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a(GO:"dendritic spine")

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Entity

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

Appears in Networks 5

Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

Activity-dependent neuroprotective protein deficiency models synaptic and developmental phenotypes of autism-like syndrome v1.0.0

The autism/neuroprotection-linked ADNP/NAP regulate the excitatory glutamatergic synapse v1.0.0

In-Edges 23

a(PUBCHEM:64627) increases a(GO:"dendritic spine") View Subject | View Object

Indeed, the reduced level of spines seen in proaggregant Tau transgenic slices are normalized when treated with 64627, whereas no significant changes are found in antiaggregant Tau transgenic slices or littermate controls (Fig. 5 A and B) PubMed:27671637

Appears in Networks:

composite(a(PUBCHEM:64627), p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del"))) causesNoChange a(GO:"dendritic spine") View Subject | View Object

Indeed, the reduced level of spines seen in proaggregant Tau transgenic slices are normalized when treated with 64627, whereas no significant changes are found in antiaggregant Tau transgenic slices or littermate controls (Fig. 5 A and B) PubMed:27671637

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) causesNoChange a(GO:"dendritic spine") View Subject | View Object

Proaggregant Tau transgenic slices showed a significant reduction of spines compared with littermate control slices, whereas spine density of antiaggregant Tau transgenic slices was similar to controls (Fig. 3 A and B) PubMed:27671637

Appears in Networks:

composite(a(PUBCHEM:64627), p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del"))) increases a(GO:"dendritic spine") View Subject | View Object

Indeed, the reduced level of spines seen in proaggregant Tau transgenic slices are normalized when treated with 64627, whereas no significant changes are found in antiaggregant Tau transgenic slices or littermate controls (Fig. 5 A and B) PubMed:27671637

Appears in Networks:

composite(a(PUBCHEM:64627), p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del"))) increases a(GO:"dendritic spine") View Subject | View Object

Having observed that 64627 restores presynaptic functioning (i.e., PPF, Fig. 4F), neuronal activity (induction of Fos, Fig. 4D), and dendritic spine levels in proaggregant Tau transgenic organotypic slices (Fig. 5 A and B), we tested whether we could restore long-term spatial memory in proaggregant Tau transgenic mice as well PubMed:27671637

Appears in Networks:
Annotations
MeSH
Mitochondria

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) negativeCorrelation a(GO:"dendritic spine") View Subject | View Object

We also observed that Tau missorts into a subgroup of proximal dendrites, which correlates with a dramatic spine loss in the affected dendrites (Fig. S2 C and F) PubMed:27671637

Appears in Networks:
Annotations
MeSH
Dendrites

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) decreases a(GO:"dendritic spine") View Subject | View Object

Proaggregant Tau transgenic slices showed a significant reduction of spines compared with littermate control slices, whereas spine density of antiaggregant Tau transgenic slices was similar to controls (Fig. 3 A and B) PubMed:27671637

Appears in Networks:

p(HGNC:HDAC3) decreases a(GO:"dendritic spine") View Subject | View Object

HDAC3 overexpression in the hippocampus increases Aß levels, activates microglia, and decreases dendritic spine density in 6-month-old APP/PS1 mice. PubMed:28771976

Appears in Networks:
Annotations
Uberon
hippocampal formation

p(HGNC:MARK4) negativeCorrelation a(GO:"dendritic spine") View Subject | View Object

Overexpression of MARK4 led to tau hyperphosphorylation, reduced expression of synaptic markers, and loss of dendritic spines and synapses, phenotypes also observed after Aβ treatment. Importantly, expression of a non-phosphorylatable form of tau with the PAR-1/MARK site mutated blocked the synaptic toxicity induced by MARK4 overexpression or Aβ treatment. To probe the involvement of endogenous MARK kinases in mediating the synaptic toxicity of Aβ, we employed a peptide inhibitor capable of effectively and specifically inhibiting the activities of all PAR-1/MARK family members. This inhibitor abrogated the toxic effects of Aβ oligomers on dendritic spines and synapses as assayed at the morphological and electrophysiological levels. PubMed:22156579

Appears in Networks:
Annotations
Uberon
hippocampal formation

p(MGI:Mapt, pmod(Ph, Ser, 262)) decreases a(GO:"dendritic spine") View Subject | View Object

Direct interaction of DAPK1 with Tau causes spine loss and subsequently neuronal death. DAPK1 phosphorylates Tau protein at Ser262 (pS(262)) in cortical neurons of stroke mice. PubMed:25995053

Appears in Networks:
Annotations
Uberon
cerebral cortex
MeSH
Stroke

p(RGD:Cdk5r2) positiveCorrelation a(GO:"dendritic spine") View Subject | View Object

p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169

Appears in Networks:

p(HGNC:DPYSL2) regulates a(GO:"dendritic spine") View Subject | View Object

In line with this, the dendritic spine-regulating activity of CRMP2 is under the control of the cyclin-dependent kinase 5 (CDK5) PubMed:30061532

Appears in Networks:

p(HGNC:CDK5) positiveCorrelation a(GO:"dendritic spine") View Subject | View Object

Both administration of amphetamines and stimulation of D1R induce a significant increase of CDK5 gene expression and protein levels, which, at molecular level, associates with increased dendritic spine density and hyper-phosphorylation of the cytoskeletal tau protein PubMed:30061532

Appears in Networks:

a(PUBCHEM:9832404) increases a(GO:"dendritic spine") View Subject | View Object

The measurements showed similar patterns in both tested brain areas, with Adnp deficiency resulting in substantial decreases in spine density (male and female mice) and increases in PSD95-asymmetric shaft synapses (males only, as indicated by increased localization of PSD95 in dendritic shafts rather than spines), which were all rescued by NAP treatment. PubMed:30106381

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Cerebral Cortex
MeSH
Pyramidal Cells
Gender
Male
Gender
Female

a(PUBCHEM:9832404) increases a(GO:"dendritic spine") View Subject | View Object

In hippocampal CA1 pyramidal cells, all dendritic spine subtypes were reduced in the Adnp+/– mice, except for the thin spines observed in males. The spine loss was rescued by NAP treatment, except for the stubby spines seen in males (Supplemental Figure 1). PubMed:30106381

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Pyramidal Cells
Gender
Male
Gender
Female

a(PUBCHEM:9832404) increases a(GO:"dendritic spine") View Subject | View Object

Supplemental Figure 2 shows the cortical spine data indicating a significant genotype effect (P < 0.01) and NAP rescue for all subtypes in males (P < 0.05). PubMed:30106381

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
Gender
Male

composite(a(PUBCHEM:9832404), p(HGNC:ADNP, pmod(MESH:Haploinsufficiency))) decreases a(GO:"dendritic spine") View Subject | View Object

Specifically, in Adnp+/+ male mice, we found that NAP treatment reduced hippocampal stubby, thin, and total spine densities (Supplemental Figure 3, P < 0.05) as well as cortical mushroom, stubby, and total densities (Supplemental Figure 4, P < 0.05). PubMed:30106381

Appears in Networks:
Annotations
MeSH
Hippocampus
Gender
Male

p(HGNC:ADNP, pmod(MESH:Haploinsufficiency)) decreases a(GO:"dendritic spine") View Subject | View Object

The measurements showed similar patterns in both tested brain areas, with Adnp deficiency resulting in substantial decreases in spine density (male and female mice) and increases in PSD95-asymmetric shaft synapses (males only, as indicated by increased localization of PSD95 in dendritic shafts rather than spines), which were all rescued by NAP treatment. PubMed:30106381

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Cerebral Cortex
MeSH
Pyramidal Cells
Gender
Male
Gender
Female

p(HGNC:ADNP, pmod(MESH:Haploinsufficiency)) decreases a(GO:"dendritic spine") View Subject | View Object

Closer inspection suggested a more severe Adnp+/– genotype effect on total spine density in the male cortex compared with the hippocampus (Figure 1A, –1.56-fold reduction compared with Figure 2A, –1.83-fold reduction compared with the Adnp+/+ genotype). PubMed:30106381

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
Gender
Male

p(HGNC:ADNP, pmod(MESH:Haploinsufficiency)) decreases a(GO:"dendritic spine") View Subject | View Object

In hippocampal CA1 pyramidal cells, all dendritic spine subtypes were reduced in the Adnp+/– mice, except for the thin spines observed in males. The spine loss was rescued by NAP treatment, except for the stubby spines seen in males (Supplemental Figure 1). PubMed:30106381

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Pyramidal Cells
Gender
Male
Gender
Female

p(HGNC:ADNP, pmod(MESH:Haploinsufficiency)) decreases a(GO:"dendritic spine") View Subject | View Object

Supplemental Figure 2 shows the cortical spine data indicating a significant genotype effect (P < 0.01) and NAP rescue for all subtypes in males (P < 0.05). PubMed:30106381

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
Gender
Male

p(HGNC:ADNP, pmod(MESH:Haploinsufficiency)) decreases a(GO:"dendritic spine") View Subject | View Object

Further sex comparisons revealed differences in excitatory synapse numbers, with the Adnp+/– male mice showing significantly reduced hippocampal spine density, coupled with increased immature pathologic excitatory shaft synapses compared with Adnp+/– female mice (P < 0.01, Supplemental Table 2) PubMed:30106381

Appears in Networks:
Annotations
MeSH
Hippocampus
Gender
Male

p(HGNC:ADNP) increases a(GO:"dendritic spine") View Subject | View Object

Also, as our previous experiments, labeling dendritic spines in vivo, showed reduction in spine density in the hippocampus and the cortex as a consequence of Adnp deficiency and protection by NAP injection, we now sought to determine possible genotype/treatment/sex effects on the vesicular glutamate transporter VGLUT1 PubMed:30664622

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

Out-Edges 4

a(GO:"dendritic spine") negativeCorrelation p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) View Subject | View Object

We also observed that Tau missorts into a subgroup of proximal dendrites, which correlates with a dramatic spine loss in the affected dendrites (Fig. S2 C and F) PubMed:27671637

Appears in Networks:
Annotations
MeSH
Dendrites

a(GO:"dendritic spine") positiveCorrelation p(RGD:Cdk5r2) View Subject | View Object

p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169

Appears in Networks:

a(GO:"dendritic spine") negativeCorrelation p(HGNC:MARK4) View Subject | View Object

Overexpression of MARK4 led to tau hyperphosphorylation, reduced expression of synaptic markers, and loss of dendritic spines and synapses, phenotypes also observed after Aβ treatment. Importantly, expression of a non-phosphorylatable form of tau with the PAR-1/MARK site mutated blocked the synaptic toxicity induced by MARK4 overexpression or Aβ treatment. To probe the involvement of endogenous MARK kinases in mediating the synaptic toxicity of Aβ, we employed a peptide inhibitor capable of effectively and specifically inhibiting the activities of all PAR-1/MARK family members. This inhibitor abrogated the toxic effects of Aβ oligomers on dendritic spines and synapses as assayed at the morphological and electrophysiological levels. PubMed:22156579

Appears in Networks:
Annotations
Uberon
hippocampal formation

a(GO:"dendritic spine") positiveCorrelation p(HGNC:CDK5) View Subject | View Object

Both administration of amphetamines and stimulation of D1R induce a significant increase of CDK5 gene expression and protein levels, which, at molecular level, associates with increased dendritic spine density and hyper-phosphorylation of the cytoskeletal tau protein PubMed:30061532

Appears in Networks:

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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.