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Appears in Networks 2

In-Edges 10

bp(GO:"neuron maturation") positiveCorrelation p(HGNC:LYNX1) View Subject | View Object

Neuronal maturation and loss of synaptic lability appear to be correlated with the onset of lynx1 expression PubMed:21482353

bp(GO:"synapse maturation") negativeCorrelation p(HGNC:LYNX1) View Subject | View Object

Neuronal maturation and loss of synaptic lability appear to be correlated with the onset of lynx1 expression PubMed:21482353

bp(GO:"synaptic transmission, cholinergic") association p(HGNC:LYNX1) View Subject | View Object

While genetic linkages of lynx family members to neurological disorders have not been found, evidence for cholinergic dysregulation has been linked to a lynx family member expressed in nonneuronal tissues and involved in human disease (Chimienti et al., 2003), and as such, alterations in lynx dosage may be useful in ameliorating cognitive decline associated with neuropsychiatric disorders. PubMed:21482353

p(FPLX:CHRN) regulates p(HGNC:LYNX1) View Subject | View Object

Abolishing receptor function through null mutations or pharmacological blockers of nAChRs abolished some of the gain-offunction phenotypes in lynx mouse models, indicating that nAChRs are necessary for the expression of lynx perturbations (Miwa et al., 2006) PubMed:21482353

path(MESH:"Cognitive Dysfunction") association p(HGNC:LYNX1) View Subject | View Object

While genetic linkages of lynx family members to neurological disorders have not been found, evidence for cholinergic dysregulation has been linked to a lynx family member expressed in nonneuronal tissues and involved in human disease (Chimienti et al., 2003), and as such, alterations in lynx dosage may be useful in ameliorating cognitive decline associated with neuropsychiatric disorders. PubMed:21482353

Out-Edges 12

p(HGNC:LYNX1) regulates act(p(FPLX:CHRN)) View Subject | View Object

Therefore, the evolutionary relationship between lynx modulators and the alpha-neurotoxins agrees with the view that lynx modulators govern critical control points in the pathway of nicotinic receptor signaling PubMed:21482353

p(HGNC:LYNX1) decreases act(p(FPLX:CHRN)) View Subject | View Object

Lynx1, the first discovered member of this family expressed in the brain (Miwa et al., 1999), has an overall inhibitory effect on nAChR function PubMed:21482353

p(HGNC:LYNX1) decreases act(p(FPLX:CHRN)) View Subject | View Object

Removal of the molecular brake provided by lynx proteins can lead to nicotinic receptor hypersensitivity—larger direct nicotinic responses, slowed desensitization kinetics (Miwa et al., 2006), and enhanced sensitivity of the EPSC frequency in the cortex to nicotine (Tekinay et al., 2009) PubMed:21482353

p(HGNC:LYNX1) regulates act(p(FPLX:CHRN)) View Subject | View Object

This indicates that lynx proteins exist, genetically, as upstream modulators of nicotinic receptor function and cholinergic signaling and can exert control over cholinergic-dependent processes PubMed:21482353

p(HGNC:LYNX1) decreases bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

Indeed, cholinergic enhancement (via cholinesterase inhibition) reopens the critical period for visual acuity in adult wild-type mice (Morishita et al., 2010), indicating that cellular mechanisms for robust plasticity are maintained in adulthood through the cholinergic system but are suppressed by the action of lynx. PubMed:21482353

p(HGNC:LYNX1) association bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

While genetic linkages of lynx family members to neurological disorders have not been found, evidence for cholinergic dysregulation has been linked to a lynx family member expressed in nonneuronal tissues and involved in human disease (Chimienti et al., 2003), and as such, alterations in lynx dosage may be useful in ameliorating cognitive decline associated with neuropsychiatric disorders. PubMed:21482353

p(HGNC:LYNX1) association path(MESH:"Cognitive Dysfunction") View Subject | View Object

While genetic linkages of lynx family members to neurological disorders have not been found, evidence for cholinergic dysregulation has been linked to a lynx family member expressed in nonneuronal tissues and involved in human disease (Chimienti et al., 2003), and as such, alterations in lynx dosage may be useful in ameliorating cognitive decline associated with neuropsychiatric disorders. PubMed:21482353

p(HGNC:LYNX1) positiveCorrelation bp(GO:"neuron maturation") View Subject | View Object

Neuronal maturation and loss of synaptic lability appear to be correlated with the onset of lynx1 expression PubMed:21482353

p(HGNC:LYNX1) negativeCorrelation bp(GO:"synapse maturation") View Subject | View Object

Neuronal maturation and loss of synaptic lability appear to be correlated with the onset of lynx1 expression PubMed:21482353

p(HGNC:LYNX1) regulates bp(GO:"generation of neurons") View Subject | View Object

Lynx1 upregulation during a critical neurodevelopmental period, the switch in the sign of GABAergic signaling, and coexpression of lynx with GABAergic subsets all indicate a possible role of lynx mediating the timing of such developmental transitions PubMed:21482353

p(HGNC:LYNX1) decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

These proteins include Lynx1, a glycophosphati- dylinositol- anchored membrane protein that can form a sta- ble complex, negatively regulates the responses of α4β2 and α7 nAChRs in heterologous systems and enhances the rate and extent of desensitisation of α4β2 nAChRs, thus acting as a molecular brake on nAChR function PubMed:28901280

p(HGNC:LYNX1) decreases act(p(HGNC:CHRNA7)) View Subject | View Object

These proteins include Lynx1, a glycophosphati- dylinositol- anchored membrane protein that can form a sta- ble complex, negatively regulates the responses of α4β2 and α7 nAChRs in heterologous systems and enhances the rate and extent of desensitisation of α4β2 nAChRs, thus acting as a molecular brake on nAChR function PubMed:28901280

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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.