INT69290

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Context Info
Confidence 0.75
First Reported 1997
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 3.69
Pain Relevance 2.52

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

endosome (Cftr) transport (Cftr) ATPase activity (Cftr)
enzyme binding (Cftr) protein complex (Cftr) transmembrane transport (Cftr)
Anatomy Link Frequency
glands 2
14.2 1
Cftr (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 143 100.00 Very High Very High Very High
sodium channel 7 99.80 Very High Very High Very High
substance P 18 99.76 Very High Very High Very High
qutenza 2 99.54 Very High Very High Very High
antagonist 3 91.36 High High
anesthesia 8 87.12 High High
adenocard 3 84.24 Quite High
Versed 3 81.76 Quite High
Bile 53 78.48 Quite High
Inflammation 24 53.36 Quite High
Disease Link Frequency Relevance Heat
Cystic Fibrosis 143 100.00 Very High Very High Very High
Targeted Disruption 21 100.00 Very High Very High Very High
Congenital Anomalies 15 99.02 Very High Very High Very High
Infection 20 93.16 High High
Multiple Myeloma 1 88.48 High High
Pulmonary Disease 22 85.72 High High
Disorder Of Lipid Metabolism 24 78.44 Quite High
Cyst 1 76.56 Quite High
Disease 14 75.60 Quite High
Cancer 2 58.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, in CFTR(-/-) mice, both forskolin- and carbachol-stimulated peak HCO3- secretions were fourfold less compared with those in CFTR(+/+) littermates (3.7 +/- 0.2 vs. 15.6 +/- 2.1 and 4.7 +/- 0.3 vs. 14.2 +/- 2.5 micromol x cm(-1) x h(-1), respectively; P < 0.01).
Localization (secretions) of CFTR in 14.2
1) Confidence 0.75 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9142920 Disease Relevance 0.13 Pain Relevance 0.22
CFTR mediates cAMP- and Ca2+-activated duodenal epithelial HCO3- secretion.
Localization (secretion) of CFTR
2) Confidence 0.75 Published 1997 Journal Am. J. Physiol. Section Title Doc Link 9142920 Disease Relevance 0.19 Pain Relevance 0.25
The aims of this series of experiments were to determine if CFTR mediates basal and stimulated duodenal epithelial HCO3- secretion.
Localization (secretion) of CFTR
3) Confidence 0.75 Published 1997 Journal Am. J. Physiol. Section Abstract Doc Link 9142920 Disease Relevance 0.19 Pain Relevance 0.26
We next examine the possibility that de novo lipogenesis could be stimulated in a state of CFTR depletion.
Localization (depletion) of CFTR
4) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864762 Disease Relevance 0.12 Pain Relevance 0
First, the protein expression of FAT/CD36, a transporter involved in FA uptake, displayed a 1,5-fold increase in CFTR-depleted cells (Figure 6A) although this difference did not reach the significance threshold (p<0.09).
Localization (increase) of CFTR
5) Confidence 0.74 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864762 Disease Relevance 0.16 Pain Relevance 0
Co-localization of CFTR and ENaC suggests that direct protein-protein interactions allow CFTR to closely regulate the activity of this channel [39,40].
Localization (localization) of CFTR associated with sodium channel
6) Confidence 0.67 Published 2001 Journal BMC Gastroenterol Section Body Doc Link PMC59644 Disease Relevance 0.39 Pain Relevance 0.41
In contrast, submucosal glands from CFTR knockout mice failed to secrete when stimulated by SP (1 micromol/l), although those from wild-type control littermates were responsive.
Neg (failed) Localization (secrete) of CFTR in glands associated with targeted disruption and substance p
7) Confidence 0.62 Published 2008 Journal Pflugers Arch. Section Abstract Doc Link 18509672 Disease Relevance 0.24 Pain Relevance 0.45
Substance P stimulates CFTR-dependent fluid secretion by mouse tracheal submucosal glands.
Localization (secretion) of CFTR in glands associated with substance p
8) Confidence 0.62 Published 2008 Journal Pflugers Arch. Section Title Doc Link 18509672 Disease Relevance 0.24 Pain Relevance 0.45
Alteration of the intracellular fate of mutant CFTR by intervening the protein processing and/or proteolytic pathway has shown promise for treating CF but selective inhibition of proteostatsis demands the controlled release of optimal amounts of drug overtime.
Localization (release) of CFTR
9) Confidence 0.56 Published 2010 Journal J Nanobiotechnology Section Body Doc Link PMC2954907 Disease Relevance 0.54 Pain Relevance 0.07
Abnormalities in sialylation of cells transfected with mutant CFTR and secretions of patients with CF have been described [9]; however, it has not been clear whether this phenomenon has been directly mediated by the presence of neuraminidases in colonizing bacteria or by the abnormal CFTR.
Localization (secretions) of CFTR associated with fibrosis and congenital anomalies
10) Confidence 0.54 Published 2009 Journal The Open Respiratory Medicine Journal Section Body Doc Link PMC2703207 Disease Relevance 0.91 Pain Relevance 0.33
effluxes could be mediated by a number of apical channels including cystic fibrosis transmembrane conductance regulator (CFTR), Ca2+-activated Cl?
Localization (channels) of CFTR associated with fibrosis and cystic fibrosis
11) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2994757 Disease Relevance 0.58 Pain Relevance 0.09

General Comments

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