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September 1, 1998AJP Renal Physiology

Partially active channels produced by PKA site mutation of the cloned renal K+ channel, ROMK2 (kir1.2)

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Population

Cloned renal K+ channel (ROMK2) mutants (S25A, S200A, S294A) and wild-type

Comparison

Mutation of PKA sites from serine to alanine and… vs Wild-type ROMK2 channels

Design

Preclinical

Authors

GMGordon G. MacGregorOrlando College of Osteopathic MedicineJXJason XuWestern UniversityCMCarmel M. McNicholasUniversity of Alabama at Birmingham

Discussion

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Implication

Should not alter management of K+ disorders; leaves open their role in native renal K+ secretion.

Structured PICO

P
Population
Cloned renal K+ channel (ROMK2) mutants (S25A, S200A, S294A) and wild-type
I
Intervention
Mutation of PKA sites from serine to alanine (S25A, S200A, S294A) and exposure to dephosphorylating conditions
C
Comparator
Wild-type ROMK2 channels
O
Outcome
Open channel probability (Po) and channel kineticssurrogate

Mutations in specific PKA phosphorylation sites of the ROMK2 channel differentially affect channel gating kinetics and membrane expression.

Cite This Study

MacGregor et al. (1998) studied this question.

synapsesocial.com/papers/6a72f2315c14dd067a154cf8https://doi.org/10.1152/ajprenal.1998.275.3.f415
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Mutations in the pore region of ROMK enhance Ba2+ block1996 · 81 citations
  2. 2Regulation of ROMK1 K+ channel activity involves phosphorylation processes.1994 · 141 citations
  3. 3Extracellular K+ and Intracellular pH Allosterically Regulate Renal Kir1.1 Channels1996 · 74 citations
  4. 4Selectivity Changes during Activation of Mutant Shaker Potassium Channels1997 · 127 citations
  5. 5Regulation of potassium channels by protein kinases1996 · 194 citations