INT325780

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Context Info
Confidence 0.69
First Reported 2010
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 13
Disease Relevance 2.86
Pain Relevance 0.36

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

signal transduction (EPOR) extracellular region (EPOR) plasma membrane (EPOR)
embryo development (EPOR)
Anatomy Link Frequency
proximal region 1
UT-7 1
EPOR (Homo sapiens)
EPOR - S462A (1)
Pain Link Frequency Relevance Heat
cytokine 52 99.18 Very High Very High Very High
Glutamate 13 84.36 Quite High
headache 39 73.24 Quite High
ischemia 13 57.52 Quite High
Disease Link Frequency Relevance Heat
Hypersensitivity 65 99.18 Very High Very High Very High
Myelodysplastic Syndromes 195 97.12 Very High Very High Very High
Erythrocytosis 143 95.56 Very High Very High Very High
Myeloproliferative Disorder 13 89.28 High High
Hyperplasia 13 82.80 Quite High
Pruritus 13 75.40 Quite High
Dyspnea 13 74.92 Quite High
Nose Bleeds 13 74.12 Quite High
Dizziness 13 73.68 Quite High
Headache 39 73.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We demonstrated a marked increase of EPOR protein on the membrane of erythroid progenitors and report its role in deregulating CD34+ cells proliferation and differentiation.
Positive_regulation (increase) of EPOR
1) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.96 Pain Relevance 0.13
Although we were unable to directly demonstrate the phosphorylation of the truncated EPOR in the absence of the cytokine, we observed, under this condition, the activation of EPOR-dependent pathway by detecting STAT5 phosphorylation in CD34+ cells cultured without EPO (Figure 5D).
Positive_regulation (activation) of EPOR associated with cytokine
2) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.07 Pain Relevance 0.05
EPO hypersensitivity might be due to both: i) the remarkable accumulation of truncated EPOR and its autoactivation, and ii) loss of the negative regulatory domain of the EPOR G1251T mutant.
Positive_regulation (accumulation) of EPOR associated with hypersensitivity
3) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.35 Pain Relevance 0
The ubiquitination mediated by beta-Trcp is a crucial signal for the C-terminus degradation of EPOR because the point mutation of Ser 462 to Ala blocks EPOR targeting to the proteasome, thereby leading to sustained activation of EPOR(S462A).
Positive_regulation (activation) of EPOR (S462A)
4) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.16 Pain Relevance 0
The observed difference of receptor turn-over is also in accord with data obtained in UT-7 cells, showing EPOR internalization and removal requires ubiquitination of the receptor's C-terminal region [34].
Positive_regulation (showing) of EPOR in UT-7
5) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0 Pain Relevance 0
The growth characteristics of the EPOR G1251T CD34+ cells and the increased levels of peripheral CEPs prompted us to investigate EPOR mRNA and protein levels during CD34+ erythroid differentiation in vitro.
Spec (investigate) Positive_regulation (investigate) of EPOR
6) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.15 Pain Relevance 0
The analysis of erythroid precursor membranes demonstrates a heretofore undescribed accumulation of the truncated EPOR, probably due to the absence of residues involved in the EPO-dependent receptor internalization and degradation.
Positive_regulation (accumulation) of EPOR
7) Confidence 0.50 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2916842 Disease Relevance 0.37 Pain Relevance 0.04
Our observation that the EPOR G1251T patients with activated EPO-EPOR signaling have an increased number of CEPs suggests the CEPs increase may be due to a constitutive EPO receptor activation in this population.
Positive_regulation (activation) of EPO receptor
8) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.09 Pain Relevance 0.05
Moreover, patient erythroid precursors present an increased activation of EPOR and its effectors, including Stat5 and Erk1/2 pathway.


Positive_regulation (activation) of EPOR
9) Confidence 0.46 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2916842 Disease Relevance 0.36 Pain Relevance 0.04
It is currently assumed that two boxes at the membrane-proximal region of the EPOR cytoplasmic domain and Y344 are the major positive motifs and that the activation of Stat5 is central for EPOR function [5].
Positive_regulation (activation) of EPOR in proximal region
10) Confidence 0.46 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.17 Pain Relevance 0.03
LLnL, that has been previously reported to induce membrane EPOR accumulation by hampering the receptor removal [34].
Positive_regulation (accumulation) of EPOR
11) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0 Pain Relevance 0
As shown in Fig. 4D, LLnL treatment causes the increase of wild-type EPOR while scarce change of mutated EPOR level was observed.
Positive_regulation (increase) of EPOR
12) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0 Pain Relevance 0
In conclusion, in this study, we report that the gain-of-function EPOR G1251T mutation results in a marked alteration of growth and differentiation of human CD34+ and in an increase of erythroid progenitors' surface EPOR peptide.
Positive_regulation (increase) of EPOR
13) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0.16 Pain Relevance 0.03

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