This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by STUART, C. A. Articles by FURLANETTO, R. W. Search for Related Content PubMed PubMed Citation Articles by STUART, C. A. Articles by FURLANETTO, R. W.

Size Discrepancy Between Somatomedin-C and Insulin Receptors^*

Department of Medicine, University of Texas Medical Branch Galveston, Texas 77550
Department of Pediatrics, Childrens Hospital of Philadelphia Philadelphia, Pennsylvania 19104

Address requests for reprints to: Dr. Charles A. Stuart, Department of Medicine,University of Texas Medical Branch, Galveston, Texas 77550.

Somatomedin-C (Sm-C) and insulin receptors have similar size and structure. Each receptor is a heterotetramer composed of two - and two β-subunits. Sodium dodecyl sulfate (SDS)-polyacrylamide gel autoradiographic studies of affinity labeled receptor preparations demonstrated that each has a whole receptor of greater than 350,000 daltons, a half-receptor of 220,000 daltons, and binding subunit (-subunit) ofabout 140,000 daltons. Using SDS-polyacrylamide disc gels and double labeling techniques,we demonstrated that the ¹²⁵I affinity labeled -subunit of the Sm-C receptorfrom human placenta was 8,000 daltons smaller than the ¹³¹I affinity labeled insulin receptor -subunit. Further double label studies demonstrated that [¹²⁵I]insulin and [¹³¹I]insulin cross-linked to placental insulin receptors precisely comigrated on SDS-disc gels, indicating that the difference between insulin and Sm-C -subunits is not an artifact of the system. The difference in ligand size (Sm-C, 7,500 daltons; insulin, 5,700 daltons) would minimize the observeddifference and is clearly not the cause of the difference in size observed. These studies provide further evidence in support of two functionally and physically distinct receptor molecules for insulin and Sm-C in human placenta. (J Clin Endocrinol Metab58: 1, 1984)

^* This work was supported in part by NIH Grant AM-26644.

Received May 10, 1983.

This article has been cited by other articles:

				W.E. Winter Type I Insulin-Dependent Diabetes Mellitus: a Model for Autoimmune Polygenic Disorders Advances in Dental Research, April 1, 1996; 10(1): 81 - 87. [Abstract] [PDF]