ABCC7 p.Glu1474*
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Sentence
Comment
43
EXPERIMENTAL PROCEDURES cRNAs for CFTR and Double Electrode Voltage Clamp-Oocytes were injected with cRNA (10 ng, 47 nl of double-distilled water) encoding wtCFTR, L1430A/L1431A, S573A, S1248A, F508del-CFTR, G551D-CFTR, S768A, S737A, S768D, S737D, E1474X, and AMPK␣1.
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ABCC7 p.Glu1474* 19095655:43:248
status: NEW184 We eliminated the PDZ binding domain of CFTR (E1474X-CFTR) and gradually increased stimulation of the oocytes as shown in Fig. 5D.
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ABCC7 p.Glu1474* 19095655:184:46
status: NEW187 In marked contrast 3 mM 8Br- -cAMP alone was unable to promote full activation of E1474X-CFTR but instead required costimulation by 8Br- -cAMP, forskolin, and IBMX, and compound C further augmented whole cell conductance (Fig. 5D) suggesting AMPK sensitivity was retained by this mutant.
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ABCC7 p.Glu1474* 19095655:187:82
status: NEW
PMID: 21647592
[PubMed]
Kongsuphol P et al: "CFTR induces extracellular acid sensing in Xenopus oocytes which activates endogenous Ca(2)-activated Cl conductance."
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Sentence
Comment
8
Because expression of CFTR-E1474X did not confer proton sensitivity, we propose that CFTR translocates a proton receptor to the plasma membrane via its PDZ-binding domain.
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ABCC7 p.Glu1474* 21647592:8:27
status: NEW121 In order to further support the concept of membrane translocation of a proton receptor by CFTR, we expressed a C-terminally truncated CFTR that lacks of the PDZBD (CFTR-E1474X) and that should no longer be able Fig. 6 The H+ -activated current is blocked by inhibitors of CaCC. a Original recording obtained from an oocyte expressing wtCFTR and exposed to extracellular pH 5.5 in the absence or presence of DIDS (100 μM) or NFA (100 μM).
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ABCC7 p.Glu1474* 21647592:121:169
status: NEW133 When expressed in Xenopus oocytes, CFTR-E1474X generated a cAMP-activated whole cell conductance of 23±3.2 μS (n=6), indicating membrane expression of functional CFTR.
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ABCC7 p.Glu1474* 21647592:133:40
status: NEW134 However, in the presence of CFTR-E1474X, Ca2+ - activated Cl- currents-conductance were no longer activated by extracellular acidic pH (ΔG=0±0.1 μS; n=6).
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ABCC7 p.Glu1474* 21647592:134:33
status: NEW
PMID: 11597353
[PubMed]
Boucherot A et al: "Role of CFTR's PDZ1-binding domain, NBF1 and Cl(-) conductance in inhibition of epithelial Na(+) channels in Xenopus oocytes."
No.
Sentence
Comment
72
In addition, we generated a CFTR mutant which only lacks the last six amino acids, encoding the PDZ-BD (E1474X-CFTR).
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ABCC7 p.Glu1474* 11597353:72:104
status: NEW77 E1474X-CFTR generated a signi'cantly larger current than wtCFTR and largely downregulated GAmil (Fig. 2).
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ABCC7 p.Glu1474* 11597353:77:0
status: NEW78 In fact, downregulation of ENaC was signi'cantly enhanced when compared to wtCFTR, which is likely due to the large Cl3 conductance generated by E1474X-CFTR.
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ABCC7 p.Glu1474* 11597353:78:145
status: NEW91 Coexpression of wtCFTR, L1480V-CFTR, E831X-CFTR and E1474X with ENaC.
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ABCC7 p.Glu1474* 11597353:91:52
status: NEW94 Stimulation of either wtCFTR, L1480V-CFTR, E831X-CFTR or E1474X signi'cantly enhanced CFTR whole cell Cl3 conductance.
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ABCC7 p.Glu1474* 11597353:94:57
status: NEW151 It was a surprising and rather unexpected result that E1474X-CFTR caused a very large Cl3 conductance which was signi'cantly enhanced compared to wtCFTR.
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ABCC7 p.Glu1474* 11597353:151:54
status: NEW