INT200786

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.69
First Reported 2006
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 9
Total Number 10
Disease Relevance 6.03
Pain Relevance 0.35

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

cell differentiation (Jak2) cytosol (Jak2) signal transduction (Jak2)
histone binding (Jak2) cytoskeleton (Jak2) nucleus (Jak2)
Anatomy Link Frequency
spleens 4
hematopoietic stem cells 2
megakaryocytes 2
Jak2 (Mus musculus)
Jak2 - V617F (7)
Pain Link Frequency Relevance Heat
fibrosis 27 100.00 Very High Very High Very High
metalloproteinase 3 87.08 High High
cva 9 75.36 Quite High
cytokine 33 74.00 Quite High
Inflammation 9 62.76 Quite High
Parenteral administration 18 24.08 Low Low
imagery 12 5.00 Very Low Very Low Very Low
anesthesia 10 5.00 Very Low Very Low Very Low
Bioavailability 9 5.00 Very Low Very Low Very Low
isoflurane 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Fibrosis 27 100.00 Very High Very High Very High
Myelofibrosis 162 99.96 Very High Very High Very High
Erythrocytosis 315 99.56 Very High Very High Very High
Myelodysplastic Syndromes 558 98.80 Very High Very High Very High
Anaemia 9 98.28 Very High Very High Very High
Disease 87 96.68 Very High Very High Very High
Malignant Neoplastic Disease 9 94.04 High High
Sprains And Strains 117 91.68 High High
Reticulocytosis 45 87.76 High High
Myeloid Leukemia 81 83.68 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Increased expression of JAK2 V617F in patients with homozygous mutations may increase severity of the phenotype in PV [41], perhaps because the mutant and WT JAK2 kinases compete for Epo receptor binding [13].
Positive_regulation (Increased) of Gene_expression (expression) of JAK2 V617F (V617F) associated with myelodysplastic syndromes
1) Confidence 0.69 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 0.86 Pain Relevance 0.06
In our model, robust polycythemia is induced by modest overexpression of JAK2 V617F in BM with two normal JAK2 genes, but further studies will be necessary to determine whether the phenotype is influenced by levels of normal JAK2.
Positive_regulation (overexpression) of Gene_expression (overexpression) of JAK2 V617F (V617F) associated with erythrocytosis
2) Confidence 0.69 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 1.04 Pain Relevance 0
There was modest (2- to 3-fold) overexpression of JAK2 in both cohorts, relative to the level of endogenous JAK2 protein (Figure 4A).
Positive_regulation (overexpression) of Gene_expression (overexpression) of JAK2
3) Confidence 0.69 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 0 Pain Relevance 0
Increased expression of JAK2 V617F in patients with homozygous mutations may increase severity of the phenotype in PV [41], perhaps because the mutant and WT JAK2 kinases compete for Epo receptor binding [13].
Spec (may) Positive_regulation (increase) of Gene_expression (expression) of JAK2 V617F (V617F) associated with myelodysplastic syndromes
4) Confidence 0.50 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 0.93 Pain Relevance 0.06
These results suggest that JAK2 V617F expression induces myelofibrosis, but the resulting impairment of erythropoiesis is due to a defect of the hematopoietic microenvironment, rather than a deficiency of malignant hematopoietic stem cells.


Positive_regulation (induces) of Gene_expression (expression) of JAK2 V617F (V617F) in hematopoietic stem cells associated with malignant neoplastic disease and myelofibrosis
5) Confidence 0.50 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 1.45 Pain Relevance 0.04
This coincided with a gradual but marked increase in fibrosis in the BM and spleen of JAK2 V617F recipients that was not observed in JAK2 WT recipients (Figure 5B).
Positive_regulation (increase) of Gene_expression (recipients) of JAK2 V617F (V617F) in spleen associated with fibrosis
6) Confidence 0.50 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 1.11 Pain Relevance 0.05
When isolated after in vitro culture in thrombopoietin, megakaryocytes from JAK2 V617F recipients were noticeably smaller than their counterparts from normal mice or JAK2 WT recipients (Figure 3D), with many micromegakaryotes undergoing proplatelet formation and mitosis.
Positive_regulation (megakaryocytes) of Gene_expression (recipients) of JAK2 V617F (V617F) in megakaryocytes
7) Confidence 0.50 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 0.39 Pain Relevance 0.04
There was increased phosphorylation of Gab2 and ERK in spleens and BM from JAK2 V617F recipients that were somewhat variable from sample to sample, but no consistent activation of Akt (data not shown).
Positive_regulation (increased) of Gene_expression (recipients) of JAK2 V617F (V617F) in spleens
8) Confidence 0.50 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 0 Pain Relevance 0
There was modest (2- to 3-fold) overexpression of JAK2 in both cohorts, relative to the level of endogenous JAK2 protein (Figure 4A).
Positive_regulation (overexpression) of Gene_expression (overexpression) of JAK2
9) Confidence 0.43 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762384 Disease Relevance 0 Pain Relevance 0
Most conspicuous is activation of the Jak/Stat pathway as indicated by elevated expression of Jak2 and Stat1, decreased expression of Socs1 and increased expression of several Stat target genes (Myc, Irf1, Igsf3g and Usp20) (Fig. 11A).
Positive_regulation (elevated) of Gene_expression (expression) of Jak2
10) Confidence 0.20 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2529338 Disease Relevance 0.25 Pain Relevance 0.11

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox