Accessory proteins for melanocortin signaling - Attractin and mahogunin
Accessory proteins for melanocortin signaling - Attractin and mahogunin
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DOI：
10.1111/j.1749-6632.2003.tb03192.x
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发表时间：
2003-01-01
期刊：
影响因子：
--
通讯作者：
Barsh, GS
中科院分区：
文献类型：
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作者：
He, L;Eldridge, AG;Barsh, GS
毛发生长过程中从真黑素合成转变为褐黑素合成是通过 Agouti 蛋白的瞬时合成来完成的，Agouti 蛋白是黑皮质素-1 受体 (Mc1r) 的反向激动剂。毛色突变桃花心木和桃花心木会阻止毛囊黑色素细胞对刺豚鼠蛋白做出反应。桃花心木中突变的基因也称为吸引素 (Atrn)，编码 I 型跨膜蛋白，充当刺鼠蛋白的辅助受体。我们最近确定，桃花心木（也称为 Mahogunin (Mgrn1)）中的突变基因编码 E3 泛素连接酶。与 Attractin 一样，Mahogunin 在无脊椎动物基因组中是保守的，它的缺失会导致多效性表型，包括海绵状神经变性。
Switching from eumelanin to pheomelanin synthesis during hair growth is accomplished by transient synthesis of Agouti protein, an inverse agonist for the melanocortin-1 receptor (Mc1r). The coat color mutations mahogany and mahoganoid prevent hair follicle melanocytes from responding to Agouti protein. The gene mutated in mahogany, which is also known as Attractin (Atrn), encodes a type I transmembrane protein that functions as an accessory receptor for Agouti protein. We have recently determined that the gene mutated in mahoganoid, which is also known as Mahogunin (Mgrn1), encodes an E3 ubiquitin ligase. Like Attractin, Mahogunin is conserved in invertebrate genomes, and its absence causes a pleiotropic phenotype that includes spongiform neurodegeneration.