Suckling defect in mice lacking the soluble haemopoietin receptor NR6
- Author(s)
- Alexander, WS; Rakar, S; Robb, L; Farley, A; Willson, TA; Zhang, JG; Hartley, L; Kikuchi, Y; Kojima, T; Nomura, H; Hasegawa, M; Maeda, M; Fabri, L; Jachno, K; Nash, A; Metcalf, D; Nicola, NA; Hilton, DJ;
- Details
- Publication Year 1999-06-03,Volume 9,Issue #11,Page 605-608
- Journal Title
- CURRENT BIOLOGY
- Publication Type
- Journal Article
- Abstract
- Cytokines control a variety of cellular responses including proliferation, differentiation, survival and functional activation, via binding to specific receptors expressed on the surface of target cells [1], The cytokine receptors of the haemopoietin family are defined by the presence of a conserved 200 amino acid extracellular domain known as the haemopoietin domain [2], We report here the isolation of NR6, a haemopoietin receptor that, like the p40 subunit of interleukin-12 (IL-12) [3] and the EB13 gene induced by Epstein-Barr virus infection in lymphocytes [4], contains a typical haemopoietin domain but lades transmembrane and cytoplasmic domains, Although in site hybridisation revealed NR6 expression at multiple sites in the developing embryo, mice lacking NR6 did not display obvious abnormalities and were born in the expected numbers. Neonatal NR6(-/-) mice failed to suckle, however, and died within 24 hours of birth, suggesting that NR6 is necessary for the recognition or processing of pheromonal signals or for the mechanics of suckling itself. In addition, NR6(-/-) mice had reduced numbers of haemopoietic progenitor cells, suggesting a potential role in the regulation of primitive haemopoiesis.
- Publisher
- CURRENT BIOLOGY LTD
- Keywords
- CYTOKINE; INTERLEUKIN-12; PROTEIN
- Publisher's Version
- https://doi.org/10.1016/S0960-9822(99)80266-8
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1999-06-03 12:00:00