Erratum: Corrigendum: WNK1 kinase balances T cell adhesion versus migration in vivo

Abstract

In the version of this article initially published, the citation of Figure 3 in the second paragraph of the third subsection (Chromatin: the nexus of phenotype and the environment) is incorrect. That should cite Figure 2, as follows: "From an evolutionary perspective, two extreme models of how such complexity might be generated and regulated can be envisaged 95 (Fig. 2). " The error has been corrected in the HTML and PDF versions of the article.Erratum: Sall1 is a transcriptional regulator defining microglia identity and function In the HTML version of this article initially published, the scale bar was missing from the inset in the top right image in Figure 2d; the bottom left plot in Figure 2e was incorrectly a duplicate of the adjacent plot at right; and the designations in Figure 4b (Sall1 f l and Sall1 creER/fl ) should have been Sall1 fl/fl and Sall1 CreER/fl (respectively). Also, the arrows in the designations above and below the plots in Supplementary Figure 3b were rendered as boxes; these should have been as follows: Sall1 +/+ →Cx3cr1 CreER -iDTR and Sall1 GFP/+ →Cx3cr1 CreER -iDTR. Finally, in Supplementary Figure 4f, the red (Ki67 + ) cells in the right set of images were not visible. These errors have been corrected for the HTML version of this article.

Phosphatidic acid-dependent localization and basal de-phosphorylation of RA-GEFs regulate lymphocyte trafficking

“…Each bar graph represents the means ± SEM phosphorylation of RA-GEF is necessary for chemokine-dependent Rap1 activation. On the other hand, WNK1-deficient T cells demonstrated an augmented chemokine-dependent Rap1 activation [37], suggesting that phosphorylation by WNK1 inhibits Rap1 activation. In this study, we demonstrated that WNK1 phosphorylated RA-GEF, and basal dephosphorylation of RA-GEF was critical for chemokinedependent Rap1 activation in lymphocytes.…”