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|Title:||Na+-H+ exchange in salivary secretory cells is controlled by an intracellular Na+ receptor|
|Citation:||Proceedings of the National Academy of Sciences of USA, 1999; 96(17):9949-9953|
|Publisher:||NATL ACAD SCIENCES|
|H. Ishibashi, A. Dinudom, K. F. Harvey, S. Kumar, J. A. Young, and D. I. Cook|
|Abstract:||It recently has been shown that epithelial Na(+) channels are controlled by a receptor for intracellular Na(+), a G protein (G(o)), and a ubiquitin-protein ligase (Nedd4). Furthermore, mutations in the epithelial Na(+) channel that underlie the autosomal dominant form of hypertension known as Liddle's syndrome inhibit feedback control of Na(+) channels by intracellular Na(+). Because all epithelia, including those such as secretory epithelia, which do not express Na(+) channels, need to maintain a stable cytosolic Na(+) concentration ([Na(+)](i)) despite fluctuating rates of transepithelial Na(+) transport, these discoveries raise the question of whether other Na(+) transporting systems in epithelia also may be regulated by this feedback pathway. Here we show in mouse mandibular secretory (endpiece) cells that the Na(+)-H(+) exchanger, NHE1, which provides a major pathway for Na(+) transport in salivary secretory cells, is inhibited by raised [Na(+)](i) acting via a Na(+) receptor and G(o). This inhibition involves ubiquitination, but does not involve the ubiquitin protein ligase, Nedd4. We conclude that control of membrane transport systems by intracellular Na(+) receptors may provide a general mechanism for regulating intracellular Na(+) concentration.|
Endosomal Sorting Complexes Required for Transport
Nedd4 Ubiquitin Protein Ligases
|Appears in Collections:||Aurora harvest|
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