INT118373

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Context Info
Confidence 0.77
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 32
Disease Relevance 29.62
Pain Relevance 1.04

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

cell differentiation (Fgf23) extracellular space (Fgf23) extracellular region (Fgf23)
Anatomy Link Frequency
osteoblasts 2
fibroblast 2
osteocyte 2
kidney 2
ulna 1
Fgf23 (Mus musculus)
Pain Link Frequency Relevance Heat
Pain 36 94.52 High High
Bile 272 82.12 Quite High
Eae 17 75.92 Quite High
Somatostatin 12 72.96 Quite High
agonist 17 66.40 Quite High
cytokine 17 35.60 Quite Low
Spinal cord 17 5.00 Very Low Very Low Very Low
sodium channel 17 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Rickets 1198 100.00 Very High Very High Very High
Cancer 235 99.96 Very High Very High Very High
Metabolic Disorder 136 99.52 Very High Very High Very High
Hypophosphatemia 214 99.26 Very High Very High Very High
Renal Failure 17 98.20 Very High Very High Very High
Hematological Disease 34 97.20 Very High Very High Very High
Hypercalcemia 36 96.56 Very High Very High Very High
Calcification 102 95.84 Very High Very High Very High
Syndrome 66 95.76 Very High Very High Very High
Disease 223 95.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Recent evidence indicates that hypophosphataemia and rickets are probably due to the over-expression of FGF23 in the lesions [8, 19].
Gene_expression (over) of FGF23 associated with rickets and hypophosphatemia
1) Confidence 0.77 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.96 Pain Relevance 0.03
As with PHEX and FGF23, DMP1 is highly expressed in cells of the osteoblasts/osteocyte lineage.
Gene_expression (expressed) of FGF23 in osteoblasts
2) Confidence 0.77 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.44 Pain Relevance 0
Later, Fgf15/19, Fgf21, and Fgf23 were generated by two large-scale genome duplication events during the evolution of early vertebrates
Gene_expression (generated) of Fgf23
3) Confidence 0.69 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0 Pain Relevance 0
The ligand-bound VDR forms a heterodimer with retinoid X receptors (RXRs) and induces the expression of Fgf23.
Gene_expression (expression) of Fgf23
4) Confidence 0.69 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.13 Pain Relevance 0.13
It does appear that DMP1 normally decreases FGF23 concentrations, as FGF23 concentrations are elevated in ARHR [21].
Gene_expression (concentrations) of FGF23 associated with rickets
5) Confidence 0.67 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.65 Pain Relevance 0
In addition to hereditary Fgf23 signaling disorders, tumors that over-produce Fgf23 also cause metabolic disorders.
Gene_expression (produce) of Fgf23 associated with metabolic disorder and cancer
6) Confidence 0.60 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.14 Pain Relevance 0
Resolution of severe, adolescent-onset hypophosphatemic rickets following resection of an FGF-23-producing tumour of the distal ulna.
Gene_expression (producing) of FGF-23 in ulna associated with cancer and rickets
7) Confidence 0.60 Published 2004 Journal Bone Section Title Doc Link 15121023 Disease Relevance 1.58 Pain Relevance 0.16
Fgf23 mutations in ADHR result in impaired proteolytic processing of Fgf23 and increased active Fgf23 levels in serum (TableĀ 2) (White et al. 2001).
Gene_expression (processing) of Fgf23 associated with rickets
8) Confidence 0.60 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.38 Pain Relevance 0
Fgf23 mutations in ADHR result in impaired proteolytic processing of Fgf23 and increased active Fgf23 levels in serum (TableĀ 2) (White et al. 2001).
Gene_expression (levels) of Fgf23 associated with rickets
9) Confidence 0.60 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.45 Pain Relevance 0
Serum Fgf23 levels are also greatly increased in patients with renal failure, partly owing to decreased renal clearance.
Gene_expression (levels) of Fgf23 associated with renal failure
10) Confidence 0.60 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.92 Pain Relevance 0
Serum levels of FGF23 are found to be elevated in most but not all patients with proven TIO.
Gene_expression (levels) of FGF23 associated with rickets
11) Confidence 0.60 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.97 Pain Relevance 0.04
Recent evidence indicates that hypophosphataemia and rickets are probably due to the over-expression of FGF23 in the lesions [8, 19].
Gene_expression (expression) of FGF23 associated with rickets and hypophosphatemia
12) Confidence 0.60 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.96 Pain Relevance 0.03
Recent evidence indicates that hypophosphataemia and rickets are probably due to the over-expression of FGF23 in the lesions [8, 19].
Gene_expression (-) of FGF23 associated with rickets and hypophosphatemia
13) Confidence 0.60 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.96 Pain Relevance 0.03
It is of interest that the mRNA of all three factors (FGF23, PHEX and DMP1) involved in the pathogenesis of hypophosphataemic rickets are highly expressed in cells of the osteoblasts/osteocyte lineage.
Gene_expression (expressed) of FGF23 in osteocyte associated with rickets
14) Confidence 0.60 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.42 Pain Relevance 0
DMP1 appears to suppress FGF23 production directly [17].
Gene_expression (production) of FGF23
15) Confidence 0.60 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.75 Pain Relevance 0
The renal phosphate wasting is not intrinsic to the kidney but likely due to an increase in serum levels of fibroblast growth factor-23 (FGF-23), and perhaps other phosphate-wasting peptides previously known as phosphatonins.
Gene_expression (levels) of FGF-23 in fibroblast
16) Confidence 0.60 Published 2006 Journal Pediatr. Nephrol. Section Abstract Doc Link 16721588 Disease Relevance 1.08 Pain Relevance 0.17
The renal phosphate wasting is not intrinsic to the kidney but likely due to an increase in serum levels of fibroblast growth factor-23 (FGF-23), and perhaps other phosphate-wasting peptides previously known as phosphatonins.
Gene_expression (levels) of fibroblast growth factor-23 in fibroblast
17) Confidence 0.60 Published 2006 Journal Pediatr. Nephrol. Section Abstract Doc Link 16721588 Disease Relevance 1.07 Pain Relevance 0.16
Active vitamin D produced in the kidney increases the expression of Fgf23 in the bone and serum Fgf23 levels in mice.
Gene_expression (expression) of Fgf23 in kidney
18) Confidence 0.54 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.14 Pain Relevance 0.09
Fgf23 is mainly expressed in the bone.
Gene_expression (expressed) of Fgf23
19) Confidence 0.54 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.76 Pain Relevance 0.04
The ligand-bound VDR forms a heterodimer with retinoid X receptors (RXRs) and induces the expression of Fgf23 in the bone.
Gene_expression (expression) of Fgf23
20) Confidence 0.54 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.18 Pain Relevance 0.03

General Comments

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