Famsin (mouse) (rec.) (His)

AdipoGen Life Sciences

Famsin (mouse) (rec.) (His)

2

Research Use Only

1 mg/ml

>95%

Gm11437

predicted gene 11437

uncharacterized protein C17orf78 homolog

Uncharacterized protein C17orf78 homolog

Famsin, coded by the gene Gm11437, promotes metabolic adaptations to fasting. Famsin is cleaved by furin from a single-pass transmembrane protein, Gm11437, during fasting. Famsin is primarily expressed by enterocytes and enteroendocrine cells in the intestine. Famsin binds to the olfactory G-protein-coupled receptor OLFR796 to activate intracellular calcium mobilization and to induce glucagon secretion. This famsin-OLFR796-glucagon signaling axis promotes gluconeogenesis and ketogenesis in the liver for energy mobilization. OLFR796, which is highly expressed in olfactory epithelium (OE) and olfactory bulb (OB) and in intestinal crypts and islets, promotes torpor for energy conservation and fasting-induced enhancement of energy mobilization in mice, thus enhancing mouse metabolic adaptations to fasting. Deficiency of famsin signaling in humans and mice attenuates glucagon secretion and reduces blood glucose levels, showing the importance of gut-islet-liver endocrine crosstalk, mediated by a famsin-glucagon axis, in glucose homeostasis. - Recombinant Protein. Mouse Famsin (aa 22-191) is fused at the C-terminus to a His-tag. Lyophilized. Contains PBS. Famsin, coded by the gene Gm11437, promotes metabolic adaptations to fasting. Famsin is cleaved by furin from a single-pass transmembrane protein, Gm11437, during fasting. Famsin is primarily expressed by enterocytes and enteroendocrine cells in the intestine. Famsin binds to the olfactory G-protein-coupled receptor OLFR796 to activate intracellular calcium mobilization and to induce glucagon secretion. This famsin-OLFR796-glucagon signaling axis promotes gluconeogenesis and ketogenesis in the liver for energy mobilization. OLFR796, which is highly expressed in olfactory epithelium (OE) and olfactory bulb (OB) and in intestinal crypts and islets, promotes torpor for energy conservation and fasting-induced enhancement of energy mobilization in mice, thus enhancing mouse metabolic adaptations to fasting. Deficiency of famsin signaling in humans and mice attenuates glucagon secretion and reduces blood glucose levels, showing the importance of gut-islet-liver endocrine crosstalk, mediated by a famsin-glucagon axis, in glucose homeostasis.

-20°C,2°C to 8°C

41116100

Mouse