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. 2017 Oct 3;7:12600. doi: 10.1038/s41598-017-12707-7

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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RANKL inhibits NUMBL expression and induces NUMBL K48-poly UB in TAK1-dependent manner. (A) Bone marrow cells, from WT and TAK1-cKO mice were cultured in presence or absence of RANKL and M-CSF for 1 day followed by mRNA isolation and qPCR for NUMBL. RANKL treatment significantly decreases NUMBL expression but in WT cells but failed to inhibit NUMBL expression under TAK1 deletion condition. (B) Bone marrow cells from WT and TAK1-cKO mice were treated with RANKL as indicated. Total cell lysates and NUMBL-immunoprecipitates were then immunoblotted with anti-NUMBL and anti-K48-UB specific antibodies, respectively. Hypo K48-polu-Ubiquitinaion in TAK1-cKO cells indicates that TAK1 mediates poly-ubiquitination of NUMBL destined for proteasome degradation. (*P < 0.05).