Abstract
Studies of mice deficient for proopiomelanocortin (Pomc) yield surprising results, and finally take us beyond the Ay model of melanocortin deficiency (pages 1066–1070).
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References
Cuénot, L. Les races pures et leurs combinasisons chez les souris (4me note). Arch. Zool. exp. gen., 4e ser 3, cxxiii– cxxxii (1905).
Miltenberger, R.J., Mynatt, R.L., Wilkinson, J.E. & Woychik, R.P. The role of the agouti gene in the yellow obese syndrome. J. Nutr. 127, 1902S–1907S ( 1997).
Krude, H. et al. Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans. Nat. Genet. 19, 155–157 (1998).
Yaswen, L., Diehl, N., Brennan, M.B. & Hochgeschwender, U. Obesity in the mouse model of Pro-opiomelanocortin deficiency responds to peripheral melanocortin. Nature Med. 1066–1070 (1999).
Cone, R.D. et al. The melanocortin receptors: agonists, antagonists, and the hormonal control of pigmentation. Recent Prog. Horm. Res. 51, 287–318 (1996).
Weber, A. et al. Adrenocorticotropin receptor gene mutations in familial glucocorticoid deficiency: relationships with clinical features in four families. J. Clin. Endocrinol. Metab. 80, 65– 71 (1995).
Huszar, D. et al. Targeted disruption of the melanocortin-4 receptor results in obesity in mice. Cell 88, 131– 141 (1997).
Vaisse, C., Clement, K., Guy-Grand, B. & Froguel, P. A frameshift mutation in human MC4R is associated with a dominant form of obesity [letter]. Nature Genet. 20, 113– 114 (1998).
Chen, W. et al. Exocrine gland dysfunction in MC5-R-deficient mice: evidence for coordinated regulation of exocrine gland function by melanocortin peptides. Cell 91, 789–798 (1997).
Ollmann, M.M., Lamoreux, M.L., Wilson, B.D. & Barsh, G.S. Interaction of Agouti protein with the melanocortin 1 receptor in vitro and in vivo. Genes Dev. 12, 316–330 (1998).
Cole, T.J. et al. Targeted disruption of the glucocorticoid receptor gene blocks adrenergic chromaffin cell development and severely retards lung maturation. Genes Dev. 9, 1608–1621 (1995).
Muglia, L., Jacobson, L., Dikkes, P. & Majzoub, J.A. Corticotropin-releasing hormone deficiency reveals major fetal but not adult glucocorticoid need. Nature 373, 427–432 (1995).
Versteeg, D.H., Van Bergen, P., Adan, R.A. & De Wildt, D.J. Melanocortins and cardiovascular regulation. Eur. J. Pharmacol. 360, 1–14 ( 1998).
Tatro, J.B. Receptor biology of the melanocortins, a family of neuroimmunomodulatory peptides. Neuroimmunomodulation 3, 259– 284 (1996).
Vergoni, A.V., Bertolini, A., Mutulis, F., Wikberg, J.E. & Schioth, H.B. Differential influence of a selective melanocortin MC4 receptor antagonist (HS014) on melanocortin-induced behavioral effects in rats. Eur. J. Pharmacol. 362, 95–101 (1998).
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Barsh, G. From Agouti to Pomc—100 years of fat blonde mice. Nat Med 5, 984–985 (1999). https://doi.org/10.1038/12415
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DOI: https://doi.org/10.1038/12415
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