Talk:Agouti signalling peptide
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The comment(s) below were originally left at several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section., and are posted here for posterity. Following
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|This page has a number of slight but important mistakes in the description of agouti peptide function.
-ASIP acts an antagonist and inverse agonist of melanocortin receptors, not the peptide hormones that act on them (alpha-Melanocyte-stimulating hormone).
-Ecopic , not constitutive, expression of agouti signalling peptide results in the syndrome of metabolic disruption, hyperphagia, and pheomelanic propenderance. Constitutive activation is a distinct term used to describe a constant level of action by a receptor (e.g. mutations causing constitutive MC1R activation result in melanistic individuals).
-The "similar to the mouse protein" part fails to mention it is referring specifically to gene ASIP which is the human homologue of the mouse Agouti gene, and produces functionally homologous proteins.
-Central neurological action of ASIP, including the hyperphagia induced obesity and MC3R/MC4R antagonism, has only been shown to be relevant in cases of ectopic agouti peptide expression, as in the case of the classic mouse mutants. These functions should not be implied to be primary actions as they are the result of a serious and in some mutants lethal shift from typical patterns of expression.
Further review of literature and editing of this page is needed. I will perhaps perform this duty myself in the near future.
Last edited at 18:31, 11 October 2009 (UTC). Substituted at 06:50, 29 April 2016 (UTC)