INT266822

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Context Info
Confidence 0.10
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 11
Disease Relevance 8.12
Pain Relevance 0.17

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
HeLa 1
smooth muscle cells 1
nucleus 1
brush 1
Grxcr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Osteoarthritis 2 91.68 High High
Pain 8 69.20 Quite High
ketamine 3 22.60 Low Low
Somatostatin 8 5.00 Very Low Very Low Very Low
cva 4 5.00 Very Low Very Low Very Low
anesthesia 3 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
Hypercalcemia 24 99.74 Very High Very High Very High
Disease 80 99.68 Very High Very High Very High
Rickets 584 99.58 Very High Very High Very High
Calcification 12 99.16 Very High Very High Very High
Pressure And Volume Under Development 2 98.96 Very High Very High Very High
Nephrotoxicity 8 97.04 Very High Very High Very High
Phosphate Metabolism Disorders 16 96.64 Very High Very High Very High
Cerebellooculorenal Syndrome 8 95.36 Very High Very High Very High
Apoptosis 74 94.88 High High
Dent Disease 8 94.56 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
PI (-) was nuclear swelling characterized by enlargement of the nucleus, and a decrease in PI fluorescence intensity.
Negative_regulation (decrease) of PI in nucleus associated with pressure and volume under development
1) Confidence 0.10 Published 2008 Journal Clinical and Experimental Otorhinolaryngology Section Body Doc Link PMC2671795 Disease Relevance 0.46 Pain Relevance 0
This apparently surprising finding is in keeping with experiments using the mouse homologue of XLH, the Hyp mouse, in which convincing evidence for a circulating factor causing the renal Pi loss in the disease has been found [16].
Negative_regulation (loss) of Pi associated with rickets and disease
2) Confidence 0.07 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.71 Pain Relevance 0
The major rate-limiting factor in the renal reabsorption of Pi is the Pi transporter located at the brush border membrane of the proximal renal tubular cells.
Negative_regulation (reabsorption) of Pi in brush
3) Confidence 0.06 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0 Pain Relevance 0
Numerous diseases are associated with rickets and increased renal Pi loss; however, it is the isolated phosphaturic entities that have attracted the most attention over the past decade, as the isolation of the genetic mutations responsible for their pathogenesis has resulted in a new understanding of the hormonal axis between bone mineralisation, renal Pi handling and vitamin D metabolism (TableĀ 2).


Negative_regulation (loss) of Pi associated with rickets and disease
4) Confidence 0.05 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.48 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.
Negative_regulation (loss) of Pi associated with hypercalcemia
5) Confidence 0.05 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.50 Pain Relevance 0.06
A calculated TmPi/GFR below this range indicates inappropriate renal Pi loss (similar to that which occurs in hyperparathyroidism or renal tubular Pi leaks, e.g.
Negative_regulation (loss) of Pi associated with hypercalcemia
6) Confidence 0.05 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.56 Pain Relevance 0
This paper briefly describes the control of serum phosphorus (Pi) concentrations in children and then discusses the advances made in elucidating the pathogenesis of various forms of hypophosphataemic rickets, concentrating on those associated with isolated renal tubular Pi loss.


Negative_regulation (loss) of Pi associated with rickets
7) Confidence 0.05 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.18 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.
Negative_regulation (loss) of Pi associated with hypercalcemia
8) Confidence 0.05 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.55 Pain Relevance 0.07
This review concentrates on those conditions associated with isolated renal tubular Pi loss rather than diseases associated with complex renal tubular defects, such as in the Fanconi syndrome (OMIM 134600), Lowe syndrome (OMIM 309000) [2], Dent disease (OMIM 300009) [2] or as a result of ifosfamide nephrotoxicity [22].


Negative_regulation (loss) of Pi associated with nephrotoxicity, phosphate metabolism disorders, dent disease, disease and cerebellooculorenal syndrome
9) Confidence 0.05 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 1.18 Pain Relevance 0
Therefore it is tempting to speculate that as in MEFs, HepG2 and HeLa cells [9], a PiT2 overexpression in mutant livers could compensate for a loss of Na+-Pi transport activity (as it is shared by PiT1 and PiT2), but not for a loss of a PiT1-specific function such as the proliferation-related function of PiT1.
Negative_regulation (loss) of Pi in HeLa
10) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0 Pain Relevance 0
Particularly, inhibition of Pi uptake by PiT1 small hairpin RNA in cultured vascular smooth muscle cells (VSMCs) blocked the expression of Pi-induced osteogenic differentiation markers, Runx2 and osteopontin, indicating that PiT1 might be a major mechanism for controlling vascular calcification and VSMC phenotypic state [18], [19].
Negative_regulation (inhibition) of Pi in smooth muscle cells associated with calcification
11) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.51 Pain Relevance 0.05

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