INT118371

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Context Info
Confidence 0.69
First Reported 2004
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 15
Total Number 21
Disease Relevance 25.34
Pain Relevance 0.85

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
fibroblast 2
fat 1
cleavage 1
Fgf23 (Mus musculus)
Pain Link Frequency Relevance Heat
Pain 25 94.16 High High
Bile 112 81.12 Quite High
Somatostatin 11 74.96 Quite High
cytokine 7 5.00 Very Low Very Low Very Low
Spinal cord 7 5.00 Very Low Very Low Very Low
agonist 7 5.00 Very Low Very Low Very Low
sodium channel 7 5.00 Very Low Very Low Very Low
Eae 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Rickets 945 99.84 Very High Very High Very High
Familial Hypophosphatemia 35 99.36 Very High Very High Very High
Renal Failure 7 99.28 Very High Very High Very High
Hypophosphatemia 163 99.00 Very High Very High Very High
Cancer 173 98.80 Very High Very High Very High
Disease 153 97.44 Very High Very High Very High
Diabetes Mellitus 14 97.36 Very High Very High Very High
Targeted Disruption 259 95.60 Very High Very High Very High
Hypercalcemia 33 95.24 Very High Very High Very High
Paraneoplastic Syndromes 11 95.04 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Serum levels of FGF23 are found to be elevated in most but not all patients with proven TIO.
Positive_regulation (elevated) of FGF23 associated with rickets
1) Confidence 0.69 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.98 Pain Relevance 0.04
Although FGF23 concentrations are not invariably increased in XLH, an inverse relationship between FGF23 and the degree of hypophosphataemia has been found [25].
Neg (not) Positive_regulation (increased) of FGF23 associated with rickets and hypophosphatemia
2) Confidence 0.69 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.95 Pain Relevance 0
However, in the short-term, the new discoveries underline the evidence that current forms of treatment with calcitriol and phosphate supplements only partially address some of the defects in the disease (hypophosphataemia and low to normal 1,25(OH)2D concentrations), but do not alter the disturbed underlying mechanisms, such as elevated FGF23 and MEPE levels and the peri-osteocytic mineralisation defects.
Positive_regulation (elevated) of FGF23 associated with hypophosphatemia and disease
3) Confidence 0.69 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.20 Pain Relevance 0
More recent evidence indicates that elevated FGF23 plays a central role in hypophosphataemia, disturbed vitamin D metabolism and the development of osteomalacia and rickets characteristic of XLH [27].
Positive_regulation (elevated) of FGF23 associated with rickets and hypophosphatemia
4) Confidence 0.69 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.02 Pain Relevance 0
It appears that the biochemical features of hypophosphataemia, renal phosphate loss and inappropriately low 1,25(OH)2D, are due to the secondary elevation of FGF23 concentrations.
Positive_regulation (elevation) of FGF23 associated with hypophosphatemia
5) Confidence 0.69 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.01 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.
Positive_regulation (increase) of FGF-23 in fibroblast
6) Confidence 0.69 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.
Positive_regulation (increase) of fibroblast growth factor-23 in fibroblast
7) Confidence 0.69 Published 2006 Journal Pediatr. Nephrol. Section Abstract Doc Link 16721588 Disease Relevance 1.08 Pain Relevance 0.16
The increased Fgf23 suppresses the expression of Cyp27b1 and induces the expression of Cyp24 by activating the ?
Positive_regulation (increased) of Fgf23
8) Confidence 0.62 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.18 Pain Relevance 0.13
These results indicate that the hypophosphatemia in patients with loss-of-function Dmp1 mutations is induced by increased serum Fgf23 levels (Liu et al. 2008).
Positive_regulation (increased) of Fgf23 associated with hypophosphatemia
9) Confidence 0.54 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.50 Pain Relevance 0
X-linked hypophosphatemia (XLH) is caused by loss-of-function Phex mutations that increase serum Fgf23 levels (Table 2) (Johnson et al. 2009).
Positive_regulation (increase) of Fgf23 associated with hypophosphatemia
10) Confidence 0.54 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.52 Pain Relevance 0
Autosomal recessive hypophosphatemic rickets/osteomalacia (ARHR) is caused by loss-of-function Dmp1 mutations that increase serum Fgf23 levels (Table 2) (Lorenz-Depiereux et al. 2006).
Positive_regulation (increase) of Fgf23 associated with rickets
11) Confidence 0.54 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.57 Pain Relevance 0
These findings raise concerns about the possible role of treatment (calcitriol) in stimulating FGF23 concentrations and, thus, increasing renal Pi loss, inducing a vicious cycle of increasing Pi supplements, increasing secondary hyperparathyroidism and further Pi loss.
Positive_regulation (stimulating) of FGF23 associated with hypercalcemia
12) Confidence 0.50 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.49 Pain Relevance 0.06
Inactivating mutations of PHEX, thus, result in an increase in circulating concentrations of FGF23 with resultant phosphaturia [28].
Positive_regulation (increase) of FGF23 associated with familial hypophosphatemia
13) Confidence 0.50 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.84 Pain Relevance 0
Circulating 1,25-(OH)(2) vitamin D was very low (14 pM; N: 40-140) while the FGF-23 serum level was markedly elevated [359.5 reference units (RU)/ml, N: 33-105].
Positive_regulation (elevated) of FGF-23
14) Confidence 0.47 Published 2004 Journal Bone Section Abstract Doc Link 15121023 Disease Relevance 1.56 Pain Relevance 0.16
It does appear that DMP1 normally decreases FGF23 concentrations, as FGF23 concentrations are elevated in ARHR [21].
Positive_regulation (elevated) of FGF23 associated with rickets
15) Confidence 0.46 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.69 Pain Relevance 0
Fig. 2The effects of increased FGF23 on bone and mineral homeostasis.
Positive_regulation (increased) of FGF23
16) Confidence 0.46 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.08 Pain Relevance 0
A recent report found that FGF23 values were, surprisingly, not consistently elevated in patients with ADHR and that serum concentrations fluctuated between normal and elevated values, depending on whether or not the individual subject was hypophosphataemic (symptomatic) [9].
Neg (not) Positive_regulation (elevated) of FGF23 associated with rickets
17) Confidence 0.46 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.28 Pain Relevance 0.07
However, a number of laboratories have been unable to show that FGF23 is the substrate for PHEX; thus, it is now believed that PHEX may prevent the cleavage of an intermediate, such as matrix extracellular phosphoglycoprotein (MEPE), which controls circulating levels of FGF23 [6].
Positive_regulation (circulating) of FGF23 in cleavage
18) Confidence 0.44 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.78 Pain Relevance 0
Serum Fgf23 levels are also greatly increased in patients with renal failure, partly owing to decreased renal clearance.
Positive_regulation (increased) of Fgf23 associated with renal failure
19) Confidence 0.42 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 0.93 Pain Relevance 0
Fgf23 mutations in ADHR result in impaired proteolytic processing of Fgf23 and increased active Fgf23 levels in serum (Table 2) (White et al. 2001).
Positive_regulation (increased) of Fgf23 associated with rickets
20) Confidence 0.36 Published 2010 Journal Cell Tissue Res Section Body Doc Link PMC2948652 Disease Relevance 1.44 Pain Relevance 0

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