ABCC7 p.Tyr512Ala
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PMID: 18391167
[PubMed]
Chen TY et al: "CLC-0 and CFTR: chloride channels evolved from transporters."
No.
Sentence
Comment
410
However, the corresponding mutation of Y512A in CLC-0 is almost without functional consequence (4).
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ABCC7 p.Tyr512Ala 18391167:410:39
status: NEW
PMID: 24178769
[PubMed]
Cesaro L et al: "Phosphorylation of cystic fibrosis transmembrane conductance regulator (CFTR) serine-511 by the combined action of tyrosine kinases and CK2: the implication of tyrosine-512 and phenylalanine-508."
No.
Sentence
Comment
49
As shown in Table 1 neither the parent peptide nor any of the substituted peptides were significantly phosphorylated by CK2, with the notable exception of the peptide in which Tyr512 was replaced by alanine (peptide 4).
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ABCC7 p.Tyr512Ala 24178769:49:176
status: NEW105 Peptides reproducing the 500-523 sequence of F508delCFTR were synthesized either as such (see legend of Fig. 2) or with Tyr512 replaced by Ala (Y512A) or by phospho-tyrosine (pY512).
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ABCC7 p.Tyr512Ala 24178769:105:120
status: NEWX
ABCC7 p.Tyr512Ala 24178769:105:144
status: NEW108 Lanes 1, 2 and 3 refer to unsubstituted, Y512A and pY512 peptides, respectively.
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ABCC7 p.Tyr512Ala 24178769:108:41
status: NEW119 The mechanism of Ser511 phosphorylation outlined here can also provide an explanation for the finding that two CFTR mutants, in which Tyr512 has been replaced by Ala and Asp, respectively, undergo defective maturation with reduced cell surface exposition (Luz et al. 2011).
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ABCC7 p.Tyr512Ala 24178769:119:134
status: NEW
PMID: 24566881
[PubMed]
Venerando A et al: "A "SYDE" effect of hierarchical phosphorylation: possible relevance to the cystic fibrosis basic defect."
No.
Sentence
Comment
29
A scenario like this would also account for a number of phenomenological observations already available in the literature, notably the defective maturation and reduced cell surface exposition of the CFTR mutant Y512A [20], which, unlike the wild type, is expected to be susceptible to phosphorylation by CK2 at S511 (see Fig. 1) and the increased accumulation of F508delCFTR upon cell treatment with a very specific CK2 inhibitor [21].
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ABCC7 p.Tyr512Ala 24566881:29:211
status: NEW