PubMed:21687501 JSONTXT

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":50,"end":59},"obj":"HP_0000716"}],"text":"Pharmacogenetics of antidepressants.\nUp to 60% of depressed patients do not respond completely to antidepressants (ADs) and up to 30% do not respond at all. Genetic factors contribute for about 50% of the AD response. During the recent years the possible influence of a set of candidate genes as genetic predictors of AD response efficacy was investigated by us and others. They include the cytochrome P450 superfamily, the P-glycoprotein (ABCB1), the tryptophan hydroxylase, the catechol-O-methyltransferase, the monoamine oxidase A, the serotonin transporter (5-HTTLPR), the norepinephrine transporter, the dopamine transporter, variants in the 5-hydroxytryptamine receptors (5-HT1A, 5-HT2A, 5-HT3A, 5-HT3B, and 5-HT6), adrenoreceptor beta-1 and alpha-2, the dopamine receptors (D2), the G protein beta 3 subunit, the corticotropin releasing hormone receptors (CRHR1 and CRHR2), the glucocorticoid receptors, the c-AMP response-element binding, and the brain-derived neurotrophic factor. Marginal associations were reported for angiotensin I converting enzyme, circadian locomotor output cycles kaput protein, glutamatergic system, nitric oxide synthase, and interleukin 1-beta gene. In conclusion, gene variants seem to influence human behavior, liability to disorders and treatment response. Nonetheless, gene × environment interactions have been hypothesized to modulate several of these effects."}

{"project":"NEUROSES","denotations":[{"id":"T1","span":{"begin":20,"end":35},"obj":"CHEBI_35469"},{"id":"T2","span":{"begin":98,"end":113},"obj":"CHEBI_35469"},{"id":"T3","span":{"begin":115,"end":118},"obj":"CHEBI_73344"},{"id":"T4","span":{"begin":229,"end":235},"obj":"PATO_0001484"},{"id":"T6","span":{"begin":426,"end":438},"obj":"CHEBI_17089"},{"id":"T7","span":{"begin":452,"end":462},"obj":"CHEBI_27897"},{"id":"T8","span":{"begin":452,"end":462},"obj":"CHEBI_16828"},{"id":"T9","span":{"begin":480,"end":488},"obj":"CHEBI_18135"},{"id":"T10","span":{"begin":514,"end":523},"obj":"CHEBI_63534"},{"id":"T11","span":{"begin":514,"end":523},"obj":"CHEBI_25375"},{"id":"T12","span":{"begin":539,"end":548},"obj":"CHEBI_350546"},{"id":"T13","span":{"begin":539,"end":548},"obj":"CHEBI_28790"},{"id":"T14","span":{"begin":647,"end":666},"obj":"CHEBI_28790"},{"id":"T15","span":{"begin":577,"end":591},"obj":"CHEBI_33569"},{"id":"T16","span":{"begin":577,"end":591},"obj":"CHEBI_18357"},{"id":"T17","span":{"begin":609,"end":617},"obj":"CHEBI_18243"},{"id":"T18","span":{"begin":761,"end":769},"obj":"CHEBI_18243"},{"id":"T19","span":{"begin":609,"end":617},"obj":"CHEBI_59905"},{"id":"T20","span":{"begin":761,"end":769},"obj":"CHEBI_59905"},{"id":"T21","span":{"begin":737,"end":741},"obj":"CHEBI_10545"},{"id":"T22","span":{"begin":800,"end":804},"obj":"CHEBI_10545"},{"id":"T23","span":{"begin":1175,"end":1179},"obj":"CHEBI_10545"},{"id":"T24","span":{"begin":748,"end":753},"obj":"PATO_0001344"},{"id":"T25","span":{"begin":748,"end":753},"obj":"CHEBI_30216"},{"id":"T26","span":{"begin":792,"end":799},"obj":"CHEBI_16541"},{"id":"T27","span":{"begin":1103,"end":1110},"obj":"CHEBI_16541"},{"id":"T28","span":{"begin":792,"end":799},"obj":"CHEBI_36080"},{"id":"T29","span":{"begin":1103,"end":1110},"obj":"CHEBI_36080"},{"id":"T31","span":{"begin":885,"end":899},"obj":"CHEBI_24261"},{"id":"T32","span":{"begin":917,"end":920},"obj":"CHEBI_28971"},{"id":"T33","span":{"begin":917,"end":920},"obj":"CHEBI_456215"},{"id":"T34","span":{"begin":917,"end":920},"obj":"CHEBI_16027"},{"id":"T35","span":{"begin":930,"end":937},"obj":"CHEBI_33250"}],"text":"Pharmacogenetics of antidepressants.\nUp to 60% of depressed patients do not respond completely to antidepressants (ADs) and up to 30% do not respond at all. Genetic factors contribute for about 50% of the AD response. During the recent years the possible influence of a set of candidate genes as genetic predictors of AD response efficacy was investigated by us and others. They include the cytochrome P450 superfamily, the P-glycoprotein (ABCB1), the tryptophan hydroxylase, the catechol-O-methyltransferase, the monoamine oxidase A, the serotonin transporter (5-HTTLPR), the norepinephrine transporter, the dopamine transporter, variants in the 5-hydroxytryptamine receptors (5-HT1A, 5-HT2A, 5-HT3A, 5-HT3B, and 5-HT6), adrenoreceptor beta-1 and alpha-2, the dopamine receptors (D2), the G protein beta 3 subunit, the corticotropin releasing hormone receptors (CRHR1 and CRHR2), the glucocorticoid receptors, the c-AMP response-element binding, and the brain-derived neurotrophic factor. Marginal associations were reported for angiotensin I converting enzyme, circadian locomotor output cycles kaput protein, glutamatergic system, nitric oxide synthase, and interleukin 1-beta gene. In conclusion, gene variants seem to influence human behavior, liability to disorders and treatment response. Nonetheless, gene × environment interactions have been hypothesized to modulate several of these effects."}

{"project":"Allie","denotations":[{"id":"SS1_21687501_1_0","span":{"begin":98,"end":113},"obj":"expanded"},{"id":"SS2_21687501_1_0","span":{"begin":115,"end":118},"obj":"abbr"}],"relations":[{"id":"AE1_21687501_1_0","pred":"abbreviatedTo","subj":"SS1_21687501_1_0","obj":"SS2_21687501_1_0"}],"text":"Pharmacogenetics of antidepressants.\nUp to 60% of depressed patients do not respond completely to antidepressants (ADs) and up to 30% do not respond at all. Genetic factors contribute for about 50% of the AD response. During the recent years the possible influence of a set of candidate genes as genetic predictors of AD response efficacy was investigated by us and others. They include the cytochrome P450 superfamily, the P-glycoprotein (ABCB1), the tryptophan hydroxylase, the catechol-O-methyltransferase, the monoamine oxidase A, the serotonin transporter (5-HTTLPR), the norepinephrine transporter, the dopamine transporter, variants in the 5-hydroxytryptamine receptors (5-HT1A, 5-HT2A, 5-HT3A, 5-HT3B, and 5-HT6), adrenoreceptor beta-1 and alpha-2, the dopamine receptors (D2), the G protein beta 3 subunit, the corticotropin releasing hormone receptors (CRHR1 and CRHR2), the glucocorticoid receptors, the c-AMP response-element binding, and the brain-derived neurotrophic factor. Marginal associations were reported for angiotensin I converting enzyme, circadian locomotor output cycles kaput protein, glutamatergic system, nitric oxide synthase, and interleukin 1-beta gene. In conclusion, gene variants seem to influence human behavior, liability to disorders and treatment response. Nonetheless, gene × environment interactions have been hypothesized to modulate several of these effects."}