Platelet-derived growth factor-BB activates calcium/calmodulin-dependent and -independent mechanisms that mediate Akt phosphorylation in the neurofibromin-deficient human Schwann cell line ST88-14

Robert G. Farrer; Jason R. Farrer; George H. DeVries

doi:10.1074/jbc.M112.442244

Platelet-derived growth factor-BB activates calcium/calmodulin-dependent and -independent mechanisms that mediate Akt phosphorylation in the neurofibromin-deficient human Schwann cell line ST88-14

Robert G. Farrer^*, Jason R. Farrer, George H. DeVries

^*Corresponding author for this work

Anesthesiology

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Background: Malignant peripheral nerve sheath tumor (MPNST) cells overexpress PDGF receptor-β, which increases intracellular calcium when activated. Results: Calcium/calmodulin (CaM) is involved in sustained phosphorylation of Akt and promotion of cell survival in an MPNST cell line. Conclusion: MPNST cells evade normal cell death through CaM-dependent sustained activation of Akt. Significance: Activation of CaM by abnormally expressed growth factor receptors may contribute to NF1 tumor formation.

Original language	English (US)
Pages (from-to)	11066-11073
Number of pages	8
Journal	Journal of Biological Chemistry
Volume	288
Issue number	16
DOIs	https://doi.org/10.1074/jbc.M112.442244
State	Published - Apr 19 2013

ASJC Scopus subject areas

Molecular Biology
Biochemistry
Cell Biology

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title = "Platelet-derived growth factor-BB activates calcium/calmodulin-dependent and -independent mechanisms that mediate Akt phosphorylation in the neurofibromin-deficient human Schwann cell line ST88-14",

abstract = "Background: Malignant peripheral nerve sheath tumor (MPNST) cells overexpress PDGF receptor-β, which increases intracellular calcium when activated. Results: Calcium/calmodulin (CaM) is involved in sustained phosphorylation of Akt and promotion of cell survival in an MPNST cell line. Conclusion: MPNST cells evade normal cell death through CaM-dependent sustained activation of Akt. Significance: Activation of CaM by abnormally expressed growth factor receptors may contribute to NF1 tumor formation.",

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Platelet-derived growth factor-BB activates calcium/calmodulin-dependent and -independent mechanisms that mediate Akt phosphorylation in the neurofibromin-deficient human Schwann cell line ST88-14. / Farrer, Robert G.; Farrer, Jason R.; DeVries, George H.
In: Journal of Biological Chemistry, Vol. 288, No. 16, 19.04.2013, p. 11066-11073.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Platelet-derived growth factor-BB activates calcium/calmodulin-dependent and -independent mechanisms that mediate Akt phosphorylation in the neurofibromin-deficient human Schwann cell line ST88-14

AU - Farrer, Robert G.

AU - Farrer, Jason R.

AU - DeVries, George H.

PY - 2013/4/19

Y1 - 2013/4/19

N2 - Background: Malignant peripheral nerve sheath tumor (MPNST) cells overexpress PDGF receptor-β, which increases intracellular calcium when activated. Results: Calcium/calmodulin (CaM) is involved in sustained phosphorylation of Akt and promotion of cell survival in an MPNST cell line. Conclusion: MPNST cells evade normal cell death through CaM-dependent sustained activation of Akt. Significance: Activation of CaM by abnormally expressed growth factor receptors may contribute to NF1 tumor formation.

AB - Background: Malignant peripheral nerve sheath tumor (MPNST) cells overexpress PDGF receptor-β, which increases intracellular calcium when activated. Results: Calcium/calmodulin (CaM) is involved in sustained phosphorylation of Akt and promotion of cell survival in an MPNST cell line. Conclusion: MPNST cells evade normal cell death through CaM-dependent sustained activation of Akt. Significance: Activation of CaM by abnormally expressed growth factor receptors may contribute to NF1 tumor formation.

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Platelet-derived growth factor-BB activates calcium/calmodulin-dependent and -independent mechanisms that mediate Akt phosphorylation in the neurofibromin-deficient human Schwann cell line ST88-14

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