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Appears in Networks 3

In-Edges 4

a(CHEBI:genistein) decreases p(HGNC:CHRNA7, pmod(Ph)) View Subject | View Object

Genistein enhances the amplitude of ACh responses when human alpha7 nAChRs are expressed in Xe- nopus laevis oocytes by inhibiting phosphorylation of the receptor in the intracellular loop (Charpantier et al., 2005; Grønlien et al., 2007) and shows similar actions on alpha7 nAChRs of rat hippocampal and supraoptic nucleus neurons as well as human SH-SY5Y cells (Charpantier et al., 2005). PubMed:19293145

a(CHEBI:genistein) decreases p(HGNC:CHRNA7, pmod(Ph)) View Subject | View Object

Dephosphorylation of the α7 receptor by genistein causes a significant increase of ACh-evoked responses without modifying the response time course or ACh sensitivity (71, 72). PubMed:17009926

act(p(FPLX:SRC), ma(kin)) increases p(HGNC:CHRNA7, pmod(Ph)) View Subject | View Object

Furthermore, Src-family kinases (SFKs) directly phosphorylate the cytoplasmic loop of α7 nAChRs in the plasma membrane. PubMed:17009926

Out-Edges 3

p(HGNC:CHRNA7, pmod(Ph)) decreases act(a(CHEBI:acetylcholine)) View Subject | View Object

Genistein enhances the amplitude of ACh responses when human alpha7 nAChRs are expressed in Xe- nopus laevis oocytes by inhibiting phosphorylation of the receptor in the intracellular loop (Charpantier et al., 2005; Grønlien et al., 2007) and shows similar actions on alpha7 nAChRs of rat hippocampal and supraoptic nucleus neurons as well as human SH-SY5Y cells (Charpantier et al., 2005). PubMed:19293145

p(HGNC:CHRNA7, pmod(Ph)) increases act(a(MESH:"Motor Endplate"), ma(GO:localization)) View Subject | View Object

In nAChRs, several phosphorylation sites (104) that control desensitization in mus- cle and 􏰀7-nAChR also contribute to end plate localization by agrin-induced tyrosine phosphorylation of the cytoskeletal protein 43K-rapsyn PubMed:23038257

p(HGNC:CHRNA7, pmod(Ph)) decreases act(p(HGNC:CHRNA7)) View Subject | View Object

Dephosphorylation of the α7 receptor by genistein causes a significant increase of ACh-evoked responses without modifying the response time course or ACh sensitivity (71, 72). PubMed:17009926

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.