INT101866

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.52
First Reported 2002
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 49
Total Number 49
Disease Relevance 17.47
Pain Relevance 2.14

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
endothelial cells 2
muscle 2
lenses 2
RL95-2 2
OGE 2
AKT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 2 98.32 Very High Very High Very High
metalloproteinase 6 97.36 Very High Very High Very High
mu opioid receptor 10 97.26 Very High Very High Very High
cytokine 62 94.64 High High
aspirin 21 94.36 High High
Immobilon 4 92.64 High High
Inflammation 57 92.28 High High
cINOD 59 81.88 Quite High
withdrawal 4 79.12 Quite High
opiate 18 77.16 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 1050 100.00 Very High Very High Very High
Pancreatic Cancer 84 99.84 Very High Very High Very High
Glioblastoma 38 99.72 Very High Very High Very High
Death 173 99.14 Very High Very High Very High
Metastasis 47 98.92 Very High Very High Very High
Cancer 739 98.80 Very High Very High Very High
Cataract 57 98.76 Very High Very High Very High
Adhesions 45 97.12 Very High Very High Very High
Targeted Disruption 29 96.36 Very High Very High Very High
Fibromyalgia 1 96.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
CA-Akt transfection induced Akt and I?
Positive_regulation (transfection) of Gene_expression (transfection) of CA-Akt
1) Confidence 0.52 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.24 Pain Relevance 0
In the presence of IND 12, MDCK-f3 cells show regenerated expression and activity ratios of the small GTPases Rac and Rho normally found in untransformed MDCK cells.
Positive_regulation (regenerated) of Gene_expression (expression) of Rac in MDCK
2) Confidence 0.49 Published 2002 Journal Cancer Res. Section Abstract Doc Link 11912145 Disease Relevance 0.40 Pain Relevance 0.07
A biological ISEL sub-study was performed including the assessment of EGFR gene copy number by fluorescent in situ hybridization (FISH), EGFR and p-AKT protein expression by immunohistochemistry (IHC), EGFR, K-RAS and B-RAF mutational status (Figure 1).31 It showed that a high EGFR gene copy number in patients treated with gefitinib represents a predictive factor of survival benefit when compared with placebo (HR: 0.61 versus 1.16 for high and low gene copy number, respectively; interaction test, P = 0.045), such as EGFR expression (HR: 0.77 versus 1.57 for positive and negative protein expression, respectively; interaction test, P = 0.049) (Table 1).
Positive_regulation (fluorescent) of Gene_expression (expression) of AKT
3) Confidence 0.49 Published 2010 Journal Drug design, development and therapy Section Body Doc Link PMC2880339 Disease Relevance 0.07 Pain Relevance 0
The phosphoinositide 3-OH kinase (PI3K)/Akt pathway, which is frequently amplified or activated in pancreatic cancer, may also contribute to resistance in several ways including the inhibition of proapoptotic proteins BAD and caspase 9 (Schlieman et al. 2003), dysregulation of the mammalian target of rapamycin (mTOR)-S6K1 signaling pathway (Asano et al. 2005), and activation of the nuclear factor kappa B (NF?
Positive_regulation (activated) of Gene_expression (pathway) of Akt associated with pancreatic cancer
4) Confidence 0.49 Published 2007 Journal Core Evidence Section Body Doc Link PMC3012429 Disease Relevance 0.93 Pain Relevance 0
The phosphorylation of a conserved threonine residue (Thr308 in Akt1, Thr309 in Akt2 and Thr305 in Akt3), upon growth factor stimulation, is required for Akt activation, while the phosphorylation of a serine residue (Ser473 in Akt1, Ser474 in Akt2 and Ser474 in Akt3) is only required for maximal Akt activity [21,24-26].
Positive_regulation (required) of Gene_expression (activation) of Akt
5) Confidence 0.46 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.46 Pain Relevance 0.04
Flow cytometry analysis revealed that butyrate was able to induce significant apoptotic death in the control cells but not in the cells expressing the constitutively active Akt (Fig. 4A).
Positive_regulation (active) of Gene_expression (expressing) of Akt associated with apoptosis and death
6) Confidence 0.46 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.84 Pain Relevance 0
Currently, three mammalian isoforms have been identified, namely Akt1/PKB?
Positive_regulation (namely) of Gene_expression (identified) of Akt1
7) Confidence 0.46 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.75 Pain Relevance 0.13
Myristoylated Akt (MyrAkt) transfected U87MG glioblastoma cells showed increase invasiveness, whereas DN-Akt transfected cells showed decrease invasiveness indicating that Akt potently promoted glioblastoma cell invasion.
Positive_regulation (transfected) of Gene_expression (transfected) of Myristoylated Akt associated with glioblastoma
8) Confidence 0.44 Published 2005 Journal J. Cell. Biochem. Section Abstract Doc Link 15546138 Disease Relevance 0.57 Pain Relevance 0.12
Myristoylated Akt (MyrAkt) transfected U87MG glioblastoma cells showed increase invasiveness, whereas DN-Akt transfected cells showed decrease invasiveness indicating that Akt potently promoted glioblastoma cell invasion.
Positive_regulation (transfected) of Gene_expression (transfected) of MyrAkt associated with glioblastoma
9) Confidence 0.44 Published 2005 Journal J. Cell. Biochem. Section Abstract Doc Link 15546138 Disease Relevance 0.57 Pain Relevance 0.12
Myristoylated Akt (MyrAkt) transfected U87MG glioblastoma cells showed increase invasiveness, whereas DN-Akt transfected cells showed decrease invasiveness indicating that Akt potently promoted glioblastoma cell invasion.
Positive_regulation (Myristoylated) of Gene_expression (transfected) of Myristoylated Akt associated with glioblastoma
10) Confidence 0.44 Published 2005 Journal J. Cell. Biochem. Section Abstract Doc Link 15546138 Disease Relevance 0.57 Pain Relevance 0.12
Myristoylated Akt (MyrAkt) transfected U87MG glioblastoma cells showed increase invasiveness, whereas DN-Akt transfected cells showed decrease invasiveness indicating that Akt potently promoted glioblastoma cell invasion.
Positive_regulation (Myristoylated) of Gene_expression (transfected) of MyrAkt associated with glioblastoma
11) Confidence 0.44 Published 2005 Journal J. Cell. Biochem. Section Abstract Doc Link 15546138 Disease Relevance 0.57 Pain Relevance 0.12
As shown previously [42], CA-Akt transfection induced COX-2 expression.


Positive_regulation (induced) of Gene_expression (transfection) of CA-Akt
12) Confidence 0.43 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.24 Pain Relevance 0
As hypothesized, CA-Akt transfection induced COX-2 expression and confirmed the results obtained with DN-Akt inhibition and PI 3-K inhibition studies.
Positive_regulation (induced) of Gene_expression (transfection) of CA-Akt
13) Confidence 0.43 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.14 Pain Relevance 0
As hypothesized, CA-Akt transfection induced COX-2 expression and confirmed the results obtained with DN-Akt inhibition and PI 3-K inhibition studies.
Positive_regulation (transfection) of Gene_expression (transfection) of CA-Akt
14) Confidence 0.43 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.14 Pain Relevance 0
As shown previously [42], CA-Akt transfection induced COX-2 expression.


Positive_regulation (transfection) of Gene_expression (transfection) of CA-Akt
15) Confidence 0.43 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.24 Pain Relevance 0
Irradiation of LEC significantly induced expression of pAkt at both 8 (p<0.05; Figure 2A) and 24 (p<0.01; Figure 2B) h compared to controls, as observed by western blot analysis.
Positive_regulation (induced) of Gene_expression (expression) of pAkt
16) Confidence 0.41 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994344 Disease Relevance 0.26 Pain Relevance 0
Moreover, the nuclear p65 signal tended to be reduced upon AKT1 knockdown in native cells (Figure 6; p65 panels for scrambled and pshAkt1), analogous to the confocal and Western results found in Par-4-overexpressing versus empty vector-transfected cells (Figure 5C).
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of AKT1
17) Confidence 0.41 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2883962 Disease Relevance 0.05 Pain Relevance 0
Following AKT1 knockdown, the cytoplasmic Par-4/p65 colocalized signal was significantly enhanced (Figure 6; Par4/p65 colocalize panel for pshAkt1).
Positive_regulation (enhanced) of Gene_expression (knockdown) of AKT1
18) Confidence 0.41 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2883962 Disease Relevance 0 Pain Relevance 0
Following AKT1 knockdown, the cytoplasmic Par-4/p65 colocalized signal was significantly enhanced (Figure 6; Par4/p65 colocalize panel for pshAkt1).
Positive_regulation (Following) of Gene_expression (knockdown) of AKT1
19) Confidence 0.41 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2883962 Disease Relevance 0 Pain Relevance 0
Various PI 3-kinase inhibitors such as Wortmannin, LY294002 and dominant-negative Akt expression vector were used to fully prove the involvement of PI 3-K/Akt pathway in the regulation of NF-?
Positive_regulation (vector) of Gene_expression (expression) of Akt
20) Confidence 0.37 Published 2004 Journal Mol Cancer Section Body Doc Link PMC394342 Disease Relevance 0.21 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox