Retracted: FoxP3 acts as a cotranscription factor with STAT3 in tumor-induced regulatory T cells
Dewan Md Sakib Hossain1, Abir K Panda1, Argha Manna1
1Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata 700054, India.
Abstract:
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the authors. This study provided an explanation for why loss of FoxP3 in inducible regulatory T cells results in reduced expression of interleukin (IL)-10 despite the absence of FoxP3 binding sites in the IL-10 promoter. STAT3 binding sites do exist in the promoter, and evidence for a direct molecular interaction between FoxP3 and STAT3 proteins was provided as an explanation of the effect of loss of FoxP3. As supporting evidence, we reported modeling of a structural interaction between these two transcription factors in Figure 4D. As the N-terminal region of FoxP3, which consists of the Exon-2 region, had not been solved at structural resolution, we mistakenly used what we deduced to be a FoxP3 related transcription factor, NFAT, in the modeling. The model depicted in Figure 4D therefore did not represent a putative interaction between FoxP3 and STAT3 as labeled, but rather a putative interaction between NFAT and STAT3. Given the incorrect labeling of Figure 4D, the lack of documentation in the paper describing exactly how the modeling was performed, the lack of evidence shown in the paper for the choice of NFAT as the modeling partner, and the limited supporting evidence for a cooperative interaction between FoxP3 and STAT3, the editors have concluded with the corresponding author that the appropriate course of action is to retract the paper. We apologize for any confusion and inconvenience caused to readers.
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