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p(HGNC:NGF)

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Entity

Name
NGF
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

In-Edges 13

composite(p(HGNC:CHRNA7), p(HGNC:NGF)) hasComponent p(HGNC:NGF) View Subject | View Object

Appears in Networks:

bp(GO:"GO:0048485") association p(HGNC:NGF) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

bp(GO:"GO:0007269") association p(HGNC:NGF) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

bp(GO:"GO:0060384") association p(HGNC:NGF) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

complex(p(HGNC:NGF), p(HGNC:NGFR)) hasComponent p(HGNC:NGF) View Subject | View Object

Appears in Networks:

complex(p(HGNC:NGF), p(HGNC:NTRK1)) hasComponent p(HGNC:NGF) View Subject | View Object

Appears in Networks:

g(HGNC:NGF) directlyIncreases p(HGNC:NGF) View Subject | View Object

The ex vivo Phase I trial attempted to move beyond currently available treatments for AD [113]. The goal of this NGF trial was to protect CBF neurons from degeneration, as well as augment the function of remaining cholinergic neurons by delivery of human NGF. After obtaining informed consent, skin biopsies were attained to generate primary cultures of autologous fibroblasts that were transfected to produce human NGF [184]. If fibroblasts were found to be acceptable based on NGF production rates, then grafts were stereotaxically placed into multiple locations within the region of the CBF neurons. Following a period of 22 months, no long-term post-surgical adverse effects were found and the rate of cognitive decline appeared to be reduced [113]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Fibroblasts
MeSH
Cognitive Dysfunction

path(MESH:D002100) association p(HGNC:NGF) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

path(MESH:D000544) increases p(HGNC:NGF) View Subject | View Object

Thus, the concomitant reduction of TrkA and accumulation of proNGF in the cortex may be an early pathobiological marker for the onset of AD (Figure 1A). In fact, significantly increased cerebrospinal fluid (CSF) levels of NGF are detectable in AD [65], demonstrating the potential utility of NGF as a diagnostic biomarker. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cerebrospinal Fluid
MeSH
Cognitive Dysfunction

path(MESH:D006930) association p(HGNC:NGF) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

a(HBP:"peripheral nervous system injury") increases p(HGNC:NGF) View Subject | View Object

Here we show through systematic epigenetic studies that the histone acetyltransferase p300/CBP-associated factor (PCAF) promotes acetylation of histone 3 Lys 9 at the promoters of established key regeneration-associated genes following a peripheral but not a central axonal injury. Furthermore, we find that extracellular signal-regulated kinase (ERK)-mediated retrograde signalling is required for PCAF-dependent regenerative gene reprogramming. Finally, PCAF is necessary for conditioning-dependent axonal regeneration and also singularly promotes regeneration after spinal cord injury. PubMed:24686445

Appears in Networks:
Annotations
Uberon
dorsal root ganglion

composite(a(MESH:"amyloid beta-protein (25-35)"), complex(GO:"NF-kappaB complex")) increases sec(p(HGNC:NGF)) View Subject | View Object

Stimulation with the Aβ25-35 fragments induces secretion of cytokines such as TNF-α and of neurotrophic factors such as nerve growth factor (NGF) and brain derived nerve factor (BDNF) in NF-κB-dependent manner PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:TNF) increases p(HGNC:NGF) View Subject | View Object

Stimulation of neuronal cells by TNF-α has been shown to upregulate transactivation of anti-apoptotic gene products and neurotrophins such as Bcl-2 and NGF respectively PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

Out-Edges 16

act(p(HGNC:NGF)) increases bp(GO:"MAPK cascade") View Subject | View Object

In cell lines, this interaction of trans-activating components is also under the regulation of the Ras-dependent MAPK and pathways related to phosphoinositide-3-kinase (PI3K) and MEK activation whose response to trophic factors such as nerve growth factor (NGF) contributes to regulating transcript initiation. PubMed:19126755

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Annotations
Text Location
Review

act(p(HGNC:NGF)) increases complex(p(HGNC:JUN), p(HGNC:SP1)) View Subject | View Object

Subsequent studies have revealed that the DNA binding Sp-1 transcriptional factor interacts in response to NGF with the c-Jun coactivator (317) to increase beta4 transcription. PubMed:19126755

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Annotations
Text Location
Review

p(HGNC:NGF) regulates r(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits") View Subject | View Object

As was noted above, in different laboratories, these cells were reported to regulate nAChR mRNA expression differently in response to nerve growth factor, and to exhibit dramatically different expression of alpha7 nAChRs. PubMed:19126755

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:NGF) isA a(MESH:D009414) View Subject | View Object

Appears in Networks:

act(p(HGNC:NGF)) increases bp(GO:"GO:0000165") View Subject | View Object

For example, NGF signal transduction activates the MAPK pathway, which participates in a wide array of biologic functions, including cell survival, differentiation and apoptosis [82–84]. MAPK is a serine/ threonine protein kinase which becomes activated upon phosphorylation and affects a wide variety of transcription factors [85]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) causesNoChange path(MESH:D003929) View Subject | View Object

NGF therapy has been tested in clinical trials of diabetic peripheral neuropathy and HIV-associated neuropathy, as well as patients with AD [177]. Each of these clinical trials met with disappointment owing to lack of efficacy, toxicity or both. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) causesNoChange path(MESH:D016263) View Subject | View Object

NGF therapy has been tested in clinical trials of diabetic peripheral neuropathy and HIV-associated neuropathy, as well as patients with AD [177]. Each of these clinical trials met with disappointment owing to lack of efficacy, toxicity or both. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) causesNoChange path(MESH:D000544) View Subject | View Object

NGF therapy has been tested in clinical trials of diabetic peripheral neuropathy and HIV-associated neuropathy, as well as patients with AD [177]. Each of these clinical trials met with disappointment owing to lack of efficacy, toxicity or both. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) association bp(GO:"GO:0060384") View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) association bp(GO:"GO:0007269") View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) association bp(GO:"GO:0048485") View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) association path(MESH:D002100) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) association path(MESH:D006930) View Subject | View Object

In addition, indirect effects and unwanted side effects appeared with systemic administration including unregulated neurotransmitter release, hyperinnervation, sprouting of neurons, sympathetic stimulation, induction of antibodies, cachexia and hyperalgesia [178–181]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

p(HGNC:NGF) decreases path(MESH:D060825) View Subject | View Object

The ex vivo Phase I trial attempted to move beyond currently available treatments for AD [113]. The goal of this NGF trial was to protect CBF neurons from degeneration, as well as augment the function of remaining cholinergic neurons by delivery of human NGF. After obtaining informed consent, skin biopsies were attained to generate primary cultures of autologous fibroblasts that were transfected to produce human NGF [184]. If fibroblasts were found to be acceptable based on NGF production rates, then grafts were stereotaxically placed into multiple locations within the region of the CBF neurons. Following a period of 22 months, no long-term post-surgical adverse effects were found and the rate of cognitive decline appeared to be reduced [113]. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Fibroblasts
MeSH
Cognitive Dysfunction

p(HGNC:NGF) increases p(FPLX:ERK, pmod(Ph)) View Subject | View Object

Here we show through systematic epigenetic studies that the histone acetyltransferase p300/CBP-associated factor (PCAF) promotes acetylation of histone 3 Lys 9 at the promoters of established key regeneration-associated genes following a peripheral but not a central axonal injury. Furthermore, we find that extracellular signal-regulated kinase (ERK)-mediated retrograde signalling is required for PCAF-dependent regenerative gene reprogramming. Finally, PCAF is necessary for conditioning-dependent axonal regeneration and also singularly promotes regeneration after spinal cord injury. PubMed:24686445

Appears in Networks:
Annotations
Uberon
dorsal root ganglion

p(HGNC:NGF) increases act(p(HGNC:KAT2B)) View Subject | View Object

Here we show through systematic epigenetic studies that the histone acetyltransferase p300/CBP-associated factor (PCAF) promotes acetylation of histone 3 Lys 9 at the promoters of established key regeneration-associated genes following a peripheral but not a central axonal injury. Furthermore, we find that extracellular signal-regulated kinase (ERK)-mediated retrograde signalling is required for PCAF-dependent regenerative gene reprogramming. Finally, PCAF is necessary for conditioning-dependent axonal regeneration and also singularly promotes regeneration after spinal cord injury. PubMed:24686445

Appears in Networks:
Annotations
Uberon
dorsal root ganglion

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