help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hoelscher, S. R.
Right arrow Articles by Ascoli, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoelscher, S. R.
Right arrow Articles by Ascoli, M.

Endocrinology, Vol 136, 5004-5013, Copyright © 1995 by Endocrine Society


ARTICLES

Decreased stathmin expression does not affect the actions of human choriogonadotropin or epidermal growth factor in Leydig tumor cells

SR Hoelscher and M Ascoli
Department of Pharmacology, University of Iowa College of Medicine, Iowa City 52242, USA.

Although hCG and mouse epidermal growth factor (mEGF) activate different signaling systems in a clonal strain of murine Leydig tumor cells (designated MA-10), both compounds ultimately elicit several common effects such as increased steroidogenesis, decreased transcription of the LH receptor gene and attenuation of adenylyl cyclase. A 21-kilodalton protein whose phosphorylation state increases after hCG and mEGF stimulation has previously been described and identified as stathmin. To determine whether stathmin is involved in the signaling pathways of hCG and mEGF, an expression vector containing the full-length stathmin complementary DNA in an antisense orientation was constructed and used to establish two novel clonal MA-10 cell lines that have a decreased level of stathmin expression. Characterization of these mutant cell lines revealed no differences from MA-10 cells or neomycin-resistant subclones of MA-10 cells with respect to the ability of hCG or mEGF to increase steroidogenesis, decrease transcription of the LH receptor, or attenuate the adenylyl cyclase activity. Thus, it appears that stathmin is not involved in mediating the common actions of hCG and mEGF in MA-10 cells.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1995 by The Endocrine Society