The authors have provided unedited and high resolution data from gels used in Figure 4A in the above mentioned article published in 2009 in Human Molecular Genetics. One of the cropped gels is illustrated for two distinct times of exposure, illustrating the absence of background in controls.
These details have been corrected only in this corrigendum/erratum to preserve the published version of record.
SWI/SNF and Rest/Nrsf interactions and the regulation of L1cam (a REST/NRSF target gene) via Dyrk1a. (A) Dyrk1a interacts with a complex containing Brg1 and Ini1. N18 cells were transiently transfected with Dyrk1a-EGFP or control p-EGFP. N18 cells were immunoprecipitated (IP) using anti-Brg1 antibody. IP was performed with the anti-Brg1 antibody. The precipitated fractions and supernatants were then resolved by sodium dodecyl sulphate– polyacrylamide gel electrophoresis (SDS–PAGE) and analysed by western blot using anti-Brg1, anti-Ini or anti-EGFP antibody. The same IP extracts were blotted on two distinct SDS–PAGE in order to detect proteins of 80–200 and 15–80 kDa, respectively. Note the band of 115 kDa expected for the Dyrk1a-EGFP fusion protein and the 25 kDa band expected for the EGFP. Note that no cross-reaction was found with the EGFP protein. (B) The mutation of the RE1/NRSE site modifies the gene expression induced by Dyrk1a-EGFP overexpression. Relative differences are shown in Lac-Z expression levels in (i) N18 cells co-transfected with the Dyrk1a-EGFP expression vector and the L1LacZ vector with respect to N18 cells co-transfected with the EGFP control vector and the L1LacZ vector and (ii) in N18 cells co-transfected with the Dyrk1a-EGFP expression vector and the L1LacZΔN vector with respect to N18 cells co-transfected with the EGFP control vector and the L1LacZΔN vector. The significant decrease (***P < 0.0001) in the LacZ expression is consistent with an interaction betweenDYRK1Aand REST/NRSF with RE1/NRSE sites. SEM is indicated by the bar.
