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Genes Newly Identified as Regulated by Glucocorticoids in Murine Thymocytes

Gail Baughman, Maureen T. Harrigan^*, N. Faith Campbell, Stephen J. Nurrishf and Suzanne Bourgeois

Regulatory Biology Laboratory, The Salk Institute for Biological Studies San Diego, California 92186-5800

Address requests for reprints to: Dr. Suzanne Bourgeois, Regulatory Biology Laboratory, The Salk Institute for Biological Studies, San Diego, California 92186–5800.

Abstract

Glucocorticoids induce dramatic biochemical andmorphological changes in lymphocytes through anunknown process that requires RNA and proteinsynthesis. In order to identify genes involved in thisresponse, we previously isolated 11 cDNA clonesfrom the murine WEHI-7TG thymoma cell line thatcorrespond to mRNAs induced by glucocorticoids.We now report the isolation of two new cDNA cloneswhose gene expression is regulated by glucocorticoidsin WEHI-7TG cells. We further characterize thetwo new cDNA clones, as well as those describedpreviously, by examining the response of each ofthe corresponding mRNAs to glucocorticoids in murinethymocytes. With the exception of two, allcDNAs correspond to genes that are induced byglucocorticoids in murine thymocytes within 4 h oftreatment. We previously identified two of the cDNAsas the mouse VL30 retrovirus-like element and themouse homolog of chondroitin sulfate proteoglycancore protein. We have now identified four additionalcDNA clones that correspond to the genes for calmodulin,mitochondrial phosphate carrier protein,immunoglobulin (Ig)-related glycoprotein (GP-70),and the 70 kilodalton autoantigen for Lupus andGraves diseases. Two other cDNA clones representpreviously undescribed genes: one shares a highsimilarity to known sequences for the family of Gprotein-coupled receptors and the other to a humanplacental-specific protein, PP11. Another cDNA appearsto contain sequences for an unknown geneand the remnants of a mouse transposon, ETn. Theremaining clones represent new, unidentified genesinduced by glucocorticoids in murine thymocytes and in the WEHI-7TG cell line.

FOOTNOTES

This work was supported by USPHS Grant CA-36146 (to S.B.) and by Core Grant CA-14195 from the NIH and by a grant from the Elsa U. Pardee Foundation (to S.B.).

^* Supported by USPHS Training Grant 5T32CA-09254 (Director, Melvin Conn) and by a fellowship from The Leukemia Society of America and by the J. Aron Charitable Foundation.

Current address: Imperial Cancer Research Foundation, PO Box 123, Lincoln's Inn Fields, London, WC2A 3PX U.K.

Received for publication December 26, 1990. Revision received March 4, 1991. Accepted for publication March 6, 1991.

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