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[Cancer Research 57, 215-220, January 15, 1997]
© 1997 American Association for Cancer Research

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Id Genes Encoding Inhibitors of Transcription Are Expressed during in Vitro Astrocyte Differentiation and in Cell Lines Derived from Astrocytic Tumors1

Pedro J. Andres-Barquin2, Maria-Clemencia Hernandez2, Timothy E. Hayes, Ronald D. G. McKay and Mark A. Israel3

Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, School of Medicine, University of California, San Francisco, San Francisco, California 94143 [P. J. A-B., M-C. H., M. A. I.], and Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892 [T. E. H., R. D. G. M.]

Id proteins belong to a class of nuclear transcription factors known as helix-loop-helix proteins. It has been reported that Id genes function as negative regulators of differentiation, and Id gene expression is down-regulated during cell differentiation. We examined the regulation of Id genes during astrocyte differentiation in a murine nervous system precursor cell line, NSEHip2-28, which is able to differentiate along the astroglial lineage, as well as in human astroglial tumor cell lines. Upon induction of NSEHip2-28 differentiation, at a time when glial fibrillary acidic protein expression became detectable, the expression of all four Id family members initially increased dramatically, and subsequently decreased. Furthermore, varying levels of Id gene expression were found in astroglial tumor cell lines displaying variable degrees of lineage-specific differentiation. These results suggest that the expression of Id family members may play an important role in the control of astrocyte differentiation.

1 This work was supported in part by grants from the Pediatric Brain Tumor Foundation of the U.S., the Preuss Foundation, the Betz Foundation, and the Nissen Family, P. J. A-B. is the recipient of a Postdoctoral Research Fellowship from the Spanish Ministry of Education and Science.

2 These authors contributed equally to this work.

3 To whom requests for reprints should be addressed, at Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research Center, Department of Neurological Surgery, HSE 722, University of California, San Francisco. 513 Parnassus Avenue, San Francisco, CA 94143-0520.

Received 10/ 9/96. Accepted 12/ 3/96.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1997 by the American Association for Cancer Research.