INT167957

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Context Info
Confidence 0.10
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 13
Disease Relevance 3.43
Pain Relevance 0.14

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
plasma 1
HeLa 1
smooth muscle cells 1
hearts 1
brush 1
Grxcr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Analgesic 3 97.16 Very High Very High Very High
Osteoarthritis 6 87.24 High High
cva 12 5.00 Very Low Very Low Very Low
anesthesia 7 5.00 Very Low Very Low Very Low
isoflurane 6 5.00 Very Low Very Low Very Low
Pain 3 5.00 Very Low Very Low Very Low
Somatostatin 3 5.00 Very Low Very Low Very Low
headache 2 5.00 Very Low Very Low Very Low
imagery 2 5.00 Very Low Very Low Very Low
ketamine 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 152 99.92 Very High Very High Very High
Hypercalcemia 9 99.64 Very High Very High Very High
Targeted Disruption 70 99.48 Very High Very High Very High
Phosphate Metabolism Disorders 6 99.44 Very High Very High Very High
Calcification 36 94.72 High High
Rickets 219 93.60 High High
Heart Rate Under Development 3 92.80 High High
Osteoarthritis 6 87.24 High High
Hypocalcemia 3 83.76 Quite High
Osteoporosis 30 82.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
Gene_expression (is) of Pi in brush
1) Confidence 0.10 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0 Pain Relevance 0
The CrP/Pi ratio in the MECR transgenic hearts (1.26±0.17) (mean±SD) after pacing at 7.5 Hz tended to be lower than that in controls (1.40±0.43).
Gene_expression (ratio) of Pi in hearts associated with targeted disruption
2) Confidence 0.09 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2680037 Disease Relevance 0.43 Pain Relevance 0
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.
Gene_expression (loss) of Pi associated with hypercalcemia
3) Confidence 0.08 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.56 Pain Relevance 0
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.
Gene_expression (leaks) of Pi associated with hypercalcemia
4) Confidence 0.08 Published 2008 Journal Eur J Pediatr Section Body Doc Link PMC2668657 Disease Relevance 0.59 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].
Gene_expression (expression) of Pi in smooth muscle cells associated with calcification
5) Confidence 0.08 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.49 Pain Relevance 0.04
Notably, a recent report shows that under physiological conditions, the Pi-transport activity of PiT1 is saturated [49], implying that only an increase in the capacity (i.e. enhanced expression of functional Pi transporters) can mediate an increase in Pi influx.
Gene_expression (expression) of Pi
6) Confidence 0.08 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.23 Pain Relevance 0
MATERIALS AND METHODS: Mice were pretreated with TDE (250, 500 and 1,000 mg/kg body weight) for 28 days and then received i.c.v. injection of Abeta25-35 peptides.
Gene_expression (pretreated) of TDE in body
7) Confidence 0.08 Published 2010 Journal J Ethnopharmacol Section Abstract Doc Link 20435125 Disease Relevance 0.15 Pain Relevance 0.10
Maintenance of a normal Pi uptake in PiT1-null MEFs supports the idea that the defect in MEF proliferation was not a consequence of Pi deprivation but resulted in a transport-independent function of PiT1, consistent with our recent data obtained in HepG2 and HeLa cells [9].
Gene_expression (deprivation) of Pi in HeLa
8) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.06 Pain Relevance 0
5 MEFs was abolished, this was associated with a 1.8-fold overexpression of PiT2 mRNA (Fig. 8C), which could account for the maintenance of normal Na+-Pi transport in PiT1-null MEFs.
Gene_expression (overexpression) of Pi
9) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.06 Pain Relevance 0
Interestingly, our results showed that Na+-Pi uptake in PiT1-null MEFs was unaffected (Fig. 8B), with no change in its kinetic properties (Vmax ?
Gene_expression (uptake) of Pi
10) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2818845 Disease Relevance 0.07 Pain Relevance 0
PiT1 (or SLC20a1) encodes a widely expressed plasma membrane protein functioning as a high-affinity Na+-phosphate (Pi) cotransporter.
Gene_expression (expressed) of Pi in plasma
11) Confidence 0.05 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2818845 Disease Relevance 0.05 Pain Relevance 0
Annexin V-FITC/PI assay
Gene_expression (assay) of PI
12) Confidence 0.03 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2222640 Disease Relevance 0.48 Pain Relevance 0
The cells were then stained with PI and analyzed DNA content by flow cytometry.
Gene_expression (stained) of PI
13) Confidence 0.03 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2222640 Disease Relevance 0.26 Pain Relevance 0

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