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complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))

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Components

Appears in Networks 6

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

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

Chaperoning α7 neuronal nicotinic acetylcholine receptors v1.0.0

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

In-Edges 15

a(MESH:"Cell Line") regulates complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

All cell lines appeared to produce alpha4beta2 nAChRs, although at considerably variable levels relative to each other. Therefore, cell and receptor identity combine to collectively determine the efficiency of nAChR expression on the cell surface. PubMed:19126755

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Text Location
Review

composite(g(HGNC:CHRNA4), g(HGNC:CHRNB2)) increases complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

Only two of these cell lines expressed alpha7 nAChRs: GH4C1 cells expressed substantially greater numbers of surface receptors than did SH-EP1 cells, which exhibited poor assembly efficiency. PubMed:19126755

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Experimental Factor Ontology (EFO)
GH4-C1 cell
Text Location
Review

a(CHEBI:"amyloid-beta") increases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Abeta action on nAChRs depends on subunit composition; it has been reported to block alpha7, transiently potentiate alpha4beta2 before blocking, and to have no action on alpha3beta4 (Pym et al., 2005). However, in contrast to its reported transient enhancement when expressed in oocytes, an inhibition of alpha4beta2 has been reported when expressed in human SH-EP1 cells (Wu et al., 2004). PubMed:19293145

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a(CHEBI:"amyloid-beta") decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Abeta action on nAChRs depends on subunit composition; it has been reported to block alpha7, transiently potentiate alpha4beta2 before blocking, and to have no action on alpha3beta4 (Pym et al., 2005). However, in contrast to its reported transient enhancement when expressed in oocytes, an inhibition of alpha4beta2 has been reported when expressed in human SH-EP1 cells (Wu et al., 2004). PubMed:19293145

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a(CHEBI:"amyloid-beta") decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Again, despite numerous reports of a block of alpha7, one study indicated that Abeta failed to block alpha7, even though it blocked alpha4beta2, alpha2beta2 and alpha4alpha5beta2 receptors (Lamb et al., 2005). PubMed:19293145

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composite(a(CHEBI:nicotine), complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) hasComponent complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

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g(HGNC:APOE) causesNoChange complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

The APOE-epsilon4 gene-dose effect was also found to correlate with the loss of nAChR binding sites in patients with AD, as well as a reduced respon- siveness to the therapeutic AChE inhibitor tacrine (Poirier et al., 1995). Within an AD cohort, APOE-epsilon4 dose dependently correlates with higher losses of ChAT but not with losses in alpha4beta2 nAChRs (Lai et al., 2006). PubMed:19293145

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MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") decreases complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

A stereological approach, in which specific, identified regions of cortex were excised as a by-product of therapeutic surgery, revealed an approximately 50% decrease in the number of alpha7-containing neurons in the temporal cortices of patients with AD, without overall loss in neuron number (Banerjee et al., 2000). In addition to loss of neurons, there are reports of reduced expression of specific nAChR subtypes, particularly of alpha4beta2 and alpha7 subunits, in many brain areas in AD. PubMed:19293145

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MeSH
Neurons

path(MESH:"Alzheimer Disease") decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Binding studies using subtypeselective labeled ligands suggest that alpha4beta2 receptors are lost in brains from patients with AD (Warpman and Nordberg, 1995; Martin-Ruiz et al., 1999). Regions showing reduced binding levels include the frontal lobe and the temporal cortex (Lai et al., 2006). PubMed:19293145

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MeSH
Brain
MeSH
Frontal Lobe
MeSH
Temporal Lobe

a(MESH:"Dopaminergic Neurons") association complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

For example, as discussed above, at least five functional nAChR subtypes have been identified in dopaminergic terminals in the striatum: α4α6β2β3, α6β2β3 and α6β2, which have the highest sensitivity to nicotine, and α4β2 and α4α5β2, which are more numerous than the α6-containing subtypes, yet with lower affinity for nicotine105,106,204. PubMed:19721446

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MeSH
Corpus Striatum
Text Location
Review

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

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a(MESH:Nicotine) decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

α4β2* subtypes, in which the presence of different accessory subunits changes their pharmacological and biophysical properties, and their sensitivity to allosteric modulators and up-regulation by nicotine PubMed:28901280

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a(MESH:Nicotine) increases complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) View Subject | View Object

By activating the α4β2 receptors on inhibitory GABAergic inputs to the VTA or GABAergic interneurons, smoked concentrations of nicotine transiently increase the release of GABA and subse- quently depress it for about one hour PubMed:28901280

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Annotations
MeSH
GABAergic Neurons

a(MESH:Nicotine) decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82]. PubMed:28901280

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

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

Appears in Networks:
Annotations
MeSH
GABAergic Neurons

Out-Edges 4

complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) hasComponent p(HGNC:CHRNA4) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) hasComponent p(HGNC:CHRNB2) View Subject | View Object

Appears in Networks:

complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) increases a(HBP:"alpha-4 beta-2 nAChR") View Subject | View Object

This subunit commonly forms heteropentameric receptors in combination with the alpha4 subunit PubMed:25514383

Appears in Networks:

complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2)) association a(MESH:"Dopaminergic Neurons") View Subject | View Object

For example, as discussed above, at least five functional nAChR subtypes have been identified in dopaminergic terminals in the striatum: α4α6β2β3, α6β2β3 and α6β2, which have the highest sensitivity to nicotine, and α4β2 and α4α5β2, which are more numerous than the α6-containing subtypes, yet with lower affinity for nicotine105,106,204. PubMed:19721446

Appears in Networks:
Annotations
MeSH
Corpus Striatum
Text Location
Review

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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.