INT135556

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Context Info
Confidence 0.69
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 38
Total Number 38
Disease Relevance 12.78
Pain Relevance 1.17

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 (AKT1) nucleoplasm (AKT1) transport (AKT1)
small molecule metabolic process (AKT1) enzyme binding (AKT1) carbohydrate metabolic process (AKT1)
Anatomy Link Frequency
plasma 5
HL-60 1
epithelial cells 1
HT-1080 1
MDA-MB-231 1
AKT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 51 100.00 Very High Very High Very High
cytokine 24 91.28 High High
Immobilon 5 88.08 High High
Inflammation 91 75.00 Quite High
imagery 13 70.80 Quite High
Osteoarthritis 35 69.28 Quite High
Pain 7 64.96 Quite High
cINOD 34 63.80 Quite High
withdrawal 3 51.32 Quite High
metalloproteinase 22 50.00 Quite Low
Disease Link Frequency Relevance Heat
Shock 12 100.00 Very High Very High Very High
Prostate Cancer 91 99.60 Very High Very High Very High
Sarcoma 24 99.52 Very High Very High Very High
Breast Cancer 187 99.28 Very High Very High Very High
Cervical Cancer 16 99.00 Very High Very High Very High
Apoptosis 397 98.88 Very High Very High Very High
Adenocarcinoma 10 95.60 Very High Very High Very High
Fibrosarcoma 9 95.36 Very High Very High Very High
Endometrial Hyperplasia 4 94.88 High High
Disease 118 93.68 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Akt3 is the most abundant of Akt isoforms, about 2 and 4 fold more than Akt1 and Akt2 respectively (Fig. 1C), which is not a normal Akt isoform expression pattern for cervical epithelial cells.
Localization (abundant) of Akt in epithelial cells
1) Confidence 0.69 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.21 Pain Relevance 0
Akt prevents cytochrome release by maintaining structural integrity of the mitochondria and is also involved in post-mitochondrial events through phosphorylation of caspase-9 [24,35-37].
Localization (release) of Akt
2) Confidence 0.69 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.46 Pain Relevance 0.03
As shown in Fig. 2A, a decline in the abundance of Akt protein was apparent following 16 hours of valproic acid or butyrate treatment, which became more evident after 24 hours of treatment.
Localization (abundance) of Akt
3) Confidence 0.69 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.09 Pain Relevance 0
Evidence is provided to indicate that PKB is targeted by robust caspase activation due to sulindac sulfide.
Localization (targeted) of PKB
4) Confidence 0.68 Published 2006 Journal Int. J. Oncol. Section Abstract Doc Link 16685448 Disease Relevance 0.31 Pain Relevance 0.05
Akt also blocks cytochrome C release from the mitochondria through the regulation of Bcl-2 [31] and regulates expression of cIAP-1 [32].
Localization (release) of Akt
5) Confidence 0.64 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 1.06 Pain Relevance 0.17
Following AKT1 knockdown, the cytoplasmic Par-4/p65 colocalized signal was significantly enhanced (Figure 6; Par4/p65 colocalize panel for pshAkt1).
Localization (colocalize) of pshAkt1
6) Confidence 0.53 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2883962 Disease Relevance 0 Pain Relevance 0
As described above, PTEN antagonizes the PI3K/AKT pathway by dephosphorylating PIP3, resulting in decreased translocation of AKT activation.
Localization (translocation) of AKT
7) Confidence 0.50 Published 2010 Journal Obstetrics and Gynecology International Section Body Doc Link PMC2846683 Disease Relevance 1.79 Pain Relevance 0
The siRNA for human mTOR, Src, Rictor, FKBP12 and Akt were purchased from Santa Cruz Biotechnology (Santa Cruz, CA) and were utilized according to the manufacturer's specifications.
Localization (purchased) of Akt
8) Confidence 0.49 Published 2010 Journal J Angiogenes Res Section Body Doc Link PMC2831839 Disease Relevance 0 Pain Relevance 0.04
The siRNA for human mTOR, Src, Rictor, FKBP12 and Akt were purchased from Santa Cruz Biotechnology (Santa Cruz, CA) and were utilized according to the manufacturer's specifications.
Localization (utilized) of Akt
9) Confidence 0.49 Published 2010 Journal J Angiogenes Res Section Body Doc Link PMC2831839 Disease Relevance 0 Pain Relevance 0.04
Rather, this action of celecoxib involved generation of mitochondria-derived reactive oxygen species, Akt phosphorylation, and nuclear translocation of the transcription factor Nrf2, with N-acetylcysteine, PI-3K antagonist LY290042, and dominant-negative Akt abrogating the effects.
Localization (translocation) of Akt associated with antagonist
10) Confidence 0.44 Published 2010 Journal Free Radic. Biol. Med. Section Abstract Doc Link 20083195 Disease Relevance 0.34 Pain Relevance 0.45
As evaluated by immunohistochemisty, normal canine LEC had minimal to no detectable pAkt protein present (Figure 1A), while immunostaining for pAkt was strong predominantly in the cytoplasm of naturally occurring cataractous canine LEC (Figure 1B) and clinical samples of canine PCO (Figure 1C).
Neg (no) Localization (present) of pAkt associated with capsule opacification
11) Confidence 0.44 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994344 Disease Relevance 0.24 Pain Relevance 0.04
Immunohistochemical staining was performed as previously described [38] using antibodies against TERT (1:350; Calbiochem, San Diego CA), pAkt (1:350; Santa Cruz, Santa Cruz, CA), cleaved caspase-3 (1:20; Oncogene, San Diego CA), ILK (1:200; Stressgen, San Diego CA), ?
Localization (1:350) of pAkt
12) Confidence 0.44 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994344 Disease Relevance 0 Pain Relevance 0
Activation of PI3K leads to phosphorylation of inositol lipids, in response to activation and membrane translocation of Akt/Protein kinase B.
Localization (translocation) of Akt
13) Confidence 0.39 Published 2009 Journal Lipids Health Dis Section Body Doc Link PMC2667508 Disease Relevance 0.10 Pain Relevance 0
In the setting of hormone receptor positive breast cancer, mTOR inhibition and the resulting increase in Akt signaling could result in ER phosphorylation on Ser167 and negate the effects of aromatase inhibition, thus limiting the therapeutic benefit of this combination.


Localization (increase) of Akt associated with breast cancer
14) Confidence 0.38 Published 2007 Journal Breast Cancer Res Section Body Doc Link PMC2242654 Disease Relevance 0.65 Pain Relevance 0
AKT1, a serine/threonin kinase also known as PKB, functions as a key mediator of the PI3K/AKT pathway.
Localization (known) of AKT1
15) Confidence 0.35 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2955614 Disease Relevance 0.17 Pain Relevance 0
AKT1, a serine/threonin kinase also known as PKB, functions as a key mediator of the PI3K/AKT pathway.
Localization (known) of PKB
16) Confidence 0.35 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2955614 Disease Relevance 0.17 Pain Relevance 0
At this time (45 min), both p38 kinase and Akt phosphorylated forms were diminished.
Localization (forms) of Akt
17) Confidence 0.33 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1065327 Disease Relevance 0.38 Pain Relevance 0.03
HSP90 inhibitors affect AKT activity indirectly through depletion of upstream signaling molecules (for example, ERBB family members) and directly by preventing HSP90-dependent conformational stability of AKT [17,21,22].
Localization (stability) of AKT
18) Confidence 0.29 Published 2008 Journal Breast Cancer Res Section Body Doc Link PMC2397535 Disease Relevance 0.59 Pain Relevance 0.03
mol/l, celecoxib caused slight increase in pAkt in MDA-MB-231 cells.
Localization (increase) of pAkt in MDA-MB-231
19) Confidence 0.25 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1175053 Disease Relevance 0.79 Pain Relevance 0
For phosphorylated forms of PKB (PKB Ser473), mTOR (mTOR Ser2448), p70S6k (p70S6k Thr389), eIF-4E-BP1 (eIF-4E-BP1 Thr37/46), eukaryotic elongation factor 2 (eEF2 Thr56), and glycogen synthase kinase 3-?
Localization (forms) of PKB
20) Confidence 0.25 Published 2008 Journal American Journal of Physiology - Endocrinology and Metabolism Section Body Doc Link PMC2536736 Disease Relevance 0 Pain Relevance 0

General Comments

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