May 1, 1994Journal of Biological ChemistryOpen Access

Mutation of calmodulin-binding site renders the Na+/H+ exchanger (NHE1) highly H(+)-sensitive and Ca2+ regulation-defective.

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Population

Exchanger-deficient fibroblasts (PS120) expressing wild-type or mutant Na+/H+ exchanger (NHE1)

Comparison

Ca2+ ionophore ionomycin or thrombin vs Wild-type vs mutant NHE1 transfectants

Design

Preclinical

Authors

SWS. WakabayashiJapan Aerospace Exploration Agency BBBénédicte BertrandUniversidad Autónoma del Estado de Morelos TIToshitaro IkedaToho University

Discussion

Member takes

Implication

No immediate clinical implications; leaves open NHE1 region A as a research target in cardiovascular ion transport disorders.

Structured PICO

Population

Exchanger-deficient fibroblasts (PS120) expressing wild-type or mutant Na+/H+ exchanger (NHE1)

Intervention

Ca2+ ionophore ionomycin (short incubation up to 1 min) or thrombin

Comparator

Wild-type vs mutant NHE1 transfectants

Outcome

Intracellular pH (pHi) dependence of the rate of 5-(N-ethyl-N-isopropyl) amiloride-sensitive 22Na+ uptakesurrogate

Calmodulin acts as a major signal transducer that activates the Na+/H+ exchanger (NHE1) by binding to an autoinhibitory domain (region A), relieving its inhibitory effect.

Cite This Study

Wakabayashi et al. (1994) studied this question.

synapsesocial.com/papers/6a6f7beef44fa9f079dceef6 https://doi.org/10.1016/s0021-9258(17)36888-6

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Mutation of calmodulin-binding site renders the Na+/H+ exchanger (NHE1) highly H(+)-sensitive and Ca2+ regulation-defective.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Mutation of calmodulin-binding site renders the Na+/H+ exchanger (NHE1) highly H(+)-sensitive and Ca2+ regulation-defective.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider