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Appears in Networks 3

In-Edges 11

complex(GO:"proteasome complex") regulates p(HGNC:RIC3) View Subject | View Object

Furthermore, the proteasome in- directly regulates synaptic transmission mediated by AChRs via regu- lation of RIC-3 [113]. PubMed:22040696

path(MESH:"Bipolar Disorder") negativeCorrelation act(p(HGNC:RIC3), ma(chap)) View Subject | View Object

Interestingly, levels of RIC-3 mRNA are elevat- ed in postmortem brains of individuals with bipolar disorder and schizophrenia [181], and a link has been suggested between defi- cient RIC-3 mediated chaperoning of an AChR subunit and individ- uals with bipolar disorder and psychotic symptoms [181]. PubMed:22040696

path(MESH:"Psychotic Disorders") negativeCorrelation act(p(HGNC:RIC3), ma(chap)) View Subject | View Object

Interestingly, levels of RIC-3 mRNA are elevat- ed in postmortem brains of individuals with bipolar disorder and schizophrenia [181], and a link has been suggested between defi- cient RIC-3 mediated chaperoning of an AChR subunit and individ- uals with bipolar disorder and psychotic symptoms [181]. PubMed:22040696

Out-Edges 16

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

Resistance to inhibitor of cholinesterase-3 (RIC-3) is required for nAChR function in C. elegans (Nguyen et al., 1995) PubMed:28445721

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

Whereas RIC-3 can enhance function of certain mammalian nAChRs, RIC-3 is not essential (Koperniak et al., 2013) PubMed:28445721

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

In C. elegans, RIC-3 protein is essential for nAChR function (Nguyen et al., 1995), and mammalian RIC-3 has modest and mixed effects on nAChRs (Halevi et al., 2003; Millar, 2008) PubMed:28445721

p(HGNC:RIC3) causesNoChange complex(a(CHEBI:epibatidine), a(MESH:"nicotinic receptor alpha3beta2")) View Subject | View Object

For alpha7 and alpha3beta2, RIC-3 did not enable detectable [3H]epibatidine binding, yet RIC-3 profoundly augmented the effects of NACHO on [3H]epibatidine binding to either receptor subtype (Figures 3A and S1A) PubMed:28445721

p(HGNC:RIC3) causesNoChange complex(a(CHEBI:epibatidine), a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

For alpha7 and alpha3beta2, RIC-3 did not enable detectable [3H]epibatidine binding, yet RIC-3 profoundly augmented the effects of NACHO on [3H]epibatidine binding to either receptor subtype (Figures 3A and S1A) PubMed:28445721

p(HGNC:RIC3) increases surf(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

As previously reported using fluorescently labeled alpha-bungarotoxin (Gu et al., 2016), NACHO enabled formation of assembled surface alpha7 receptors, and RIC-3 further enhanced this (Figures 3E and 3F) PubMed:28445721

act(p(HGNC:RIC3), ma(chap)) increases p(FPLX:CHRN) View Subject | View Object

More re- cently, the transmembrane protein resistant to inhibitors of cholines- terase (RIC-3), originally identified in Caenorhabditis elegans, has been classed as a much more selective chaperone of the AChR [71,107–112]. PubMed:22040696

p(HGNC:RIC3) increases act(p(FPLX:CHRN)) View Subject | View Object

Co-expression with RIC-3 was shown to be required for AChR ac- tivity in C. elegans body muscles and for enhanced AChR activity in Xenopus oocytes [110,112]. PubMed:22040696

act(p(HGNC:RIC3), ma(chap)) increases p(FPLX:CHRN) View Subject | View Object

Interestingly, levels of RIC-3 mRNA are elevat- ed in postmortem brains of individuals with bipolar disorder and schizophrenia [181], and a link has been suggested between defi- cient RIC-3 mediated chaperoning of an AChR subunit and individ- uals with bipolar disorder and psychotic symptoms [181]. PubMed:22040696

p(HGNC:RIC3) increases bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

In C. elegans, RIC-3 is necessary for synaptic transmission mediated by neuronal AChRs but not by other LGICs [71,77,109]. PubMed:22040696

p(HGNC:RIC3) decreases act(complex(p(HGNC:CHRNA3), p(HGNC:CHRNB4))) View Subject | View Object

In contrast, RIC-3 caused a marked inhibition of functional responses with hetero- meric α3β4 and α4β2 AChRs in Xenopus oocytes [109]. PubMed:22040696

p(HGNC:RIC3) decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

In contrast, RIC-3 caused a marked inhibition of functional responses with hetero- meric α3β4 and α4β2 AChRs in Xenopus oocytes [109]. PubMed:22040696

p(HGNC:RIC3) increases p(HGNC:CHRNA9) View Subject | View Object

Osman et al. [122] find that RIC-3 expression increases the total amount of α9 AChR in CL4 cells, supporting the view that RIC-3 regulates AChR trafficking by increasing the number of mature or correctly folded receptor subunits reaching the cell surface. PubMed:22040696

p(HGNC:RIC3) increases p(HGNC:CHRNA7) View Subject | View Object

It is noteworthy that RIC-3 has been shown to increase α7 AChR heterologous expression both in X. laevis oocytes and in HEK-293, CHO and SHE-P1 mammalian cell lines [66,71,77,107–112,119,125]. PubMed:22040696

act(p(HGNC:RIC3), ma(chap)) negativeCorrelation path(MESH:"Bipolar Disorder") View Subject | View Object

Interestingly, levels of RIC-3 mRNA are elevat- ed in postmortem brains of individuals with bipolar disorder and schizophrenia [181], and a link has been suggested between defi- cient RIC-3 mediated chaperoning of an AChR subunit and individ- uals with bipolar disorder and psychotic symptoms [181]. PubMed:22040696

act(p(HGNC:RIC3), ma(chap)) negativeCorrelation path(MESH:"Psychotic Disorders") View Subject | View Object

Interestingly, levels of RIC-3 mRNA are elevat- ed in postmortem brains of individuals with bipolar disorder and schizophrenia [181], and a link has been suggested between defi- cient RIC-3 mediated chaperoning of an AChR subunit and individ- uals with bipolar disorder and psychotic symptoms [181]. PubMed:22040696

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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.