Ionic regulation of MEL cell commitment

Robert Levenson; Ian Macara; Lewis Cantley; David Housman

doi:10.1002/jcb.240210102

Ionic regulation of MEL cell commitment

Robert Levenson, Ian Macara, Lewis Cantley, David Housman

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6 Scopus citations

Abstract

A key event in the initiation of the dimethyl sulfoxide (DMSO)‐induced program of murine erythroleukemia (MEL) cell differentiation is a rise in the level of cytoplasmic calcium ions. Our interest in the present study is whether other inducers of the terminal erythroid differentiation program also act via a calcium‐dependent pathway. Inhibition of calcium transport has been found to prevent the induction of MEL cell commitment by DMSO, butyric acid (BA), or hypoxanthine (HX). Enhancement of the calcium flux rate with A23187 or elevation of cytoplasmic calcium levels with FCCP stimulates the kinetics of commitment in response to all three inducers. These results suggest that of the inducers we have tested (DMSO, BA, and HX), all three act to initiate commitment via a common mechanism which involves modulation of cytoplasmic calcium levels.

Original language	English (US)
Pages (from-to)	1-8
Number of pages	8
Journal	Journal of cellular biochemistry
Volume	21
Issue number	1
DOIs	https://doi.org/10.1002/jcb.240210102
State	Published - 1983

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Biology
Cell Biology

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abstract = "A key event in the initiation of the dimethyl sulfoxide (DMSO)‐induced program of murine erythroleukemia (MEL) cell differentiation is a rise in the level of cytoplasmic calcium ions. Our interest in the present study is whether other inducers of the terminal erythroid differentiation program also act via a calcium‐dependent pathway. Inhibition of calcium transport has been found to prevent the induction of MEL cell commitment by DMSO, butyric acid (BA), or hypoxanthine (HX). Enhancement of the calcium flux rate with A23187 or elevation of cytoplasmic calcium levels with FCCP stimulates the kinetics of commitment in response to all three inducers. These results suggest that of the inducers we have tested (DMSO, BA, and HX), all three act to initiate commitment via a common mechanism which involves modulation of cytoplasmic calcium levels.",

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T1 - Ionic regulation of MEL cell commitment

AU - Levenson, Robert

AU - Macara, Ian

AU - Cantley, Lewis

AU - Housman, David

PY - 1983

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N2 - A key event in the initiation of the dimethyl sulfoxide (DMSO)‐induced program of murine erythroleukemia (MEL) cell differentiation is a rise in the level of cytoplasmic calcium ions. Our interest in the present study is whether other inducers of the terminal erythroid differentiation program also act via a calcium‐dependent pathway. Inhibition of calcium transport has been found to prevent the induction of MEL cell commitment by DMSO, butyric acid (BA), or hypoxanthine (HX). Enhancement of the calcium flux rate with A23187 or elevation of cytoplasmic calcium levels with FCCP stimulates the kinetics of commitment in response to all three inducers. These results suggest that of the inducers we have tested (DMSO, BA, and HX), all three act to initiate commitment via a common mechanism which involves modulation of cytoplasmic calcium levels.

AB - A key event in the initiation of the dimethyl sulfoxide (DMSO)‐induced program of murine erythroleukemia (MEL) cell differentiation is a rise in the level of cytoplasmic calcium ions. Our interest in the present study is whether other inducers of the terminal erythroid differentiation program also act via a calcium‐dependent pathway. Inhibition of calcium transport has been found to prevent the induction of MEL cell commitment by DMSO, butyric acid (BA), or hypoxanthine (HX). Enhancement of the calcium flux rate with A23187 or elevation of cytoplasmic calcium levels with FCCP stimulates the kinetics of commitment in response to all three inducers. These results suggest that of the inducers we have tested (DMSO, BA, and HX), all three act to initiate commitment via a common mechanism which involves modulation of cytoplasmic calcium levels.

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Ionic regulation of MEL cell commitment

Abstract

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