INT141499

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Context Info
Confidence 0.64
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 17
Total Number 18
Disease Relevance 7.46
Pain Relevance 0.71

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

Anatomy Link Frequency
myocytes 2
skeletal muscle 2
muscle 1
pancreas 1
myotubes 1
MIR133B (Homo sapiens)
Pain Link Frequency Relevance Heat
tolerance 182 98.26 Very High Very High Very High
Chronic pancreatitis 2 91.16 High High
Paracetamol 4 11.60 Low Low
withdrawal 14 5.00 Very Low Very Low Very Low
cINOD 14 5.00 Very Low Very Low Very Low
Pain 14 5.00 Very Low Very Low Very Low
local anesthetic 14 5.00 Very Low Very Low Very Low
lidocaine 14 5.00 Very Low Very Low Very Low
Potency 14 5.00 Very Low Very Low Very Low
spastic colon 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 1107 99.84 Very High Very High Very High
Apoptosis 2 99.24 Very High Very High Very High
Impaired Glucose Tolerance 182 98.26 Very High Very High Very High
Coronary Heart Disease 24 97.14 Very High Very High Very High
Repression 2 95.84 Very High Very High Very High
Adenocarcinoma 9 92.52 High High
Pancreatitis 2 91.16 High High
Insulin Resistance 490 89.36 High High
Hypertrophy 14 89.20 High High
Aging 2 89.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The expression of miR-216 and -217 and lack of expression of miR-133a were identified as characteristic of pancreas tissue.
Gene_expression (expression) of miR-133a in pancreas
1) Confidence 0.64 Published 2007 Journal Oncogene Section Abstract Doc Link 17237814 Disease Relevance 0.79 Pain Relevance 0.16
The Northern probe detects both miR-133a and miR-133b due to sequence similarity.
Gene_expression (detects) of miR-133a
2) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.63 Pain Relevance 0.04
The Northern probe detects both miR-133a and miR-133b due to sequence similarity.
Gene_expression (detects) of miR-133b
3) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.63 Pain Relevance 0.04
Thus, we found that altered miR-133a expression modestly related to important clinical parameters.
Gene_expression (expression) of miR-133a
4) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.14 Pain Relevance 0.04
However, evidence of distinct binding proteins that modulate processing of pri-miRNA to mature miRNA [92] has emerged and we clearly demonstrate that expression of miR-1 and miR-133a are not co-regulated in vivo in human skeletal muscle.
Gene_expression (expression) of miR-133a in skeletal muscle
5) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.32 Pain Relevance 0
A clear stepwise reduction in mature miR-133a expression was observed across the three clinical groups.
Gene_expression (expression) of miR-133a
6) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.43 Pain Relevance 0.08
In addition, miR-133a expression was significantly associated with HbA1c, an indicator of long-term glucose homeostasis (R2 = 0.29, P < 0.01) and also correlated with HOMA1 (R2 = 0.15, P = 0.04).
Gene_expression (expression) of miR-133a
7) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.29 Pain Relevance 0.07
Over-expression of miR-1 [55] or miR-206 [86] in mouse myoblasts accelerates differentiation into myotubes whereas over-expression of miR-133 promotes proliferation [55].
Gene_expression (expression) of miR-133 in myotubes
8) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.40 Pain Relevance 0
We found that expression of miR-133a was associated with fasting glucose and 2 hour glucose tolerance data (R2 = 0.37, P < 0.001), with higher fasting glucose levels associated with lower miR-133a expression (Figure 2d).
Gene_expression (expression) of miR-133a associated with tolerance and impaired glucose tolerance
9) Confidence 0.28 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.37 Pain Relevance 0.08
Skeletal muscle miR-133a expression was reduced by five-fold in T2D (P < 0.001).
Gene_expression (expression) of miR-133a in Skeletal muscle associated with diabetes mellitus
10) Confidence 0.24 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.44 Pain Relevance 0.08
We found that expression of miR-133a was associated with fasting glucose and 2 hour glucose tolerance data (R2 = 0.37, P < 0.001), with higher fasting glucose levels associated with lower miR-133a expression (Figure 2d).
Gene_expression (expression) of miR-133a associated with tolerance and impaired glucose tolerance
11) Confidence 0.24 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.30 Pain Relevance 0.08
An oligonucleotide was synthesized to probe for miR-133a/b (5'-AGCUGGUUGAAGGGGACCAAA-3').
Gene_expression (synthesized) of miR-133a
12) Confidence 0.24 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0 Pain Relevance 0
ANOVA indicated that miR-133a (F = 11.8, P < 0.0001) was significantly different between the three groups, miR-206 expression more modestly altered (F = 4.5, P = 0.02) and miR-1 and miR-133b were unchanged (Figure 2c).
Gene_expression (expression) of miR-133b
13) Confidence 0.21 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.75 Pain Relevance 0.05
Several groups have used microarray data to examine the expression changes when a single miRNA changes, and we used the mean absolute expression approach described recently by Arora and Simpson [49] and also the tissue-centric approach described by Sood et al. [50] to determine whether we could detect shifts in the average expression of mRNA targets of the muscle-specific miRNAs (miR-1, miR-133a/b and miR-206, collectively known as 'myomirs') in human skeletal muscle.
Gene_expression (expression) of miR-133a in muscle
14) Confidence 0.21 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0 Pain Relevance 0
Regulation of miRNA production, post-transcriptionally, is proving to be potentially important for determining stem cell differentiation [93,94] while the protein or signaling factors that inhibit miR-133a production in T2D remain to be determined, this process clearly has the potential to alter muscle differentiation [28].


Gene_expression (production) of miR-133a in stem cell associated with diabetes mellitus
15) Confidence 0.21 Published 2010 Journal Genome Med Section Body Doc Link PMC2847700 Disease Relevance 0.51 Pain Relevance 0
Both miR-1 and -133 seem to play a crucial role in the regulation of cardiac hypertrophy and their down-regulation allows for the de-repression of growth-related genes that are involved in cardiac hypertrophy.6 Intriguingly, miR-1 and -133 play opposing roles in cell fate determination; miR-1 has a pro-apoptotic function31,32 that is rescued by the expression of miR-133 (32). miR-1 and miR-133 also regulate cardiac electrical properties; miR-1 is known to trigger cardiac arrhythmias33 and both miR-1 and -133 have been shown to target the pacemaker current If.34 miR-499-5p is highly expressed in the myocardium25,35 and its up-regulation is associated with cell senescence, suggesting that it may play a role in terminal differentiation.36,37 Further, miR-499 has also been shown to promote the differentiation of cardiac progenitor cells into myocytes;38 therefore, it may play a role in the activation of repair mechanisms following MI.
Gene_expression (expression) of miR-133 in myocytes associated with aging, repression, apoptosis, coronary heart disease and myocardial infarction
16) Confidence 0.01 Published 2010 Journal European Heart Journal Section Body Doc Link PMC2980809 Disease Relevance 0.69 Pain Relevance 0
Both miR-1 and -133 seem to play a crucial role in the regulation of cardiac hypertrophy and their down-regulation allows for the de-repression of growth-related genes that are involved in cardiac hypertrophy.6 Intriguingly, miR-1 and -133 play opposing roles in cell fate determination; miR-1 has a pro-apoptotic function31,32 that is rescued by the expression of miR-133 (32). miR-1 and miR-133 also regulate cardiac electrical properties; miR-1 is known to trigger cardiac arrhythmias33 and both miR-1 and -133 have been shown to target the pacemaker current If.34 miR-499-5p is highly expressed in the myocardium25,35 and its up-regulation is associated with cell senescence, suggesting that it may play a role in terminal differentiation.36,37 Further, miR-499 has also been shown to promote the differentiation of cardiac progenitor cells into myocytes;38 therefore, it may play a role in the activation of repair mechanisms following MI.
Gene_expression (expression) of miR-133 in myocytes associated with aging, repression, apoptosis, coronary heart disease and myocardial infarction
17) Confidence 0.01 Published 2010 Journal European Heart Journal Section Body Doc Link PMC2980809 Disease Relevance 0.69 Pain Relevance 0
Recently, Kim and Bartel (40) tested the effect of 67 pDSPs altering target sites for miR-1/206, miR-133 and miR-122 in the 3?
Gene_expression (/) of miR-133
18) Confidence 0.00 Published 2010 Journal Nucleic Acids Research Section Body Doc Link PMC2808989 Disease Relevance 0.08 Pain Relevance 0

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