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Entity

Name
calcium-mediated signaling
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 4

In-Edges 12

act(a(CHEBI:"amyloid-beta")) association bp(GO:"calcium-mediated signaling") View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

a(CHEBI:nicotine) association bp(GO:"calcium-mediated signaling") View Subject | View Object

Nicotine protects PC12 cells from cell death resulting from serum depletion through a mechanism that depends upon the function of IP3 receptors, L-type calcium channels, ryanodine receptors, and ERK, suggesting that the protective effect of nicotine is mediated by calcium signaling pathways (Ren et al., 2005). PubMed:19293145

bp(MESH:Neuroprotection) association bp(GO:"calcium-mediated signaling") View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

act(p(HGNC:CHRNA7)) association bp(GO:"calcium-mediated signaling") View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

composite(p(HGNC:JAK2), p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) association bp(GO:"calcium-mediated signaling") View Subject | View Object

JAK-2, also implicated in the neuroprotective pathway, may play a role in linking nAChR action with calcium signaling, because JAK-2 phosphorylates inositol 1,4,5-triphosphate receptors through its activation of FYN (Wallace et al., 2005). PubMed:19293145

p(HGNC:CHRNA7, var("p.345A"), var("p.346A"), var("p.347A"), var("p.348A")) decreases bp(GO:"calcium-mediated signaling") View Subject | View Object

These findings in N2a cells are consistent with data from PC12 cells and suggest that α7345–348A nAChR expression impairs nAChR calcium signaling. PubMed:26088141

a(CHEBI:nifedipine) increases bp(GO:"calcium-mediated signaling") View Subject | View Object

As shown in Fig. 5, A–C, nifedipine was found to decrease the peak calcium response to choline in PC12 cells (peak: 795.00% ΔF/Fθ ± 107.1%) by 56.94% (p = 0.003), whereas prolonging the duration of the choline-induced calcium transient (AUC: 749.50% ΔF/Fθ2 × s ± 64.02%) in the same cell. PubMed:26088141

a(CHEBI:nifedipine) causesNoChange bp(GO:"calcium-mediated signaling") View Subject | View Object

In α7345–348A nAChR expressing cells, nifedipine had no effect on the peak or the duration of the calcium transient (peak: 957.00% ΔF/Fθ ± 252.2%; AUC: 333.33% ΔF/Fθ2 × s ± 91.53%) relative to choline treatment alone (Fig. 5, A–C). The findings suggest that choline-induced calcium responses in PC12 cells involve the activity of VGCC (37, 38). PubMed:26088141

a(MESH:"xestospongin C") decreases bp(GO:"calcium-mediated signaling") View Subject | View Object

We confirmed the involvement of IP3Rs in choline-induced calcium transients at the GC of PC12 cells. Cells were preincubated with the IP3R blocker xestospongin C (1 μM) prior to imaging. As shown in Fig. 7, A–C, pretreatment with xestospongin C reduced the α7 nAChR calcium response peak by 46.82% in α7 cells (peak: 1308.43% ΔF/Fθ ± −238.13%; + xestospongin C = 695.80% ΔF/Fθ ± 101.46%). PubMed:26088141

a(MESH:Barium) causesNoChange bp(GO:"calcium-mediated signaling") View Subject | View Object

As shown in Fig. 5, A–C, barium replacement had little to no effect on the peak and total calcium transient observed in α7 (peak: 1474.83% ΔF/Fθ ± 162.00%; AUC: 693.5% ΔF/Fθ2 × s ± 154.15%) and α7345–348A expressing cells (peak: 794% ΔF/Fθ ± 81.36%; AUC: 543.5% ΔF/Fθ2 × s ± 89.59%). PubMed:26088141

p(FPLX:HSP90) association bp(GO:"calcium-mediated signaling") View Subject | View Object

Accordingly, Hsp90 affects many key cellular processes, including cell cycle progression, steroid signaling, calcium signaling, protein trafficking, protein secretion, the immune re- sponse, and the heat shock response (HSR) (45, 48, 82). PubMed:23746257

g(HGNC:"IQCJ-SCHIP1") increases bp(GO:"calcium-mediated signaling") View Subject | View Object

In the 3-month-old hippocampi (Figure 4B), we found significant sex-dependent changes for Adnp+/– gene regulation and NAP rescue in the following genes in male mice: (a) apolipoprotein E (Apoe), the lead gene for Alzheimer’s disease risk, which was shown before to be a major gene regulated by ADNP (10, 13); (b) Gm21949, which is suggested to play a role in calcium-mediated responses, action potential conduction in myelinated cells, and axonal outgrowth and guidance (6); (c) lipase A (Lipa), which is related to lipid metabolism and was previously shown to be regulated by the Adnp genotype in mice (3); (d) autism-associated neuroligin 2 (Nlgn2), a postsynaptic membrane cell adhesion protein that mediates the formation and maintenance of synapses between neurons (12); (e) paired box protein 6 (Pax6), a key regulator in glutamatergic neuronal differentiation (38) and cortical development (39), which was shown before by us to be regulated by ADNP (complete knockout of Adnp rendered Pax6 expression undetectable in the brain primordium, contrasting with increased expression in Adnp+/– embryos [ref. 1] and in subcortical brain domains of 2-month-old male Adnp+/– mice [ref. 3]); and (f) Wolframin endoplasmic reticulum transmembrane glycoprotein (Wfs1), which is associated with neurodegeneration and cellular calcium homeostasis regulation and was previously shown to be regulated by NAP (34). PubMed:30106381

Out-Edges 6

bp(GO:"calcium-mediated signaling") association act(a(CHEBI:"amyloid-beta")) View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

bp(GO:"calcium-mediated signaling") association bp(MESH:Neuroprotection) View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

bp(GO:"calcium-mediated signaling") association act(p(HGNC:CHRNA7)) View Subject | View Object

Calcium signaling pathways are involved both in the toxic action of Abeta and in the protection against that toxicity offered by nicotinic ligands. Given that alpha7 homomeric nAChRs are much more permeable to calcium ions than are most other nAChRs (Bertrand et al., 1993), it is to be expected that nicotinic neuroprotection mediated by nAChRs, notably alpha7, would depend upon the activation of calcium signaling pathways. ABT-418 is a nicotinic agonist that protects primary rat cortical neurons from glutamate toxicity through its activation of alpha7 nAChRs, and this is blocked when calcium is removed from the extracellular medium (Donnelly-Roberts et al., 1996). PubMed:19293145

bp(GO:"calcium-mediated signaling") association a(CHEBI:nicotine) View Subject | View Object

Nicotine protects PC12 cells from cell death resulting from serum depletion through a mechanism that depends upon the function of IP3 receptors, L-type calcium channels, ryanodine receptors, and ERK, suggesting that the protective effect of nicotine is mediated by calcium signaling pathways (Ren et al., 2005). PubMed:19293145

bp(GO:"calcium-mediated signaling") association composite(p(HGNC:JAK2), p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) View Subject | View Object

JAK-2, also implicated in the neuroprotective pathway, may play a role in linking nAChR action with calcium signaling, because JAK-2 phosphorylates inositol 1,4,5-triphosphate receptors through its activation of FYN (Wallace et al., 2005). PubMed:19293145

bp(GO:"calcium-mediated signaling") association p(FPLX:HSP90) View Subject | View Object

Accordingly, Hsp90 affects many key cellular processes, including cell cycle progression, steroid signaling, calcium signaling, protein trafficking, protein secretion, the immune re- sponse, and the heat shock response (HSR) (45, 48, 82). PubMed:23746257

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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.