ABCC7 p.Thr1471Ala

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PMID: 23067305 [PubMed] Tosoni K et al: "CFTR mutations altering CFTR fragmentation."
No. Sentence Comment
6 The F508del and S511A mutations generate different fragmentation fingerprints that are each unlike the wild-type; yet, both mutants generate new N-terminal-bearing CFTR fragments that are not observed with other CK2-related mutations (S511D, S422A/D and T1471A/D).
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ABCC7 p.Thr1471Ala 23067305:6:254
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44 Cell culture, lysis, protein solubilization and Western blotting The cell culture methods to create the stable CFTR-expressing cell lines (WT, F, WT S422A, WT S422D, WT S511A, WT S511D, WT T1471A and WT T1471D) and their culture protocols have been described recently [25].
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ABCC7 p.Thr1471Ala 23067305:44:190
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215 wt-CFTR with mutated T1471 T1471A fragmentation is very similar to the wt.
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ABCC7 p.Thr1471Ala 23067305:215:27
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220 In summary, the two S511A/S511D and T1471A/T1471D pairs manifested very different CFTR cleavage patterns and abundance of full-length CFTR when present on a wt background.
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ABCC7 p.Thr1471Ala 23067305:220:36
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PMID: 24058532 [PubMed] Venerando A et al: "Detection of phospho-sites generated by protein kinase CK2 in CFTR: mechanistic aspects of Thr1471 phosphorylation."
No. Sentence Comment
91 Cell Culture Baby hamster kidney cells (BHK) stably expressing human CFTR (hCFTR) either wild type (WT), or Phe508del, or WT T1471A were growth to reach 70-80% confluency [13].
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ABCC7 p.Thr1471Ala 24058532:91:125
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147 Accordingly a hCFTR mutant no longer susceptible to such a phosphorylation (T1471A) was overexpressed in BHK cells as compared to hCFTR wild type.
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ABCC7 p.Thr1471Ala 24058532:147:76
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162 Once blockade is removed de novo synthesis of CFTR wild type is significantly stimulated if endogenous CK2 is inhibited by cell treatment with CX4945 (Panel A), a similar effect of CX4945 being also detectable if wild type CFTR is replaced by its T1471A mutant, which is no longer susceptible to phosphorylation at Thr1471 (Panel B).
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ABCC7 p.Thr1471Ala 24058532:162:247
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172 BHK cells expressing human CFTR wild type (A), T1471A (B) and Phe508del (C) were treated for 2 h with CHX to stop protein synthesis (compare first and second lanes).
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ABCC7 p.Thr1471Ala 24058532:172:47
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193 To get clues about the possible consequences of CFTR phosphorylation by CK2, advantage has been taken of the most selective CK2 inhibitor available to date, CX-4945 [43] and of a CFTR mutant in which Thr1471 has been replaced by alanine (T1471A) [13].
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ABCC7 p.Thr1471Ala 24058532:193:200
status: NEW
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ABCC7 p.Thr1471Ala 24058532:193:238
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197 On the other hand the effect of CK2 on CFTR stability seems not to be mediated by Thr1471, at least in a wild type background, since a similar effect of CX4945 was observed with CFTR wild type and its T1471A mutant (Figure 5, compare Panels A and B).
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ABCC7 p.Thr1471Ala 24058532:197:201
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206 (TIF) Figure S4 BHK cells expressing WT, WT/T1471A or Phe508delCFTR were exposed to either cycloheximide (CHX, 100 mg/ml) or Brefeldin A (BFA, 200 ng/ml).
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ABCC7 p.Thr1471Ala 24058532:206:45
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