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α-MSH and Desacetyl-α-MSH Signaling through Melanocortin Receptors
| Content Provider | Scilit |
|---|---|
| Author | Mountjoy, Kathleen G. Wu, Chia-Shan Jenny Cornish, Jillian Callon, Karen E. |
| Copyright Year | 2003 |
| Description | Journal: Annals of the New York Academy of Sciences The functional significance of N-terminal acetylation of $ACTH[1–13]NH_{2}$ is unknown. N-terminal acetylation of $ACTH[1–13]NH_{2}$ (known as desacetyl-α-MSH) to produce α-MSH enhances some activities of $ACTH[1–13]NH_{2}$ and virtually eliminates others. To determine whether α-MSH and desacetyl-α-MSH diverge in their coupling to melanocortin receptors in vitro, we measured the sensitivity of MC1, MC3, MC4, and MC5 receptors stably expressed in HEK293 cells to these peptides, functionally coupling them to adenylyl cyclase and a calcium signaling pathway. α-MSH and desacetyl-α-MSH similarly coupled these overexpressed receptors to both signaling pathways. In contrast, we discovered that α-MSH significantly increased primary rat osteoblast proliferation while for desacetyl-α-MSH there was only a trend to do the same. Osteoblast cells expressing very low levels of endogenous melanocortin receptors, in contrast with transfected HEK293 cells overexpressing a single melanocortin receptor, may provide an in vitro model for differentiating between α-MSH and desacetyl-α-MSH signaling. |
| Related Links | https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.2003.tb03162.x |
| Ending Page | 65 |
| Page Count | 8 |
| Starting Page | 58 |
| e-ISSN | 17496632 |
| DOI | 10.1111/j.1749-6632.2003.tb03162.x |
| Journal | Annals of the New York Academy of Sciences |
| Issue Number | 1 |
| Volume Number | 994 |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 2003-06-01 |
| Access Restriction | Open |
| Subject Keyword | Journal: Annals of the New York Academy of Sciences Endocrinology and Metabolism Melanocortin Receptor |
| Content Type | Text |
| Resource Type | Article |
