INT123303

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.71
First Reported 2004
Last Reported 2010
Negated 1
Speculated 3
Reported most in Body
Documents 40
Total Number 44
Disease Relevance 15.50
Pain Relevance 1.18

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

mRNA processing (Smn1) nucleolus (Smn1) RNA binding (Smn1)
nucleus (Smn1) cytoplasm (Smn1)
Anatomy Link Frequency
HeLa 4
fibroblasts 3
motor neuron 2
spinal cord 1
Smn1 (Mus musculus)
Pain Link Frequency Relevance Heat
Spinal cord 156 97.06 Very High Very High Very High
cINOD 3 96.48 Very High Very High Very High
Central nervous system 80 87.28 High High
Action potential 2 81.44 Quite High
Intracerebroventricular 78 71.08 Quite High
palliative 2 64.80 Quite High
fibrosis 43 64.44 Quite High
Pain 4 50.00 Quite Low
diabetic neuropathy 2 48.80 Quite Low
antidepressant 2 47.28 Quite Low
Disease Link Frequency Relevance Heat
Targeted Disruption 41 99.98 Very High Very High Very High
Spinal Muscular Atrophy 1339 99.96 Very High Very High Very High
Disease 292 96.08 Very High Very High Very High
INFLAMMATION 3 95.04 Very High Very High Very High
Weight Gain 6 94.00 High High
Death 65 93.68 High High
Hepatotoxicity 14 90.48 High High
Neurodegenerative Disease 42 88.88 High High
Frailty 43 69.68 Quite High
Epidermolysis Bullosa Simplex 39 68.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To determine whether ASO-enhanced trans-splicing occurred in a more complex context of endogenous SMN gene expression, pIn711 and pM13 was co-transfected into HeLa cells to examine trans-splicing with endogenous SMN transcripts.
Gene_expression (expression) of SMN in HeLa
1) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.19 Pain Relevance 0
(Supplemental Figure S1A, S1B, see Methods) The ASO-expressing plasmids were co-transfected into HeLa cells with the SMN2 mini-gene and the pM13 which expresses the SMN trans-splicing RNA.
Gene_expression (expresses) of SMN in HeLa
2) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0 Pain Relevance 0
In addition to the identification and development of small molecules that stimulate full-length SMN2 expression, RNA modalities such as antisense oligonucleotides (ASO), TOES/bifunctional RNAs and trans-splicing RNAs have shown promise in SMA cell-based models [14]–[20].
Gene_expression (expression) of SMN2 associated with spinal muscular atrophy
3) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.64 Pain Relevance 0
The critical distinction between the two genes occurs at the RNA processing level: SMN1 produces full-length transcripts, while SMN2 primarily produces an alternatively spliced transcript lacking the final coding exon [10].
Gene_expression (produces) of SMN1
4) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 1.09 Pain Relevance 0.03
The critical distinction between the two genes occurs at the RNA processing level: SMN1 produces full-length transcripts, while SMN2 primarily produces an alternatively spliced transcript lacking the final coding exon [10].
Gene_expression (produces) of SMN2
5) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 1.13 Pain Relevance 0.03
HeLa cells express SMN1 and SMN2 genes and provide a robust level of target RNA.
Gene_expression (express) of SMN1 in HeLa
6) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.22 Pain Relevance 0
SMN levels in the co-transfected cells were comparable to SMN levels detected in the unaffected control fibroblasts, 3814 cells.
Gene_expression (levels) of SMN in fibroblasts
7) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.31 Pain Relevance 0
The cells are derived from a severe Type I SMA patient and lack endogenous SMN1, and consequently contain very low levels of SMN-enriched nuclear structures called gems and express very low levels of full-length SMN protein.
Gene_expression (express) of SMN associated with spinal muscular atrophy
8) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.28 Pain Relevance 0
HeLa cells express SMN1 and SMN2 genes and provide a robust level of target RNA.
Gene_expression (express) of SMN2 in HeLa
9) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.22 Pain Relevance 0
The SMA murine model expresses the genomic human SMN2 gene and the human SMN?
Gene_expression (expresses) of SMN2 associated with spinal muscular atrophy
10) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.39 Pain Relevance 0.07
Extracts derived from pMU3 transfected cells exhibited a two to four-fold increase compared to untreated extracts, demonstrating that the trans-splicing event not only generates higher levels of protein, but that SMN protein produced through this pathway is functional in a critical cellular process ascribed to native SMN (Figure 5A, 5B).
Gene_expression (produced) of SMN
11) Confidence 0.71 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.06 Pain Relevance 0
This single vector platform allows for the production of two individual RNAs that target distinct aspects of SMN pre-mRNA, leading to enhanced full-length SMN expression (Figure 1A).
Gene_expression (expression) of SMN
12) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.13 Pain Relevance 0
The SMA murine model expresses the genomic human SMN2 gene and the human SMN?
Gene_expression (expresses) of SMN associated with spinal muscular atrophy
13) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.39 Pain Relevance 0.07
To monitor the functionality of the SMN protein produced downstream of the trans-splicing event, SMN protein function was measured by in vitro snRNP assembly assays.
Gene_expression (produced) of SMN
14) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.09 Pain Relevance 0
Extracts generated from 3813 cells co-transfected with pM13 and increasing concentrations of ASO pIn711 were analyzed for SMN levels using a SMN monoclonal antibody.
Spec (analyzed) Gene_expression (levels) of SMN
15) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.31 Pain Relevance 0
Therefore, we initially examined SMN2 trans-splicing with the goal of devising strategies to enhance trans-splicing efficiency in vivo.
Spec (examined) Gene_expression (examined) of SMN2
16) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.31 Pain Relevance 0.07
The cells are derived from a severe Type I SMA patient and lack endogenous SMN1, and consequently contain very low levels of SMN-enriched nuclear structures called gems and express very low levels of full-length SMN protein.
Gene_expression (levels) of SMN associated with spinal muscular atrophy
17) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.28 Pain Relevance 0
SMN2 is retained in essentially all SMA patients and is a primary target for SMA therapeutic development [13].
Gene_expression (retained) of SMN2 associated with spinal muscular atrophy
18) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 1.08 Pain Relevance 0.03
To determine whether the cell-based analysis of pMU3 translated into comparable results in vivo, SMN proteins were examined in a previously described mouse model of SMA, referred to as SMN?
Spec (examined) Gene_expression (proteins) of SMN associated with spinal muscular atrophy
19) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.42 Pain Relevance 0.03
Therefore, the competition between SMN2 cis-splicing and trans-splicing is likely reduced, providing a potential advantage to trans-splicing in the SMN context compared to other alternatively regulated exons that retain fully functional splice sites.
Gene_expression (cis-splicing) of SMN2
20) Confidence 0.62 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565107 Disease Relevance 0.14 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox