Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Appears in Networks 3

In-Edges 9

a(CHEBI:"2-(2-amino-3-methoxyphenyl)chromen-4-one") decreases p(FPLX:ERK, pmod(Ph)) View Subject | View Object

ERK phosphorylation in MAPT mutant neurons was blocked by treatment with PD98059, a specific inhibitor of MEK-mediated activation of ERK (Li et al., 2001) (Figures 4B and 4C) PubMed:27594586

p(HGNC:MAPT, var("p.Ala152Thr")) increases p(FPLX:ERK, pmod(Ph)) View Subject | View Object

The level of phosphorylated ERK (p-ERK) was significantly increased in tau-A152T neurons and to a lesser extent in MAPT IVS10+16 patient neurons (Figure 4A) PubMed:27594586

p(HBP:HBP00044, var("p.Ala152Thr")) causesNoChange p(FPLX:ERK, pmod(Ph)) View Subject | View Object

ERK phosphorylation is also not affected by A152T mutation in 3R tau (Figure S4D) PubMed:27594586

p(HBP:HBP00045, var("p.Ala152Thr")) increases p(FPLX:ERK, pmod(Ph)) View Subject | View Object

Correspondingly, the level of p-ERK was also elevated in HEK293 cells expressing tau-A152T (Figure 4E) PubMed:27594586

act(p(HGNC:MMP9)) positiveCorrelation p(FPLX:ERK, pmod(Ph)) View Subject | View Object

We found the level and activity of secreted MMP-9 to correlate well with the extent of ERK phosphorylation (Figure S4A) PubMed:27594586

sec(p(HGNC:MMP9)) positiveCorrelation p(FPLX:ERK, pmod(Ph)) View Subject | View Object

We found the level and activity of secreted MMP-9 to correlate well with the extent of ERK phosphorylation (Figure S4A) PubMed:27594586

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

a(CHEBI:"methyl 3,5-di-O-caffeoyl quinate") increases p(FPLX:ERK, pmod(Ph)) View Subject | View Object

Macranthoin G inhibited the NF-B pathway and activated the phosphorylation of IB, p38 and ERK, and thus, min-imized cell damage [131]. PubMed:29179999

Out-Edges 3

p(FPLX:ERK, pmod(Ph)) positiveCorrelation act(p(HGNC:MMP9)) View Subject | View Object

We found the level and activity of secreted MMP-9 to correlate well with the extent of ERK phosphorylation (Figure S4A) PubMed:27594586

p(FPLX:ERK, pmod(Ph)) positiveCorrelation sec(p(HGNC:MMP9)) View Subject | View Object

We found the level and activity of secreted MMP-9 to correlate well with the extent of ERK phosphorylation (Figure S4A) PubMed:27594586

p(FPLX:ERK, pmod(Ph)) increases act(p(FPLX:ERK)) 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

About

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.