.
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starvation activates map kinase through the muscarinic Acetylcholine Pathway in caenorhabditis elegans pharynx
Cell Metabolism, 2006Co-Authors: Youngjai You, Jeongho Kim, Melanie H Cobb, Leon AveryAbstract:Starvation activates MAPK in the pharyngeal muscles of C. elegans through a muscarinic Acetylcholine receptor, Gqα, and nPKC as shown by the following results: (1) Starvation causes phosphorylation of MAPK in pharyngeal muscle. (2) In a sensitized genetic background in which Gqα signaling cannot be downregulated, activation of the Pathway by a muscarinic agonist causes lethal changes in pharyngeal muscle function. Starvation has identical effects. (3) A muscarinic antagonist blocks the effects of starvation on sensitized muscle. (4) Mutations and drugs that block any step of signaling from the muscarinic receptor to MAPK also block the effects of starvation on sensitized muscle. (5) Overexpression of MAPK in wild-type pharyngeal muscle mimics the effects of muscarinic agonist and of starvation on sensitized muscle. We suggest that, during starvation, the muscarinic Pathway to MAPK is activated to change the pharyngeal muscle physiology to enhance ingestion of food when food becomes available.
Melanie H Cobb - One of the best experts on this subject based on the ideXlab platform.
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starvation activates map kinase through the muscarinic Acetylcholine Pathway in caenorhabditis elegans pharynx
Cell Metabolism, 2006Co-Authors: Youngjai You, Jeongho Kim, Melanie H Cobb, Leon AveryAbstract:Starvation activates MAPK in the pharyngeal muscles of C. elegans through a muscarinic Acetylcholine receptor, Gqα, and nPKC as shown by the following results: (1) Starvation causes phosphorylation of MAPK in pharyngeal muscle. (2) In a sensitized genetic background in which Gqα signaling cannot be downregulated, activation of the Pathway by a muscarinic agonist causes lethal changes in pharyngeal muscle function. Starvation has identical effects. (3) A muscarinic antagonist blocks the effects of starvation on sensitized muscle. (4) Mutations and drugs that block any step of signaling from the muscarinic receptor to MAPK also block the effects of starvation on sensitized muscle. (5) Overexpression of MAPK in wild-type pharyngeal muscle mimics the effects of muscarinic agonist and of starvation on sensitized muscle. We suggest that, during starvation, the muscarinic Pathway to MAPK is activated to change the pharyngeal muscle physiology to enhance ingestion of food when food becomes available.
Pim Van Der Harst - One of the best experts on this subject based on the ideXlab platform.
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identifying genetic variants for heart rate variability in the Acetylcholine Pathway
PLOS ONE, 2014Co-Authors: Harriette Riese, Loretto M Munoz, Catharina A Hartman, Xiuhua Ding, Albertine J Oldehinkel, Arie M Van Roon, Peter J Van Der Most, Joop D Lefrandt, Ron T Gansevoort, Pim Van Der HarstAbstract:Heart rate variability is an important risk factor for cardiovascular disease and all-cause mortality. The Acetylcholine Pathway plays a key role in explaining heart rate variability in humans. We assessed whether 443 genotyped and imputed common genetic variants in eight key genes (CHAT, SLC18A3, SLC5A7, CHRNB4, CHRNA3, CHRNA, CHRM2 and ACHE) of the Acetylcholine Pathway were associated with variation in an established measure of heart rate variability reflecting parasympathetic control of the heart rhythm, the root mean square of successive differences (RMSSD) of normal RR intervals. The association was studied in a two stage design in individuals of European descent. First, analyses were performed in a discovery sample of four cohorts (n=3429, discovery stage). Second, findings were replicated in three independent cohorts (n=3311, replication stage), and finally the two stages were combined in a meta-analysis (n=6740). RMSSD data were obtained under resting conditions. After correction for multiple testing, none of the SNPs showed an association with RMSSD. In conclusion, no common genetic variants for heart rate variability were identified in the largest and most comprehensive candidate gene study on the Acetylcholine Pathway to date. Future gene finding efforts for RMSSD may want to focus on hypothesis free approaches such as the genome-wide association study.
