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J. Biol. Chem., Vol. 275, Issue 32, 24534-24539, August 11, 2000

This Article Full Text Full Text (PDF) All Versions of this Article: 275/32/24534    most recent M003388200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Brandt, P. C. Articles by Vanaman, T. C. Search for Related Content PubMed PubMed Citation Articles by Brandt, P. C. Articles by Vanaman, T. C. Social Bookmarking                      What's this?

Elevated Glucocorticoid Receptor Transactivation and Down-regulation of ₁ Integrin Are Associated with Loss of Plasma Membrane Ca²⁺-ATPase Isoform 1^*

Paul C. Brandt^§ and Thomas C. Vanaman^¶

From the  Department of Medical Pharmacology and Toxicology, Texas A & M System Health Science Center, College Station, Texas 77843-1114 and the ^¶ Department of Biochemistry, University of Kentucky Medical Center, Lexington, Kentucky 40536-0084

We have previously shown that inhibition of expression of the plasma membrane Ca²⁺-ATPase isoform 1 in PC6 cells leads to loss of nerve growth factor-mediated neurite extension (Brandt, P. C., Sisken, J. E., Neve, R. L., and Vanaman, T. C. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 13843-13848). Cells lacking plasma membrane Ca²⁺-ATPase 1 did not attach to collagen-coated plates as tightly as controls, suggesting that a defect in adhesion might be underlying the inability to extend neurites. We report here that cell lines lacking plasma membrane Ca²⁺-ATPase 1 do not produce ₁ integrin, which is required for both collagen adherence and neurite extension. Because ₁ integrin gene transcription can be down-regulated by glucocorticoids, the response of cells to glucocorticoids was investigated. Cortisol-dependent transactivation from the mouse mammary tumor virus promoter in cells lacking plasma membrane Ca²⁺-ATPase 1 was stimulated 145-216-fold over untreated cells compared with 15-26-fold for controls. This increase was not due to increased binding affinity of the receptor for cortisol, an increased number of cortisol-binding sites, or increased translocation of the receptor to the nucleus. Expression of additional glucocorticoid receptor-dependent genes required for neurite extension must also be altered in cells missing the plasma membrane Ca²⁺-ATPase 1 because constitutive expression of ₁ integrin did not restore their nerve growth factor-mediated neurite extension capability. The impact of plasma membrane Ca²⁺-ATPase isoform 1 on other signaling systems and the resultant profound yet subtle effects on PC6 cells strongly suggests that it plays an important role in modulating signal transduction pathways downstream of Ca²⁺-mediated signals.

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