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Appears in Networks 2

Tau Biochemistry v1.2.5

Tau Biochemistry Section of NESTOR

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 7

a(HBP:"cerebral cortex") positiveCorrelation p(HBP:RAC1b) View Subject | View Object

Because we also found Rac1b-positive neurons in the AD cortex, it will be interesting to determine whether these perikarya display a similar gene profile to that found in the NB cholinergic neurons. PubMed:22142809

Appears in Networks:
Annotations
Uberon
cerebral cortex
Disease Ontology (DO)
Alzheimer's disease
MeSH
Alzheimer Disease

p(HGNC:CAV2) negativeCorrelation p(HBP:RAC1b) View Subject | View Object

Furthermore, single-cell gene expression profiling with custom-designed microarrays showed down-regulation of caveolin 2, GNB4, and lipase A in AD Rac1b-positive/p75NTR-labeled NB neurons compared with Rac1b-negative/p75NTRpositive perikarya in NCI. These proteins are involved in Rac1 pathway/cell cycle progression and lipid metabolism. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HGNC:GNB4) negativeCorrelation p(HBP:RAC1b) View Subject | View Object

Furthermore, single-cell gene expression profiling with custom-designed microarrays showed down-regulation of caveolin 2, GNB4, and lipase A in AD Rac1b-positive/p75NTR-labeled NB neurons compared with Rac1b-negative/p75NTRpositive perikarya in NCI. These proteins are involved in Rac1 pathway/cell cycle progression and lipid metabolism. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HGNC:LIPA) negativeCorrelation p(HBP:RAC1b) View Subject | View Object

Furthermore, single-cell gene expression profiling with custom-designed microarrays showed down-regulation of caveolin 2, GNB4, and lipase A in AD Rac1b-positive/p75NTR-labeled NB neurons compared with Rac1b-negative/p75NTRpositive perikarya in NCI. These proteins are involved in Rac1 pathway/cell cycle progression and lipid metabolism. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HGNC:NGFR) association p(HBP:RAC1b) View Subject | View Object

CBF tissues harvested from people who died with a clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment, or AD were immunolabeled for both p75NTR and Rac1b. Rac1b appeared as cytoplasmic diffuse granules, loosely aggregated filaments, or compact spheres in p75NTR-positive NB neurons. Although Rac1b colocalized with tau cytoskeletal markers, the percentage of p75NTR-immunoreactive neurons expressing Rac1b was significantly increased only in AD compared with both mild cognitive impairment and NCI. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

act(a(MESH:Neurons)) positiveCorrelation act(p(HBP:RAC1b)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

Appears in Networks:

p(MGI:Cdk5) negativeCorrelation act(p(HBP:RAC1b)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

Appears in Networks:

Out-Edges 8

p(HBP:RAC1b) association p(HGNC:NGFR) View Subject | View Object

CBF tissues harvested from people who died with a clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment, or AD were immunolabeled for both p75NTR and Rac1b. Rac1b appeared as cytoplasmic diffuse granules, loosely aggregated filaments, or compact spheres in p75NTR-positive NB neurons. Although Rac1b colocalized with tau cytoskeletal markers, the percentage of p75NTR-immunoreactive neurons expressing Rac1b was significantly increased only in AD compared with both mild cognitive impairment and NCI. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HBP:RAC1b) negativeCorrelation p(HGNC:CAV2) View Subject | View Object

Furthermore, single-cell gene expression profiling with custom-designed microarrays showed down-regulation of caveolin 2, GNB4, and lipase A in AD Rac1b-positive/p75NTR-labeled NB neurons compared with Rac1b-negative/p75NTRpositive perikarya in NCI. These proteins are involved in Rac1 pathway/cell cycle progression and lipid metabolism. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HBP:RAC1b) negativeCorrelation p(HGNC:GNB4) View Subject | View Object

Furthermore, single-cell gene expression profiling with custom-designed microarrays showed down-regulation of caveolin 2, GNB4, and lipase A in AD Rac1b-positive/p75NTR-labeled NB neurons compared with Rac1b-negative/p75NTRpositive perikarya in NCI. These proteins are involved in Rac1 pathway/cell cycle progression and lipid metabolism. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HBP:RAC1b) negativeCorrelation p(HGNC:LIPA) View Subject | View Object

Furthermore, single-cell gene expression profiling with custom-designed microarrays showed down-regulation of caveolin 2, GNB4, and lipase A in AD Rac1b-positive/p75NTR-labeled NB neurons compared with Rac1b-negative/p75NTRpositive perikarya in NCI. These proteins are involved in Rac1 pathway/cell cycle progression and lipid metabolism. PubMed:22142809

Appears in Networks:
Annotations
Uberon
basal nucleus of telencephalon
Cell Ontology (CL)
cholinergic neuron
Disease Ontology (DO)
Alzheimer's disease

p(HBP:RAC1b) positiveCorrelation a(HBP:"cerebral cortex") View Subject | View Object

Because we also found Rac1b-positive neurons in the AD cortex, it will be interesting to determine whether these perikarya display a similar gene profile to that found in the NB cholinergic neurons. PubMed:22142809

Appears in Networks:
Annotations
Uberon
cerebral cortex
Disease Ontology (DO)
Alzheimer's disease
MeSH
Alzheimer Disease

act(p(HBP:RAC1b)) negativeCorrelation p(MGI:Cdk5) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

Appears in Networks:

act(p(HBP:RAC1b)) positiveCorrelation act(a(MESH:Neurons)) View Subject | View Object

Our data showed that CDK5 knock down induced an increase in p35 protein levels and Rac activity in triple transgenic Alzheimer's mice, which correlated with the recovery of cognitive function; these findings confirm that increased p35 and active Rac are involved in neuroprotection. In summary, our data suggest that p35 acts as a mediator of Rho GTPase activity and contributes to the neuroprotection induced by CDK5 RNAi. PubMed:27087442

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.