Suckling defect in mice lacking the soluble haemopoietin receptor NR6

Citation
Ws. Alexander et al., Suckling defect in mice lacking the soluble haemopoietin receptor NR6, CURR BIOL, 9(11), 1999, pp. 605-608
Citations number
13
Categorie Soggetti
Experimental Biology
Journal title
CURRENT BIOLOGY
ISSN journal
09609822 → ACNP
Volume
9
Issue
11
Year of publication
1999
Pages
605 - 608
Database
ISI
SICI code
0960-9822(19990603)9:11<605:SDIMLT>2.0.ZU;2-2
Abstract
Cytokines control a variety of cellular responses including proliferation, differentiation, survival and functional activation, via binding to specifi c receptors expressed on the surface of target cells [1], The cytokine rece ptors 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 Eps tein-Barr virus infection in lymphocytes [4], contains a typical haemopoiet in 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 bor n in the expected numbers. Neonatal NR6(-/-) mice failed to suckle, however , and died within 24 hours of birth, suggesting that NR6 is necessary for t he recognition or processing of pheromonal signals or for the mechanics of suckling itself. In addition, NR6(-/-) mice had reduced numbers of haemopoi etic progenitor cells, suggesting a potential role in the regulation of pri mitive haemopoiesis.