INT279125

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Context Info
Confidence 0.32
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 3
Disease Relevance 2.59
Pain Relevance 0.36

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

extracellular region (COL9A2)
Anatomy Link Frequency
chondrocytes 1
COL9A2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Arthritis 74 90.24 High High
Inflammation 62 63.96 Quite High
rheumatoid arthritis 16 5.00 Very Low Very Low Very Low
cytokine 10 5.00 Very Low Very Low Very Low
Inflammatory mediators 6 5.00 Very Low Very Low Very Low
chemokine 6 5.00 Very Low Very Low Very Low
Osteoarthritis 3 5.00 Very Low Very Low Very Low
methotrexate 2 5.00 Very Low Very Low Very Low
Analgesic 2 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Alpha-1-antitrypsin Deficiency 10 100.00 Very High Very High Very High
Mucocutaneous Lymph Node Syndrome 100 90.76 High High
Arthritis 68 90.24 High High
Disease 144 88.72 High High
Cleidocranial Dysplasia 4 86.00 High High
Osteochondrodysplasias 44 82.36 Quite High
Death 1 72.68 Quite High
Fever 22 66.04 Quite High
INFLAMMATION 70 63.96 Quite High
Rheumatoid Arthritis 16 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Recently there has been much speculation about the reason for this genetic heterogeneity, and a number of hypotheses have been suggested; i.e., 1) some mutations disrupt specific interactions between matrilin-3, type IX collagen, and COMP in the cartilage ECM [Briggs and Chapman, 2002]; 2) the blocked/delayed secretion of one mutant protein results in a cascade of protein retention within the rER of chondrocytes [Unger and Hecht, 2001]; or 3) a combination of both mechanisms [Dinser et al., 2002].
type IX collagen Binding (interactions) of in chondrocytes
1) Confidence 0.32 Published 2005 Journal Human Mutation Section Body Doc Link PMC2726956 Disease Relevance 0.37 Pain Relevance 0
As shown in TablesĀ 6 and 7, the 17-peptide biomarkers were found to be degradation products of eight different proteins: alpha1 antitrypsin (A1AT, two peptides having overlapping sequences), collagen type I alpha 1 (COL1A1; five peptides and three of them having overlapping sequences), collagen type I alpha 2 (COL1A2; one peptide), collagen type III alpha 1 (COL3A1; one peptide), collagen type IX alpha 2 (COL9A2; one peptide), fibrinogen alpha (FGA; two peptides having overlapping sequences), fibrinogen beta (FGB; two peptides having overlapping sequences), and uromodulin (UMOD; three peptides having overlapping sequences).
collagen type IX alpha 2 Binding (found) of associated with alpha-1-antitrypsin deficiency
2) Confidence 0.26 Published 2010 Journal Clin Proteomics Section Body Doc Link PMC2970804 Disease Relevance 1.08 Pain Relevance 0.18
As shown in TablesĀ 6 and 7, the 17-peptide biomarkers were found to be degradation products of eight different proteins: alpha1 antitrypsin (A1AT, two peptides having overlapping sequences), collagen type I alpha 1 (COL1A1; five peptides and three of them having overlapping sequences), collagen type I alpha 2 (COL1A2; one peptide), collagen type III alpha 1 (COL3A1; one peptide), collagen type IX alpha 2 (COL9A2; one peptide), fibrinogen alpha (FGA; two peptides having overlapping sequences), fibrinogen beta (FGB; two peptides having overlapping sequences), and uromodulin (UMOD; three peptides having overlapping sequences).
COL9A2 Binding (found) of associated with alpha-1-antitrypsin deficiency
3) Confidence 0.26 Published 2010 Journal Clin Proteomics Section Body Doc Link PMC2970804 Disease Relevance 1.14 Pain Relevance 0.18

General Comments

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