INT266818

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Context Info
Confidence 0.12
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 8
Disease Relevance 3.90
Pain Relevance 0

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

cilium (Grxcr1) molecular_function (Grxcr1)
Anatomy Link Frequency
renal tubule 1
vasculature 1
thyroid 1
osteoblast 1
urine 1
Grxcr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Pain 5 5.00 Very Low Very Low Very Low
Somatostatin 5 5.00 Very Low Very Low Very Low
cva 4 5.00 Very Low Very Low Very Low
ketamine 3 5.00 Very Low Very Low Very Low
anesthesia 3 5.00 Very Low Very Low Very Low
Osteoarthritis 2 5.00 Very Low Very Low Very Low
isoflurane 2 5.00 Very Low Very Low Very Low
medulla 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Calcification 12 100.00 Very High Very High Very High
Hypocalcemia 5 99.20 Very High Very High Very High
Osteoporosis 10 98.76 Very High Very High Very High
Rickets 365 98.68 Very High Very High Very High
Phosphate Metabolism Disorders 10 97.04 Very High Very High Very High
Apoptosis 74 96.68 Very High Very High Very High
Death 17 93.08 High High
Hypercalcemia 15 92.12 High High
Disease 50 91.52 High High
Hypophosphatemia 55 89.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
All the OHCs could be differentiated as 4 groups according to the F-actin and PI staining (Fig. 1).
Localization (staining) of PI
1) Confidence 0.12 Published 2008 Journal Clinical and Experimental Otorhinolaryngology Section Body Doc Link PMC2671795 Disease Relevance 0.19 Pain Relevance 0
Hypophosphataemic rickets due to decreased intestinal absorption either because of a low dietary intake or the prolonged ingestion of antacids will not be discussed further, as these do not involve a primary defect in renal Pi handling.
Localization (handling) of Pi associated with rickets
2) Confidence 0.09 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.14 Pain Relevance 0
Serum Pi homeostasis is maintained largely through the control of renal phosphate reabsorption, and, in a steady state, urine Pi excretion reflects dietary intake.
Localization (excretion) of Pi in urine
3) Confidence 0.09 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.06 Pain Relevance 0
Elevated concentrations of FGF23 internalise and reduce the NaPi-IIa and c cotransporters in the proximal renal tubule, reducing Pi reabsorption and suppressing 1 alpha-hydroxylase activity, thus, reducing 1,25-(OH)2D and serum Pi concentrations (Fig. 2) [11].
Localization (reabsorption) of Pi in renal tubule
4) Confidence 0.09 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.80 Pain Relevance 0
A number of factors influence the renal tubular reabsorption of Pi, such as dietary phosphorus content, and parathyroid hormone (PTH), growth hormone (insulin-like growth factor 1) and thyroid hormone concentrations, although these latter two hormones probably do not play a major role in the short-term control of serum Pi concentrations, but, rather, determine long-term concentrations.
Localization (reabsorption) of Pi in thyroid
5) Confidence 0.09 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.05 Pain Relevance 0
Fanconi syndrome and isolated renal phosphate loss from various forms of hypophosphataemic rickets) and a value above the normal range suggests inappropriate renal Pi retention (as that occurs in hypoparathyroidism or dietary phosphate restriction).


Localization (retention) of Pi associated with phosphate metabolism disorders, hypocalcemia and rickets
6) Confidence 0.09 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.70 Pain Relevance 0
In summary, although PiT1 does not seem to be essential to the development of a normal vasculature, it remains to be determined whether PiT1 is instrumental to a Pi-induced vascular calcification in vivo through the generation of animals carrying a tissue-specific deletion of PiT1.
Localization (deletion) of Pi in vasculature associated with calcification
7) Confidence 0.07 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.49 Pain Relevance 0
PiT1, but not PiT2, mRNA and Na+-Pi transport were found to be regulated in osteoblast-like and chondrogenic cells by various factors, mainly Pi, IGF-1, BMP2 and TGF-?
Localization (transport) of Pi in osteoblast associated with osteoporosis
8) Confidence 0.07 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.47 Pain Relevance 0

General Comments

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