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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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NHE3 inhibits PKA-dependent functional expression of CFTR by NHERF2 PDZ interactions

Cited 15 times inthomson ciCited 15 times inthomson ci
Title
NHE3 inhibits PKA-dependent functional expression of CFTR by NHERF2 PDZ interactions
Author
Favia, M.Fanelli, T.Bagorda, A.Di Sole, F.Reshkin, S. J.Suh, Pann-GhillGuerra, L.Casavola, V.
Keywords
CFTR; Ezrin; NHE3; NHERF2; PDZ domains; PKA
Issue Date
200608
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.347, no.2, pp.452 - 459
Abstract
It has been shown that when CFTR and NHE3 are co-expressed on the apical membrane of the A6-NHE3 cell monolayers, the two transporters interact via a shared regulatory complex composed of NHERF2, ezrin, and PKA. We observe here that co-expression of NHE3 reduced both PKA-dependent apical CFTR expression and its activation once in place by approximately 50%. To analyze the role of NHERF2 in this process, we transfected NHE3 expressing and non-expressing A6 monolayers with NHERF2 cDNA in which its binding domains had been deleted. When only CFTR is expressed on the apical membrane, deletion of any of the NHERF2 binding domains inhibited both PKA-dependent apical CFTR expression and its activation, while when NHE3 was co-expressed with CFTR PDZ2 deletion was without effect on CFTR sorting and activity. This suggests that when the PDZ2 domain is "sequestered" by interacting with NHE3 it can no longer participate in CFTR functional expression.
URI
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DOI
http://dx.doi.org/10.1016/j.bbrc.2006.06.112
ISSN
0006-291X
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