INT198049

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Context Info
Confidence 0.58
First Reported 2006
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 5.35
Pain Relevance 0.96

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
cardiomyocytes 4
macrophages 2
myocardium 1
nucleus 1
thymus 1
JAK2 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 133 99.16 Very High Very High Very High
chemokine 10 98.84 Very High Very High Very High
antagonist 14 85.68 High High
corticosteroid 37 80.20 Quite High
Inflammation 38 74.60 Quite High
Bioavailability 7 68.92 Quite High
Inflammatory stimuli 6 60.40 Quite High
Leflunomide 1 39.56 Quite Low
ischemia 2 6.08 Low Low
Somatostatin 22 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Carcinoma 95 99.60 Very High Very High Very High
Coronary Heart Disease 57 99.32 Very High Very High Very High
Infection 18 99.12 Very High Very High Very High
Hypertrophy 59 98.76 Very High Very High Very High
Death 15 98.08 Very High Very High Very High
Cancer 86 93.76 High High
Adhesions 73 93.40 High High
Apoptosis 148 92.40 High High
Leiomyosarcoma 59 91.40 High High
Endotoxemia 3 90.00 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In turn, activated JAK2 (in concert with other kinases) phosphorylates eight conserved tyrosines in cytoplasmic domain [4].
Positive_regulation (activated) of JAK2
1) Confidence 0.58 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2916842 Disease Relevance 0 Pain Relevance 0.03
to the type II IFN receptor, JAK1 and JAK2 are activated and phosphorylate the signal transducer and activator of transcription 1(STAT1) on the tyrosine residue at position 701 (Tyr701) and the serine residue at position 727 (Ser727) (Parmar and Platanias, 2005; Platanias, 2005) (Fig. 2).
Positive_regulation (activated) of JAK2
2) Confidence 0.38 Published 2008 Journal Gene Regulation and Systems Biology Section Body Doc Link PMC2733082 Disease Relevance 0.56 Pain Relevance 0
The same applied for Jak2 inhibitors, although Jak2 has been shown to be ubiquitously activated in human HCC [38].
Positive_regulation (activated) of Jak2 associated with carcinoma
3) Confidence 0.32 Published 2006 Journal BMC Cancer Section Body Doc Link PMC1601962 Disease Relevance 1.34 Pain Relevance 0
on the SC membrane, inducing the phosphorylation of STAT3 via GP130/JAK2 activation within the SC [17], [50], [55].
Positive_regulation (activation) of JAK2
4) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696599 Disease Relevance 0.23 Pain Relevance 0
and IL-6 [25] and enhances CC-chemokine ligand expression in cultured murine macrophage, through activation of a JAK2-STAT3 pathway [25].
Positive_regulation (activation) of JAK2 in macrophage associated with chemokine
5) Confidence 0.21 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2846344 Disease Relevance 0.39 Pain Relevance 0.33
In the thymus, Fyn acts as a tyrosine kinase that transduces the leptin signal independently of JAK2 activation and mediates some of the immunomodulatory effects of leptin in this tissue.
Positive_regulation (activation) of JAK2 in thymus
6) Confidence 0.19 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2846344 Disease Relevance 0.55 Pain Relevance 0
In addition, it accelerates cholesteryl ester accumulation in human monocyte-derived macrophages by increasing ACAT-1 expression via JAK2 and PI3K, thereby suppressing cholesterol efflux [29].
Positive_regulation (increasing) of JAK2 in macrophages
7) Confidence 0.19 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2846344 Disease Relevance 0.14 Pain Relevance 0.14
Subsequently, the activated JAK2 phosphorylates the receptor and STATs (signal transducer and activator of transcription), and dimers of the latter are translocated to the nucleus to promote gene transcription (Carter-Su and Smit 1998).
Positive_regulation (activated) of JAK2 in nucleus
8) Confidence 0.16 Published 2006 Journal International Journal of Nanomedicine Section Body Doc Link PMC2676637 Disease Relevance 0.05 Pain Relevance 0.07
Utilizing an in vivo feline right ventricular pressure-overload (RVPO) model of hypertrophy, we demonstrate that in 48 h pressure-overload (PO) myocardium, STAT3 becomes phosphorylated and redistributed to detergent-insoluble fractions with no accompanying JAK2 activation.
Neg (no) Positive_regulation (activation) of JAK2 in myocardium associated with hypertrophy
9) Confidence 0.15 Published 2008 Journal International Journal of Biological Sciences Section Abstract Doc Link PMC2443357 Disease Relevance 0.49 Pain Relevance 0
Our analysis using in vivo and in vitro models of hypertrophic stimulation did not show JAK2 phosphorylation, though JAK2 phosphorylation/activation could be observed in EGF-treated adult feline cardiomyocytes in vitro.
Positive_regulation (activation) of JAK2 in cardiomyocytes
10) Confidence 0.15 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0.03
JAK-1 and JAK-2 are activated by a broad range of cytokines that use gp130 whereas JAK-3 which is highly expressed in lymphoid cells is activated only by cytokines that bind to gamma-chain-containing receptors.
Positive_regulation (activated) of JAK-2 associated with cytokine
11) Confidence 0.14 Published 2009 Journal Journal of Transplantation Section Body Doc Link PMC2809333 Disease Relevance 0.25 Pain Relevance 0.30
To ascertain whether the classic JAK2-mediated pathway is involved during STAT3 activation, we assayed for JAK2 recruitment to the insoluble fraction and phosphorylation at Tyr1007/1008 sites at all time points of PO (Figure 2a) and RGD stimulation of cardiomyocytes (Figure 2b).
Spec (whether) Positive_regulation (involved) of JAK2 in cardiomyocytes
12) Confidence 0.11 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0
To ascertain whether the classic JAK2-mediated pathway is involved during STAT3 activation, we assayed for JAK2 recruitment to the insoluble fraction and phosphorylation at Tyr1007/1008 sites at all time points of PO (Figure 2a) and RGD stimulation of cardiomyocytes (Figure 2b).
Positive_regulation (assayed) of JAK2 in cardiomyocytes
13) Confidence 0.11 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0
An earlier study40 in a murine transverse aortic constriction PO model demonstrates that STAT3 undergoes biphasic acute (3 h) and hypertrophic responses (48 h) via the gp130-mediated JAK2 signaling where the activated STAT3 plays an autoregulatory negative feedback role by promoting the expression of a JAK2 inhibitor protein, SOCS3 (suppressor of cytokine signaling-3).
Positive_regulation (mediated) of JAK2 associated with cytokine
14) Confidence 0.11 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0.05
Although STAT3 activation has been reported via signaling through Janus Kinase 2 (JAK2) in several cardiac models of hypertrophy, the importance of other nonreceptor tyrosine kinases (NTKs) has not been explored.
Positive_regulation (activation) of Janus Kinase 2 associated with hypertrophy
15) Confidence 0.10 Published 2008 Journal International Journal of Biological Sciences Section Abstract Doc Link PMC2443357 Disease Relevance 0.43 Pain Relevance 0
Although STAT3 activation has been reported via signaling through Janus Kinase 2 (JAK2) in several cardiac models of hypertrophy, the importance of other nonreceptor tyrosine kinases (NTKs) has not been explored.
Positive_regulation (activation) of JAK2 associated with hypertrophy
16) Confidence 0.10 Published 2008 Journal International Journal of Biological Sciences Section Abstract Doc Link PMC2443357 Disease Relevance 0.43 Pain Relevance 0
RGD stimulation of adult cardiomyocytes in vitro caused both STAT3 redistribution and activation that were accompanied by the activation and redistribution of c-Src and the TEC family kinase, BMX, but not JAK2.
Positive_regulation (activation) of JAK2 in cardiomyocytes
17) Confidence 0.10 Published 2008 Journal International Journal of Biological Sciences Section Abstract Doc Link PMC2443357 Disease Relevance 0.51 Pain Relevance 0

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