ABCMdb

ABCC7 p.Ser737Asp

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Publications

PMID: 19095655 [PubMed] Kongsuphol P et al: "Mechanistic insight into control of CFTR by AMPK."

No. 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. Login to comment
129 In contrast, the S768D mutation, mimicking phosphorylation at Ser768 , produced a whole cell conductance that was significantly smaller than even wtCFTR (note that conductance not lowered with S737D; see also Fig. 3C for phenformin sensitivity of these mutants). Login to comment
147 In contrast the residual CFTR conductances generated by S768D (but not S737D) were not only further inhibited by phenformin, but neither phospho-mimic mutant could be augmented by the AMPK inhibitor compound C. Login to comment

PMID: 21059651 [PubMed] Wang G et al: "The inhibition mechanism of non-phosphorylated Ser768 in the regulatory domain of cystic fibrosis transmembrane conductance regulator."

No. Sentence Comment

181 It is reasonable that Ser737 may not form an inhibitory H-bond because S737D was not activated by curcumin even if ATP was added (Fig. 6F), further suggesting that Ser737 may be a weak inhibitory site. Login to comment
192 It is reasonable that both Q958R/S737R and Q958D/S737D were not activated by ATP because Ser737 was a weak inhibitory site (Fig. 7C). Login to comment

PMID: 9463368 [PubMed] Sugita M et al: "CFTR Cl- channel and CFTR-associated ATP channel: distinct pores regulated by common gates."

No. Sentence Comment

142 To examine this further, we expressed CFTR S-oct-D, which contains eight serine-to-aspartate substitutions in the R domain (S660D, S686D, S700D, S712D, S737D, S768D, S795D and S813D) (Figure 8A). Login to comment
150 To examine this further, we expressed CFTR S-oct-D, which contains eight serine-to-aspartate substitutions in the R domain (S660D, S686D, S700D, S712D, S737D, S768D, S795D and S813D) (Figure 8A). Login to comment

PMID: 7690753 [PubMed] Rich DP et al: "Regulation of the cystic fibrosis transmembrane conductance regulator Cl- channel by negative charge in the R domain."

No. Sentence Comment

121 The single-channel open-stateprobabil- ity for wild-type CFTR (n = 14), CFTR S-Quad-A (S600A,S737A, S712A,S737A,S768A,S795A,S813A) (n = 7), or CFTR S-Oct-D (S660D,S686D,S700D,S712D,S737D,S768D,S795D,S813D)(n = 7in ATP alone (-PKA);n = 10 inPKA and ATP (+PkX))C1-channels was determined as described under "Experimental Procedures." Login to comment
123 S795A,S813A) (n = 5). Login to comment
205 Functional analysisof serine-to-aspartate mutantsof CFTR.A, the changes in SPQ fluorescence ofHeLa cells expressing wild-type CFTR (n = 56), CFTR S-Quad-D (S600D,S737D, S795D,S813D) (n = 24), CFTR S-Hex-D (S660D,S686D,S700D, S712D,S737D,S768D,S795D,S813D)( n = 23), or virus only-infected control cells (n = 53) after substitution of NO; for Iat 0 min. Login to comment
209 B, time course of current changes inan excised, inside-outmembrane patchfrom a HeLa cell expressingCFTR S-Oct-D (S660D,S686D,S700D,S712D,S737D,S768D,S795D,S813D) C1- chan- nels.ATP (0.88 mM)and PKA (75 m)were added tothe cytosolic(bath) side of the membrane as indicated by the burs. Login to comment
213 S737D,S795D,S813D) (n = 37), CFTR S-Oct-D (S660D,S686D,S700D, vitro or in vivo (Figs.6 and 9). Login to comment
217 S737D,S795D,S813D) (n = 37), CFTR S-Oct-D (S660D,S686D,S700D, vitro or in vivo (Figs.6 and 9). Login to comment