Withdrawal: Cooperative regulation of NOTCH1 protein-phosphatidylinositol 3-kinase (PI3K) signaling by NOD1, NOD2, and TLR2 receptors renders enhanced refractoriness to transforming growth factor-β (TGF-β)- or cytotoxic T-lymphocyte antigen 4 (CTLA-4)-mediated impairment of human dendritic cell maturation.

Abstract

VOLUME 286 (2011) PAGES 31347–31360 This article has been withdrawn by the authors. The authors identified some issues and brought them to the attention of the Journal. After careful analysis of all of the original data used for preparing the figures in the publication, the following errors were identified. The actin immunoblot from Fig. 6B was reused in Figs. 9C, 10C, and 11H. The actin immunoblot in Fig. 8B was reused in Fig. 11 (A and E). The actin immunoblot in Fig. 11B was reused in Fig. 11G. The authors submitted to the Journal all of the correct actin immunoblots for all of the figures listed above. Given these issues, the authors state that the responsible course of action would be to withdraw the article to maintain the high standards and rigor of scientific literature from the authors' group as well as the Journal. The authors apologize to the scientific community for what they state are inadvertent mistakes and will seek to republish the article with suitable modifications in due course. Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-β (TGF-β)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell MaturationJournal of Biological ChemistryVol. 286Issue 36PreviewDendritic cells (DCs) as sentinels of the immune system are important for eliciting both primary and secondary immune responses to a plethora of microbial pathogens. Cooperative stimulation of a complex set of pattern-recognition receptors, including TLR2 and nucleotide-binding oligomerization domain (NOD)-like receptors on DCs, acts as a rate-limiting factor in determining the initiation and mounting of the robust immune response. It underscores the need for “decoding” these multiple receptor interactions. Full-Text PDF Open Access