INT84308
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The key question is: are these neoplasms related to previously unrecognized functions of CFTR, or are they secondary to chronic inflammation, infection, or malnutrition, which might predispose to malignancy? | |||||||||||||||
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Involvement of CFTR in mediating prostatic bicarbonate secretion | |||||||||||||||
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secretion, the CFTR-dependent bacterial killing capacity of the prostate could be due to a direct effect of HCO3? | |||||||||||||||
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Immunofluorescent staining also localized CFTR protein to the plasma membrane of the culture epithelial cells (Figure 1D, right), which was also stained positive for cytokeratin 5&8, a marker of epithelial cells (Figure 1D, middle).
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However, given the striking increase of studies suggesting capability of CFTR to conduct large anions when they are present on the intracellular side and where ATP hydrolysis can occur [44], one may suppose that, in certain physiological conditions, even normally ATP-impermeable Cl? | |||||||||||||||
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Interestingly, CFTR knockout animals, in which MRP1 expression was found to be augmented, had an increased rate of ATP release from unstimulated erythrocytes, suggesting that ATP release was mediated by MRP1 but not by CFTR. | |||||||||||||||
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CFTR-independent ATP release was observed by Takahashi et al. [54] in 3T3 fibroblasts, by Grygorczyk and Hanrahan [55] in T84, CHO, Calu-3, NIH3T3 and some other cells, by Mitchell et al. [56] in ocular ciliary epithelial cells, by Watt et al. [57] in human nasal epithelial cells in primary culture, by Hazama et al. [5861] in human Intestine 407 and mouse C127 cells, and by Donaldson et al. [62] in nasal airway surface liquid from normal and CF subjects. | |||||||||||||||
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Heterologous expression of CFTR was shown to downregulate VSOR anion channel activity in CPAE and COS cells [116] as well as in HEK293T cells [117], but upregulate swelling-induced ATP release from C127/CFTR cells [58, 60]. | |||||||||||||||
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Three features distinguish CF from controls: 1) higher basal PD, reflecting enhanced Na+ transport secondary to relative Cl- impermeability 2) greater inhibition of PD after nasal perfusion with amiloride, a Na+ channel inhibitor, and 3) little or no change in change of Cl- transport in response to perfusion with a Cl--free solution along with isoproteronol, (which reflects an absence of CFTR-mediated Cl- secretion). | |||||||||||||||
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If anionic forms of ATP are released via the CFTR channel, then actual ATP-mediated conductance should be measurable in CFTR-expressing cells under certain experimental conditions. | |||||||||||||||
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This article reviews the impact of CF on the pancreas, the role of the CFTR protein in pancreatic secretion, and some of the exciting research identifying mutations in the CFTR gene as a risk factor for idiopathic acute and chronic pancreatitis. | |||||||||||||||
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Bioresponsive matrices in drug delivery
For years, the field of drug delivery has focused on (1) controlling the release of a therapeutic and (2) targeting the therapeutic to a specific cell type. | |||||||||||||||
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General Comments
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