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In-Edges 3

path(HBP:Neurodegeneration) negativeCorrelation p(MGI:Chrnb2) View Subject | View Object

The importance of retaining the high-affinity nicotine binding sites to brain integrity has been demonstrated in studies of mice with a null mutation in the gene that encodes the beta2 nAChR subunit, a structural subunit of the high-affinity nicotine binding site (150, 184, 215, 311); these mice experience early onset neurodegeneration (528). PubMed:19126755

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Out-Edges 7

p(MGI:Chrnb2) negativeCorrelation path(HBP:Neurodegeneration) View Subject | View Object

The importance of retaining the high-affinity nicotine binding sites to brain integrity has been demonstrated in studies of mice with a null mutation in the gene that encodes the beta2 nAChR subunit, a structural subunit of the high-affinity nicotine binding site (150, 184, 215, 311); these mice experience early onset neurodegeneration (528). PubMed:19126755

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p(MGI:Chrnb2) regulates bp(MESH:Homeostasis) View Subject | View Object

The importance of beta2 in maintaining brain homeostasis during normal ageing was highlighted in the KO mouse for this subunit PubMed:25514383

p(MGI:Chrnb2) increases a(MESH:"Cerebral Cortex") View Subject | View Object

Aged beta2 null mutant mice have a thinner cortex compared to agematched wild-type controls (Zoli et al., 1999). This work should be pursued further as it indicates a “neurotrophic” action of beta2 receptor activation by endogenous ACh (Zanardi et al., 2007) PubMed:25514383

p(MGI:Chrnb2) increases path(MESH:Attention) View Subject | View Object

Null mutant beta2 mice were also tested to determine the role of this subunit in cognition. Guillem et al. (2011) showed that these mice exhibit an attention deficit which was restored by re-expression of this subunit with a lentiviral vector in the PFC PubMed:25514383

p(MGI:Chrnb2) increases bp(GO:cognition) View Subject | View Object

Null mutant beta2 mice were also tested to determine the role of this subunit in cognition. Guillem et al. (2011) showed that these mice exhibit an attention deficit which was restored by re-expression of this subunit with a lentiviral vector in the PFC PubMed:25514383

p(MGI:Chrnb2) decreases path(MESH:"Memory Disorders") View Subject | View Object

In the NPR task (7 months p.i.), the GFP-beta2 spent significantly more time exploring the novel compartment (p = 0.003; Fig. 4A), as well as APP-beta2 (p = 0.017; Fig. 4B). PubMed:27522251

p(MGI:Chrnb2) increases a(CHEBI:"amyloid-beta") View Subject | View Object

We observed intracellular Abeta staining in the polymorphic layer of the DG that was absent in GFP-beta2 (Fig. 8) PubMed:27522251

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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.