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Appears in Networks 6

In-Edges 19

composite(p(HGNC:APP), p(HGNC:CNTN2)) decreases bp(GO:neurogenesis) View Subject | View Object

Finally, a recent study reported a surprising twist, viz. that APP in conjunction with TAG1, a molecule found in the outer plasma membrane, and presenilins act to suppress neurogenesis. PubMed:18650430

a(CHEBI:acetylcholine) increases bp(GO:neurogenesis) View Subject | View Object

Recent evidences also suggest the involvement of ACh in adult neurogenesis PubMed:26813123

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) increases bp(GO:neurogenesis) View Subject | View Object

Thus, pro-aggregant TauRDΔK causes neurodegeneration, whereas anti-aggregant TauRDΔKPP leads to neurogenesis, even in regions outside the DG PubMed:29202785

act(p(HGNC:CDK5)) negativeCorrelation bp(GO:neurogenesis) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

act(p(HGNC:GSK3B)) negativeCorrelation bp(GO:neurogenesis) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

act(p(FPLX:ERK)) negativeCorrelation bp(GO:neurogenesis) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

p(HGNC:MAPT) association bp(GO:neurogenesis) View Subject | View Object

It is not clear whether the discrepancy between these results is due to the differences between the knockout mouse lines; nevertheless, both papers point to some involvement of tau in neurogenesis PubMed:26631930

p(HGNC:MAPT) increases bp(GO:neurogenesis) View Subject | View Object

In addition, as tau is involved in multiple novel functions, including iron transport, neurogenesis, LTD and neuronal DNA protection (as discussed above), the loss of function of tau may also lead to neurodegeneration via impairment of these processes. PubMed:26631930

a(CHEBI:"nitric oxide") decreases bp(GO:neurogenesis) View Subject | View Object

Furthermore, nitric oxide (NO), a well characterized repressor of NF-κB activation and signaling [174, 175], causes a mitigation in neurogenesis PubMed:28745240

a(CHEBI:"reactive oxygen species") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

a(CHEBI:"sphingosine 1-phosphate") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

bp(GO:"axon guidance") increases bp(GO:neurogenesis) View Subject | View Object

NF-κB also plays a vital role in axon guidance subsequent to neurogenesis and axon growth in response to neurotrophins, resulting in the integration of the nascent neurons PubMed:28745240

act(complex(GO:"NF-kappaB complex")) increases bp(GO:neurogenesis) View Subject | View Object

The trophic factors that evoke proliferation of NPC by inducing activation of NF-κB include epidermal growth factor (EGF) [155-161], basic fibroblast growth factor (bFGF) [155-161], vascular endothelial growth factor (VEGF) [162], tumor necrosis factor α (TNFα) [163], and erythropoietin (EPO) PubMed:28745240

act(complex(GO:"NF-kappaB complex")) increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

act(complex(GO:"NF-kappaB complex")) increases bp(GO:neurogenesis) View Subject | View Object

NF-κB also plays a vital role in axon guidance subsequent to neurogenesis and axon growth in response to neurotrophins, resulting in the integration of the nascent neurons PubMed:28745240

p(HBP:"sAPP-alpha") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

path(MESH:"Brain Injuries, Traumatic") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

path(MESH:"Cerebral Infarction") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

path(MESH:Hypoxia) increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

Out-Edges 4

bp(GO:neurogenesis) negativeCorrelation act(p(HGNC:GSK3B)) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

bp(GO:neurogenesis) negativeCorrelation act(p(HGNC:CDK5)) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

bp(GO:neurogenesis) negativeCorrelation act(p(FPLX:ERK)) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

bp(GO:neurogenesis) association p(HGNC:MAPT) View Subject | View Object

It is not clear whether the discrepancy between these results is due to the differences between the knockout mouse lines; nevertheless, both papers point to some involvement of tau in neurogenesis PubMed:26631930

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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.