INT71019

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Context Info
Confidence 0.42
First Reported 1997
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 13
Disease Relevance 6.88
Pain Relevance 0.43

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

nucleoplasm (SMAD4) intracellular (SMAD4) protein binding transcription factor activity (SMAD4)
DNA binding (SMAD4) cytoplasm (SMAD4) cytosol (SMAD4)
Anatomy Link Frequency
liver 1
SMAD4 (Homo sapiens)
Pain Link Frequency Relevance Heat
IPN 2 75.68 Quite High
cytokine 6 74.52 Quite High
long-term potentiation 7 71.32 Quite High
antagonist 3 70.56 Quite High
Chronic pancreatitis 24 69.28 Quite High
nMDA receptor 2 65.04 Quite High
Dismenorea 3 20.44 Low Low
cerebral cortex 10 5.00 Very Low Very Low Very Low
Somatosensory cortex 8 5.00 Very Low Very Low Very Low
gABA 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 442 100.00 Very High Very High Very High
Malignant Neoplastic Disease 44 99.92 Very High Very High Very High
Metastasis 45 98.40 Very High Very High Very High
Carcinoma 6 97.16 Very High Very High Very High
Noninfiltrating Intraductal Carcinoma 1 95.92 Very High Very High Very High
Pancreatic Cancer 83 95.04 Very High Very High Very High
Adenoma 2 94.52 High High
Adenocarcinoma 73 84.28 Quite High
Pancreatitis 30 80.32 Quite High
Cleidocranial Dysplasia 6 77.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Genetic alterations such as K-ras mutation, inactivation of the p53, p16 and DPC4 genes and frequent chromosomal loss of the 17p, 9p, 18q and 1p are thought to play a crucial role in the carcinogenesis of pancreatic cancer.
Negative_regulation (inactivation) of DPC4 associated with pancreatic cancer
1) Confidence 0.42 Published 1997 Journal Nippon Geka Gakkai Zasshi Section Abstract Doc Link 9276865 Disease Relevance 0.60 Pain Relevance 0.20
Loss of other tumor suppressor genes like p53, BRCA2 and DPC4 (Smad4) occurs later in neoplasia development.
Negative_regulation (Loss) of DPC4 associated with cancer
2) Confidence 0.38 Published 2003 Journal Mol Cancer Section Body Doc Link PMC151686 Disease Relevance 1.31 Pain Relevance 0
Loss of other tumor suppressor genes like p53, BRCA2 and DPC4 (Smad4) occurs later in neoplasia development.
Negative_regulation (Loss) of Smad4 associated with cancer
3) Confidence 0.38 Published 2003 Journal Mol Cancer Section Body Doc Link PMC151686 Disease Relevance 1.31 Pain Relevance 0
Hence, down-regulation of Smad4 along with loss of 18q also appear to be properties of the tumor.
Negative_regulation (regulation) of Smad4 associated with cancer
4) Confidence 0.34 Published 2010 Journal Genome Biol Section Body Doc Link PMC2945784 Disease Relevance 0.93 Pain Relevance 0
In such cases it is believed that the inactivation of the tumor suppressor protein Smad4 and the allelic loss of 18q are driving events in the formation of metastasis to the liver [20].
Negative_regulation (inactivation) of Smad4 in liver associated with cancer and metastasis
5) Confidence 0.34 Published 2010 Journal Genome Biol Section Body Doc Link PMC2945784 Disease Relevance 0.85 Pain Relevance 0
The expression level of Smad4 in the tumor was found to be very low (43-fold lower than in samples within our compendium of tumor expression data).
Negative_regulation (low) of Smad4 associated with cancer
6) Confidence 0.33 Published 2010 Journal Genome Biol Section Body Doc Link PMC2945784 Disease Relevance 0.90 Pain Relevance 0
The formed smad2/3-smad4 factor is mutually inhibited with PPAR-alpha-RXR-alpha complex.
Negative_regulation (inhibited) of smad4
7) Confidence 0.25 Published 2010 Journal BMC Bioinformatics Section Body Doc Link PMC2944280 Disease Relevance 0 Pain Relevance 0.16
However, molecular analyses demonstrate genetic alterations like the loss of DPC4 in distinct invasive forms of IPMNs, PanIN-3 as well as in DACs.
Negative_regulation (loss) of DPC4
8) Confidence 0.22 Published 2003 Journal Mol Cancer Section Body Doc Link PMC149423 Disease Relevance 0.98 Pain Relevance 0
We have demonstrated via knockdown of SMAD 4 that TGF?
Negative_regulation (knockdown) of SMAD 4
9) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2945765 Disease Relevance 0 Pain Relevance 0.07
Targeted knockdown of SMAD 4 in decidualized ESCs using two independent siRNAs (n?
Negative_regulation (knockdown) of SMAD 4
10) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2945765 Disease Relevance 0 Pain Relevance 0
In contrast, targeted knockdown of SMAD 4 prevented the TGF?
Negative_regulation (knockdown) of SMAD 4
11) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2945765 Disease Relevance 0 Pain Relevance 0
The role of the reelin receptors ApoER2 and VLVDR was evaluated using RAP, which blocks both receptors [46], [47], or using SP600125 which blocks ApoER2 by inhibiting JIP activity [49].
Negative_regulation (inhibiting) of JIP
12) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965671 Disease Relevance 0 Pain Relevance 0
We inhibited JIP activity by applying SP600125 (50 ┬ÁM).
Negative_regulation (inhibited) of JIP
13) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2965671 Disease Relevance 0 Pain Relevance 0

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