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12 rezultati
Effects of MSH on food intake, body weight and coat color of the yellow obese mouse.
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Viable yellow obese mice (Avy/a) were treated for 10 days with 5, 15, 50 or 150 micrograms/d of either alpha-MSH or desacetyl-MSH. The half-maximal effect on weight gain occurred with a dose of 5 micrograms/d for desacetyl-MSH and at a 30 fold higher level of 150 micrograms/d for alpha-MSH. In
Preservation of eumelanin hair pigmentation in proopiomelanocortin-deficient mice on a nonagouti (a/a) genetic background.
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The original strain of proopiomelanocortin (POMC)-deficient mice (Pomc-/-) was generated by homologous recombination in 129X1/SvJ (A(w)/A(w))-derived embryonic stem cells using a targeting construct that deleted exon 3, encoding all the known functional POMC-derived peptides including alpha MSH,
Role of melanocortinergic neurons in feeding and the agouti obesity syndrome.
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Dominant alleles at the agouti locus (A) cause an obesity syndrome in the mouse, as a consequence of ectopic expression of the agouti peptide. This peptide, normally only found in the skin, is a high-affinity antagonist of the melanocyte-stimulating hormone receptor (MC1-R), thus explaining the
Lack of proopiomelanocortin peptides results in obesity and defective adrenal function but normal melanocyte pigmentation in the murine C57BL/6 genetic background.
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Mice deficient in proopiomelanocortin peptides (Pomc(-/-)) generated on a 129 (A(w)/ A(w)) genetic background were back-crossed onto the C57BL/6 (a/a) genetic background. These mice exhibited most of the phenotypic characteristics previously reported on the 129 genetic background (Yaswen et al.
Molecular genetic characterization of six recessive viable alleles of the mouse agouti locus.
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The agouti locus on mouse chromosome 2 encodes a secreted cysteine-rich protein of 131 amino acids that acts as a molecular switch to instruct the melanocyte to make either yellow pigment (phaeomelanin) or black pigment (eumelanin). Mutations that up-regulate agouti expression are dominant to those
Molecular basis of the pleiotropic phenotype of mice carrying the hypervariable yellow (Ahvy) mutation at the agouti locus.
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The murine agouti locus regulates a switch in pigment synthesis between eumelanin (black/brown pigment) and phaeomelanin (yellow/red pigment) by hair bulb melanocytes. We recently described a spontaneous mutation, hypervariable yellow (Ahvy) and demonstrated that Ahvy is responsible for the largest
Agouti: from mouse to man, from skin to fat.
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The agouti protein regulates pigmentation in the mouse hair follicle producing a black hair with a subapical yellow band. Its effect on pigmentation is achieved by antagonizing the binding of alpha-melanocyte stimulating hormone (alpha-MSH) to melanocortin 1 receptor (Mc1r), switching melanin
Genetic studies of the mouse mutations mahogany and mahoganoid.
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The mouse mutations mahogany (mg) and mahoganoid (md) are negative modifiers of the Agouti coat color gene, which encodes a paracrine signaling molecule that induces a swithc in melanin synthesis from eumelanin to pheomelanin. Animals mutant for md or mg synthesize very little or no pheomelanin
Unexpected endocrine features and normal pigmentation in a young adult patient carrying a novel homozygous mutation in the POMC gene.
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BACKGROUND
Proopiomelanocortin (POMC) is the precursor to five biologically active peptides, including ACTH produced in the anterior pituitary and alpha-MSH produced in the hypothalamus. Mutations that inactivate the POMC gene have been described in children, causing a pleiotropic syndrome that
The insertion of a full-length Bos taurus LINE element is responsible for a transcriptional deregulation of the Normande Agouti gene.
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Mammalian pigmentation is controlled by the concerted action of Tyr, Tyrp1 and Dct producing eumelanin and/or pheomelanin in melanocytes. The ratio of these two pigments is determined by the agonist alpha-melanocyte stimulating hormone and the antagonist Agouti protein acting on the Mc1r. Here we
An Independent Locus Upstream of ASIP Controls Variation in the Shade of the Bay Coat Colour in Horses
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Novel coat colour phenotypes often emerge during domestication, and there is strong evidence of genetic selection for the two main genes that control base coat colour in horses-ASIP and MC1R. These genes direct the type of pigment produced, red pheomelanin (MC1R) or black
Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor.
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The genetic loci agouti and extension control the relative amounts of eumelanin (brown-black) and phaeomelanin (yellow-red) pigments in mammals: extension encodes the receptor for melanocyte-stimulating hormone (MSH) and agouti encodes a novel 131-amino-acid protein containing a signal sequence.
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