INT246755

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Context Info
Confidence 0.50
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 4
Disease Relevance 1.01
Pain Relevance 0

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

cytosol (Tsc2) signal transduction (Tsc2) Golgi apparatus (Tsc2)
nucleus (Tsc2) intracellular (Tsc2) protein complex (Tsc2)
Anatomy Link Frequency
cardiac myocyte 1
Tsc2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cytokine 2 5.00 Very Low Very Low Very Low
cerebral cortex 2 5.00 Very Low Very Low Very Low
transdermal 2 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
adenocard 2 5.00 Very Low Very Low Very Low
Angina 2 5.00 Very Low Very Low Very Low
ketamine 1 5.00 Very Low Very Low Very Low
agonist 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Congenital Anomalies 7 99.98 Very High Very High Very High
Hypertrophy 1 99.92 Very High Very High Very High
Increased Venous Pressure Under Development 2 93.40 High High
Disease 42 72.20 Quite High
Autosomal Dominant Polycystic Kidney 2 67.92 Quite High
Apoptosis 9 62.96 Quite High
Vasculitis 6 60.16 Quite High
Cancer 52 58.40 Quite High
Diabetes Mellitus 39 51.28 Quite High
Neointima 21 50.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Mayer et al. [49] performed an RNA based screening of the entire coding regions of both TSC genes applying the protein truncation test (PTT) and identified a high proportion of unusual splicing abnormalities affecting the TSC2 gene.
Regulation (affecting) of TSC2 associated with congenital anomalies
1) Confidence 0.50 Published 2008 Journal Current Genomics Section Body Doc Link PMC2691673 Disease Relevance 0.28 Pain Relevance 0
Previous reports have identified a mutation consisting of a 34 bp deletion affecting portions of exon 38 and the adjacent intron 38 of TSC2.
Regulation (affecting) of TSC2
2) Confidence 0.37 Published 2008 Journal Current Genomics Section Body Doc Link PMC2691673 Disease Relevance 0.25 Pain Relevance 0
AMPK activation suppresses protein synthesis and prevents cardiac myocyte hypertrophy by regulation of the eEF2 kinase/eEF2 axis and/or TSC2-mTOR-P70S6 pathways.22-24) LKB1 has been reported to cause G1 growth arrest in cultured cells via induction of p21WAF1/CIP111) and stimulation of Brg1 ATPase.25) LKB1 kinase activity is required for p21WAF1/CIP1 induction, and overexpression of LKB1 causes p21WAF1/CIP1-induced growth arrest in cells with undetectable or low levels of endogenous LKB1.11) In contrast to kinase activity, although Brg1-associated growth arrest also requires LKB1 kinase activity, wild-type LKB1 and the kinase-deficient form LKB1-SL26 both stimulate Brg1 ATPase.25) This suggests that some regulatory functions of LKB1 may not require its kinase activity.19) As is well known, LKB1 has an autophosphorylation activity to increased its kinase activity.
Regulation (regulation) of TSC2 in cardiac myocyte associated with hypertrophy
3) Confidence 0.26 Published 2010 Journal Korean Circulation Journal Section Body Doc Link PMC3008825 Disease Relevance 0.43 Pain Relevance 0
Phosphorylation of hamartin and/or tuberin may play an important role in the regulation of the tuberin-hamartin complex (46).
Regulation (regulation) of tuberin
4) Confidence 0.11 Published 2008 Journal Diabetes Section Body Doc Link PMC2551671 Disease Relevance 0.05 Pain Relevance 0

General Comments

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