The gas5 gene is disrupted by a frameshift mutation within its longest open reading frame in several inbred mouse strains and maps to murine Chromosome 1

The gas5 gene is disrupted by a frameshift mutation within its longest open reading frame in... Mammalian Genome 9, 773–774 (1998). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1998 The gas5 gene is disrupted by a frameshift mutation within its longest open reading frame in several inbred mouse strains and maps to murine Chromosome 1 Alexander J. Muller, Seema Chatterjee, Angelika Teresky, Arnold J. Levine Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA Received: 11 May 1998 / Accepted: 26 May 1998 The gas5 gene was identified in a screen for mRNAs induced in NIH3T3 fibroblasts following growth arrest (Schneider et al. 1988). gas5 message levels decline upon serum stimulation of quiescent mouse fibroblasts by what appears to be a post- transcriptional mechanism that may be dependent on protein ki- nase activity (Ciccarelli et al. 1990). gas5 message levels may also be subject to transcriptional regulation that occurs in response to cellular differentiation (Coccia et al. 1992). Abundant levels of gas5 message have been observed in most adult mouse tissues examined, the exceptions being liver and spleen (Coccia et al.1992). Neural tube-specific expression of gas5 message during neural tube closure has been reported to occur in embryos of the SWV/Fnn mouse strain, but not in embryos of the LM/Bc/Fnn mouse strain. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

The gas5 gene is disrupted by a frameshift mutation within its longest open reading frame in several inbred mouse strains and maps to murine Chromosome 1

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Publisher
Springer-Verlag
Copyright
Copyright © 1998 by Springer-Verlag New York Inc.
Subject
Life Sciences; Cell Biology; Animal Genetics and Genomics; Human Genetics
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s003359900862
Publisher site
See Article on Publisher Site

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