INT260921

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.34
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 5
Disease Relevance 3.12
Pain Relevance 0.94

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

transport (Khsrp) mRNA processing (Khsrp) RNA binding (Khsrp)
nucleus (Khsrp) DNA binding (Khsrp) cytoplasm (Khsrp)
Anatomy Link Frequency
finger 2
Khsrp (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 465 97.44 Very High Very High Very High
cytokine 134 96.50 Very High Very High Very High
Kinase C 17 74.16 Quite High
Arthritis 21 70.24 Quite High
Inflammatory stimuli 12 70.08 Quite High
chemokine 40 58.08 Quite High
Inflammatory response 16 47.60 Quite Low
cINOD 21 29.52 Quite Low
aspirin 4 5.00 Very Low Very Low Very Low
Inflammatory mediators 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 577 97.66 Very High Very High Very High
INFLAMMATION 482 97.44 Very High Very High Very High
Targeted Disruption 34 78.52 Quite High
Hyperplasia 20 76.48 Quite High
Breast Cancer 20 71.68 Quite High
Arthritis 17 70.24 Quite High
Stress 15 63.36 Quite High
Congenital Anomalies 11 57.28 Quite High
Hypoxia 45 54.60 Quite High
Disease 39 48.64 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Studies have determined that stability of target mRNAs (iNOS) is increased when KHSRP is immunodepleted and that KHSRP co-immunoprecipitates with ZFP36 on target mRNAs and also competes directly with ELAVL1 for ARE-binding sites on target mRNAs (Linker et al., 2005; Chou et al., 2006).
Negative_regulation (immunodepleted) of KHSRP
1) Confidence 0.34 Published 2008 Journal Molecular Human Reproduction Section Body Doc Link PMC2639449 Disease Relevance 0.20 Pain Relevance 0.04
These are modulated during cellular stimulation by inactivation of RNA decay-promoting proteins such as zinc-finger protein, tristetraprolin (TTP) [4], K-homology splicing-regulatory protein (KSRP) [5], butyrate response factor 1 and 2 [6], and certain gene products of the AU-rich element (ARE)/poly(U)-binding/degradation factor 1 (AUF1) [7].
Negative_regulation (inactivation) of K-homology splicing-regulatory protein in finger
2) Confidence 0.27 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2921490 Disease Relevance 0.50 Pain Relevance 0.18
These are modulated during cellular stimulation by inactivation of RNA decay-promoting proteins such as zinc-finger protein, tristetraprolin (TTP) [4], K-homology splicing-regulatory protein (KSRP) [5], butyrate response factor 1 and 2 [6], and certain gene products of the AU-rich element (ARE)/poly(U)-binding/degradation factor 1 (AUF1) [7].
Negative_regulation (inactivation) of KSRP in finger
3) Confidence 0.27 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2921490 Disease Relevance 0.50 Pain Relevance 0.18
One of those is the p38 MAPK pathway that leads to phosphorylation and inactivation of the activity of the RNA decay-promoting proteins such as TTP and KSRP.
Negative_regulation (inactivation) of KSRP
4) Confidence 0.24 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2921490 Disease Relevance 0.95 Pain Relevance 0.33
Continued secretion of cytokines and growth factors during chronic inflammation and cancer contribute to a prolonged state of activated pathways such as the MAPK pathway that maintains mRNA stabilization by inactivation of RNA-binding proteins that participate in mRNA decay such as TTP and KSRP (Fig. 2).
Negative_regulation (inactivation) of KSRP associated with inflammation, cancer and cytokine
5) Confidence 0.12 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2921490 Disease Relevance 0.97 Pain Relevance 0.21

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox