Skip Navigation

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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (12)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sato, K.
Right arrow Articles by Miyagi, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sato, K.
Right arrow Articles by Miyagi, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Glycobiology vol 5 no 5 pp. 511-516, 1995
© 1995

research-article

Genomic organization and the 5'-upstream sequence of the rat cytosolic sialidase gene

Kaoru Sato and Taeko Miyagi1

Division of Biochemistry, Research Institute, Miyagi Cancer Center 47-1 Nodayama, Medeshima-shiode, Natori, Miyagi 981-12, Japan

1To whom correspondence should be addressed

Received on February 21, 1995; revised on April 10, 1995; accepted on April 10, 1995

We have previously cloned a cDNA of a rat cytosolic siali-dase which is strongly expressed in skeletal muscle. Both the highest enzyme activity, as well as the highest mRNA level, are present in this tissue. To understand the basis of the expression of this sialidase, we have cloned and sequenced the rat gene and its 5'-upstream region from a rat genomic library. The gene encoding the 1.8 kb skeletal muscle mRNA was found to span 3.4 kb of genomic DNA, and to consist of two introns and three exons. Exon 1 contains the 5' noncoding region, and exons 2 and 3 encode the regions containing the AUG initiation codon and two Asp-boxes, respectively. In the 5'-upstream sequence, there are a TATA box and two E-box pairs known as consensus binding sites for muscle-specific transcription factors. Analysis of the expression of transfected sialidase enhancer/promotor expression plasmid demonstrated the sialidase enhancer/promotor to be active in rat L6 myogenic cells shown to express this gene, but inactive in rat 3Y1 fibroblasts shown not to express the enzyme. The transcription activity was increased 3-fold after induction of myoblast differentiation by serum depletion. These observations give an account of constitutive expression of the sialidase gene in skeletal muscle.

genomic sequence L6 myoblast glycoproteins sialidase


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
B. Starcher, A. d'Azzo, P. W. Keller, G. K. Rao, D. Nadarajah, and A. Hinek
Neuraminidase-1 is required for the normal assembly of elastic fibers
Am J Physiol Lung Cell Mol Physiol, October 1, 2008; 295(4): L637 - L647.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. Hinek, A. V. Pshezhetsky, M. von Itzstein, and B. Starcher
Lysosomal Sialidase (Neuraminidase-1) Is Targeted to the Cell Surface in a Multiprotein Complex That Facilitates Elastic Fiber Assembly
J. Biol. Chem., February 10, 2006; 281(6): 3698 - 3710.
[Abstract] [Full Text] [PDF]

Home page
 GlycobiologyHome page
E. Monti, A. Preti, C. Nesti, A. Ballabio, and G. Borsani
Expression of a novel human sialidaseencoded by the NEU2 gene
Glycobiology, December 1, 1999; 9(12): 1313 - 1321.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
E Bonten, A van der Spoel, M Fornerod, G Grosveld, and A d'Azzo
Characterization of human lysosomal neuraminidase defines the molecular basis of the metabolic storage disorder sialidosis.
Genes & Dev., December 15, 1996; 10(24): 3156 - 3169.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.