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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Nat Neurosci. 2013 Aug 4;16(9):1238–1247. doi: 10.1038/nn.3479

Figure 2. TDRD3 acts as a bridge connecting Top3β and FMRP.

Figure 2

(a-c) IP-western to assess whether various TDRD3-deletion mutants described in (b) co-immunoprecipitate with Top3β, FMRP, FXR1 and FXR2. The Flag-tagged TDRD3 variants were transfected into HEK293 cells, and co-IP was performed using a Flag antibody. The crossreactive polypeptides are indicated with asterisks. A mock IP from untransfected HEK293 cells was included as a control. (b) Schematic representation of different TDRD3-deletion mutants (left), and their ability to coimmunoprecipitate with Top3β and FMRP from HEK293 extracts (right). (d) IP-Western shows that the association between Top3β and FMRP was disrupted in HeLa cells depleted of TDRD3 by siRNA. The IP was performed using a Flag antibody from extracts of HeLa cells stably expressing HF-Top3β. Full-length pictures of the blots are in Supplementary Fig. 10. The representative images shown have been repeated at least twice, and the results are reproducible.