INT83728

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Context Info
Confidence 0.46
First Reported 1999
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 42
Total Number 53
Disease Relevance 0.46
Pain Relevance 5.06

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

nuclear envelope (TMPO) chromosome (TMPO) nucleus (TMPO)
DNA binding (TMPO)
Anatomy Link Frequency
tail 4
TMPO (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 3503 99.82 Very High Very High Very High
cytokine 3 90.72 High High
b2 receptor 40 76.24 Quite High
Neuropeptide 3 75.84 Quite High
bradykinin 40 69.84 Quite High
Somatostatin 2 65.04 Quite High
Nerve growth factor 2 51.92 Quite High
Enkephalin 2 47.28 Quite Low
Angina 51 5.00 Very Low Very Low Very Low
COX2 40 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 44 77.92 Quite High
Stress 113 75.20 Quite High
Thrombosis 113 70.72 Quite High
Adhesions 40 66.88 Quite High
Increased Venous Pressure Under Development 131 53.04 Quite High
Injury 40 11.20 Low Low
Hypertension 124 5.00 Very Low Very Low Very Low
Cv General 3 Under Development 51 5.00 Very Low Very Low Very Low
Apoptosis 41 5.00 Very Low Very Low Very Low
Asthma 40 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Immunocytochemical observations have shown that the secreted thymic hormones, thymosin alpha 1 and thymopoietin (and its short form, thymopentin or TP5), are produced by the same RE cells.
Localization (secreted) of thymopoietin
1) Confidence 0.46 Published 1999 Journal In Vivo Section Abstract Doc Link 10459506 Disease Relevance 0 Pain Relevance 0.14
The secreted thy nic hormones, thymulin, thymosin-alpha 1 and thymopoietin (its short form, thymopentin or TP5) were detected immunocytochemically to be produced by RE cells.
Localization (secreted) of thymopoietin
2) Confidence 0.45 Published 2000 Journal Anticancer Res. Section Abstract Doc Link 10928121 Disease Relevance 0 Pain Relevance 0.11
Hence, collectively, both NO-donors and the vasodilatory prostanoids prostacyclin and PGD2 readily desensitize TP-mediated Rho activation and cytoskeletal signaling in 1° h.AoSMCs, findings entirely predicted from and in keeping with outcomes from other systems [6,8,35,36].
Localization (desensitize) of TP
3) Confidence 0.34 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.09
Hence, through the use of TP isoform-specific siRNA, we sought to determine whether TP?
Localization (use) of TP isoform
4) Confidence 0.34 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.06 Pain Relevance 0.06
itself and is entirely consistent with previous findings involving both prostacyclin- and NO-mediated desensitization of TP?
Localization (desensitization) of TP
5) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.04
is not affected by either prostacyclin or NO again suggests that the effects of both vasodilators are due to direct effects on TP?
Localization (effects) of TP
6) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.05
activation, both the NO and prostacyclin analogues SIN-1 and Cicaprost impair TP-mediated cytoskeletal changes involving RhoA activation and cofilin phosphorylation in 1° h.AoSMCs and that they do so, at least in part, by specifically and directly targeting TP?
Localization (targeting) of TP
7) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.07 Pain Relevance 0
Consistent with those previous studies, pre-incubation with SIN-1 specifically impaired U46619-induced [Ca2+]i mobilization in HEK.TP?
Localization (mobilization) of TP
8) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.03
was also significantly impaired by either Cicaprost or SIN-1, while neither agent affected such responses in HEK.TP?
Localization (responses) of TP
9) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
independently contribute to U46619-induced RhoA activation and signaling in 1° h.AoSMCs and to ascertain whether the inhibitory effects of NO and/or Cicaprost may directly target TP?
Localization (target) of TP
10) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.08 Pain Relevance 0.05
Hence, both the NO and prostacyclin impair TP-mediated cytoskeletal changes involving RhoA activation, F-actin polymerization and cofilin phosphorylation in 1° h.AoSMCs and they do so, at least in part, by specifically and directly targeting TP?
Localization (targeting) of TP
11) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
More specifically, by directly targeting TP?
Localization (targeting) of TP
12) Confidence 0.29 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.03
S329,331A cell lines stably over-expressing hemagglutinin (HA) -tagged forms of TP?
Localization (forms) of TP
13) Confidence 0.28 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
Similarly, the sGC and NOS inhibitors LY 83583 (30%) and l-NAME (40%), respectively, yielded significant impairments in agonist-induced desensitization of TP?.
Localization (desensitization) of TP associated with agonist
14) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.21
Investigation of the role of Nitric oxide signalling in homologous desensitization of TP?
Localization (desensitization) of TP
15) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.08
, it is evident that its target PKC-sensitive site(s) is located at sites other than within the C-tail domain of TP?
Localization (located) of TP in tail
16) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.10
On the other hand, pre-treatment of HEK.TP
Localization (treatment) of TP
17) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0.08 Pain Relevance 0.14
Whilst pre-incubation with GF 109203X had no significant effect on [Ca2+]i mobilization by TP?
Localization (mobilization) of TP
18) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.14
S145A , respectively, we have previously established that Ser145 actually corresponds to the GF 109203X-sensitive, PKC site that accounts for the partial agonist-induced desensitization of both TP?
Localization (desensitization) of TP associated with agonist
19) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.08
, clearly indicating that other factors may also contribute to agonist-induced desensitization of TP?.
Localization (desensitization) of TP associated with agonist
20) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.13

General Comments

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