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Molecular Endocrinology Vol. 4, No. 1 59-68
doi:10.1210/mend-4-1-59
Copyright © 1990 by the Endocrine Society.
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Activation of {alpha}-Protein Kinase C Leads to Association with Detergent-Insoluble Components of GH4C1 Cells

Susan C. Kiley and Susan Jaken

W. Alton Jones Cell Science Center, Inc. Lake Placid, New York 12946

Address requests for reprints to: Dr. Susan Jaken, W. Alton Jones All Science Center Inc., 10 Old Barn Road, Lake Placid, New York.

Abstract

TRH and phorbol dibutyrate (PDBu) stimulate PRL secretion and synthesis from GH4C1 rat pituitary cells through activation of protein kinase C (PKC). TRH responses are mediated by increases in cellular levels of two PKC activators, Ca2+ and diacylglycerol (DAG), whereas PDBu acts as a DAG analog. We conducted experiments to compare the effects of Ca2+ and PDBu/DAG on {alpha}-PKC redistribution and to determine to what components of the particulate fraction activated {alpha}-PKC associates. Subcellular fractionation experiments demonstrated that TRH and PDBu both caused chelator-stable association of {alpha}-PKC with the particulate fraction. In contrast, Ca2+-mediated association with the particulate fraction was not chelator stable. Immunocytofluorescence experiments also demonstrated that TRH, PDBu, and increased cytosolic Ca2+ (due to ionomycin or K+ depolarization) caused redistribution. The effect of TRH was rapid and transient, similar to TRH stimulation of phospholipase C. The translocated {alpha}-PKC in the particulate fraction from TRH- or PDBu-treated cultures was not solubilized with Triton X-100. In comparable studies using an immunofluorescence assay, {alpha}-PKC immunofluorescence remained in detergent-insoluble preparations from TRH- and PDBu-stimulated, but not resting cells. The association of activated {alpha}-PKC with chelator- and detergent-insoluble material suggested that activated {alpha}-PKC may be associated with membrane and cytoskeletal components.

FOOTNOTES

This work was supported in part by NIH Grant CA-48137 Council for Tobacco Research Grant 2375.

Received for publication August 16, 1989. Revision received October 4, 1989. Accepted for publication October 11, 1989.




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