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Appears in Networks 4

In-Edges 13

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

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

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

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

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

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

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

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

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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

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

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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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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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

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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

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

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

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

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

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

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

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

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

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

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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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.