التفاصيل البيبلوغرافية
| العنوان: |
Chromosomal mapping and mutational analysis of the coding region of the glycogen synthase kinase-3α and β isoforms in patients with NIDDM. |
| المؤلفون: |
Hansen, L., Arden, K. C., Rasmussen, S. B., Viars, C. S., Vestergaard, H., Hansen, T., Møller, A. M., Woodgett, J. R., Pedersen, O. |
| المصدر: |
Diabetologia; Jul1997, Vol. 40 Issue 8, p940-946, 7p |
| مستخلص: |
Activation of glycogen synthesis in skeletal muscle in response to insulin results from the combined inactivation of glycogen synthase kinase-3 (GSK-3) and activation of the protein phosphatase-1, changing the ratio between the inactive phosphorylated state of the glycogen synthase to the active dephosphorylated state. In a search for genetic defects responsible for the decreased insulin stimulated glycogen synthesis seen in patients with non-insulin-dependent diabetes mellitus (NIDDM) and their glucose-tolerant first-degree relatives we have performed mutational analysis of the coding region of the 2 isoforms of GSK-3α and GSK-3 β in 72 NIDDM patients and 12 control subjects. No structural changes were detected apart from a few silent mutations. Mapping of the GSK-3α to chromosome 19q13.1–13.2 and the GSK-3 β to chromosome 3q13.3-q21 outside known genetic loci linked to NIDDM further makes it unlikely that these genes are involved in the pathogenesis of common forms of NIDDM. [Diabetologia (1997) 40: 940–946] [ABSTRACT FROM AUTHOR] |
|
Copyright of Diabetologia is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder