a(MESH:"Receptors, N-Methyl-D-Aspartate")
On the other hand, stimulation of Gαq coupled muscarinic receptors generates intracellular second messengers that can facilitate N-methyl-D-aspartate (NMDA) currents PubMed:26813123
On the other hand, stimulation of Gαq coupled muscarinic receptors generates intracellular second messengers that can facilitate N-methyl-D-aspartate (NMDA) currents PubMed:26813123
On the other hand, stimulation of Gαq coupled muscarinic receptors generates intracellular second messengers that can facilitate N-methyl-D-aspartate (NMDA) currents PubMed:26813123
In synapses, the projection domain of tau interacts with protein kinase Fyn (plays an important role during myelination [75]), postsynaptic density protein 95 (PSD-95) [76], and N-methyl-D-aspartate receptors (NMDAR). PubMed:26751493
PP2A enzymes can also associate with protein kinases that have been linked to AD, such as glycogen synthase kinase 3β (GSK3β) and cyclin-dependent kinase 5 (cdk5; Plattner et al.,2006), and neuronal receptors, e.g., the NMDA receptor (Chan and Sucher, 2001) and the metabotropic glutamate receptor 5 (Mao et al., 2005; Arif et al., 2014). PubMed:24653673
Glutamate induced stimulation of cerebellar granule cells via the N-methyl-D-aspartate (NMDA) receptor activate p65:p50 dimers and enhance transactivation of pro-apoptotic factors PubMed:25652642
There are reports showing that the protein and mRNA levels of KPI-containing APP isoforms are elevated in AD brain and associated with increased Ab deposition [9]; and prolonged activation of extrasynaptic NMDA receptor in neurons can shift APP expression from APP695 to KPI-containing APP isoforms, accompanied with increased production of Ab [10] PubMed:21214928
There are reports showing that the protein and mRNA levels of KPI-containing APP isoforms are elevated in AD brain and associated with increased Ab deposition [9]; and prolonged activation of extrasynaptic NMDA receptor in neurons can shift APP expression from APP695 to KPI-containing APP isoforms, accompanied with increased production of Ab [10] PubMed:21214928
There are reports showing that the protein and mRNA levels of KPI-containing APP isoforms are elevated in AD brain and associated with increased Ab deposition [9]; and prolonged activation of extrasynaptic NMDA receptor in neurons can shift APP expression from APP695 to KPI-containing APP isoforms, accompanied with increased production of Ab [10] PubMed:21214928
The levels of APP isoforms with a KPI domain seem to be elevated in patients with AD (Menendez- Gonzalez et al. 2005) and a splicing shift in neurons from APP695 to KPI-containing APP isoforms, along with increased Abeta generation, is observed when the NMDA receptor is activated (Bordji et al. 2010) PubMed:22122372
The levels of APP isoforms with a KPI domain seem to be elevated in patients with AD (Menendez- Gonzalez et al. 2005) and a splicing shift in neurons from APP695 to KPI-containing APP isoforms, along with increased Abeta generation, is observed when the NMDA receptor is activated (Bordji et al. 2010) PubMed:22122372
The levels of APP isoforms with a KPI domain seem to be elevated in patients with AD (Menendez- Gonzalez et al. 2005) and a splicing shift in neurons from APP695 to KPI-containing APP isoforms, along with increased Abeta generation, is observed when the NMDA receptor is activated (Bordji et al. 2010) PubMed:22122372
The incubation with S 24795 was able to normalize Ca++ influx mediated by both alpha7 nAChR and NMDAR (Wang et al., 2009, 2010) PubMed:25514383
In synapses, the projection domain of tau interacts with protein kinase Fyn (plays an important role during myelination [75]), postsynaptic density protein 95 (PSD-95) [76], and N-methyl-D-aspartate receptors (NMDAR). PubMed:26751493
CaMKs functionally link NMDA (N-methyl-d-aspartate) receptors to Rac1 activation via the phosphorylation of specific guanine nucleotide exchange factors (GEFs) such as Kalirin-7, TIAM1 and β-PIX PubMed:27796283
CaMKs functionally link NMDA (N-methyl-d-aspartate) receptors to Rac1 activation via the phosphorylation of specific guanine nucleotide exchange factors (GEFs) such as Kalirin-7, TIAM1 and β-PIX PubMed:27796283
Hence, LTD-inducing NMDA receptor activation leads to an increase in tau phosphorylation at sites PHF-1, AT180, as well as AT8 and to a reduction at AT100. PubMed:22833681
Hence, LTD-inducing NMDA receptor activation leads to an increase in tau phosphorylation at sites PHF-1, AT180, as well as AT8 and to a reduction at AT100. PubMed:22833681
Hence, LTD-inducing NMDA receptor activation leads to an increase in tau phosphorylation at sites PHF-1, AT180, as well as AT8 and to a reduction at AT100. PubMed:22833681
Hence, LTD-inducing NMDA receptor activation leads to an increase in tau phosphorylation at sites PHF-1, AT180, as well as AT8 and to a reduction at AT100. PubMed:22833681
PP2A enzymes can also associate with protein kinases that have been linked to AD, such as glycogen synthase kinase 3β (GSK3β) and cyclin-dependent kinase 5 (cdk5; Plattner et al.,2006), and neuronal receptors, e.g., the NMDA receptor (Chan and Sucher, 2001) and the metabotropic glutamate receptor 5 (Mao et al., 2005; Arif et al., 2014). PubMed:24653673
The molecular mechanism underlying constitutive activation of NF-κB by glutamate-induced excitatory synaptic neurotransmission has been ascribed to NMDA receptor mediated Ca2+ influx and subsequent activation of CaMKII PubMed:28745240
The molecular mechanism underlying constitutive activation of NF-κB by glutamate-induced excitatory synaptic neurotransmission has been ascribed to NMDA receptor mediated Ca2+ influx and subsequent activation of CaMKII PubMed:28745240
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.