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Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

In-Edges 1

p(HGNC:CHRNA7) association a(CHEBI:clozapine) View Subject | View Object

However, the atypical antipsychotic drug clozapine normalizes auditory gating in DBA/2 mice — an effect which involves an alpha7 nAChR mechanism181. PubMed:19721446

Out-Edges 9

a(CHEBI:clozapine) increases bp(MESH:"Sensory Gating") View Subject | View Object

However, the atypical antipsychotic drug clozapine normalizes auditory gating in DBA/2 mice — an effect which involves an alpha7 nAChR mechanism181. PubMed:19721446

a(CHEBI:clozapine) association p(HGNC:CHRNA7) View Subject | View Object

However, the atypical antipsychotic drug clozapine normalizes auditory gating in DBA/2 mice — an effect which involves an alpha7 nAChR mechanism181. PubMed:19721446

a(CHEBI:clozapine) increases bp(GO:autophagy) View Subject | View Object

Recently, in vitro studies on the effects of second-generation, atypical antipsychotics demonstrated that sertindole and clozapine are potent autophagy inducers in both neuronal and non-neuronal cell lines PubMed:30061532

a(CHEBI:clozapine) increases bp(GO:autophagy) View Subject | View Object

Similar to pimozide, clozapine activates the autophagy process via the AMPK–ULK1–Beclin1 pathway, as evidenced by increased levels of autophagy markers (i.e., LC3-II and Atg5–Atg12 conjugate); increased phosphorylation of AMPK and its downstream substrates, namely ULK1 and beclin1; and an increased number of autophagosomes in the frontal cortex in clozapine-treated rats PubMed:30061532

a(CHEBI:clozapine) increases p(HGNC:PRKAA1, pmod(Ph)) View Subject | View Object

Similar to pimozide, clozapine activates the autophagy process via the AMPK–ULK1–Beclin1 pathway, as evidenced by increased levels of autophagy markers (i.e., LC3-II and Atg5–Atg12 conjugate); increased phosphorylation of AMPK and its downstream substrates, namely ULK1 and beclin1; and an increased number of autophagosomes in the frontal cortex in clozapine-treated rats PubMed:30061532

a(CHEBI:clozapine) increases p(HGNC:ULK1, pmod(Ph)) View Subject | View Object

Similar to pimozide, clozapine activates the autophagy process via the AMPK–ULK1–Beclin1 pathway, as evidenced by increased levels of autophagy markers (i.e., LC3-II and Atg5–Atg12 conjugate); increased phosphorylation of AMPK and its downstream substrates, namely ULK1 and beclin1; and an increased number of autophagosomes in the frontal cortex in clozapine-treated rats PubMed:30061532

a(CHEBI:clozapine) increases p(HGNC:BECN1, pmod(Ph)) View Subject | View Object

Similar to pimozide, clozapine activates the autophagy process via the AMPK–ULK1–Beclin1 pathway, as evidenced by increased levels of autophagy markers (i.e., LC3-II and Atg5–Atg12 conjugate); increased phosphorylation of AMPK and its downstream substrates, namely ULK1 and beclin1; and an increased number of autophagosomes in the frontal cortex in clozapine-treated rats PubMed:30061532

a(CHEBI:clozapine) increases a(GO:autophagosome) View Subject | View Object

Similar to pimozide, clozapine activates the autophagy process via the AMPK–ULK1–Beclin1 pathway, as evidenced by increased levels of autophagy markers (i.e., LC3-II and Atg5–Atg12 conjugate); increased phosphorylation of AMPK and its downstream substrates, namely ULK1 and beclin1; and an increased number of autophagosomes in the frontal cortex in clozapine-treated rats PubMed:30061532

a(CHEBI:clozapine) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

Chronic clozapine treatment (20 mg/kg/day) reduces Abeta deposition PubMed:30061532

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.