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Pnas11110correction 3895..3895 Corrections BIOCHEMISTRY NEUROSCIENCE Correction for “Mechanism of ligand-gated potassium efflux in Correction for “Bioluminescence imaging of Aβ deposition in bi- bacterial pathogens,” by Tarmo P. Roosild, Samantha Castronovo, genic mouse models of Alzheimer’s disease,” by Joel C. Watts, Kurt Jess Healy, Samantha Miller, Christos Pliotas, Tim Rasmussen, Giles, Sunny K. Grillo, Azucena Lemus, Stephen J. DeArmond, Wendy Bartlett, Stuart J. Conway, and Ian R. Booth, which ap- and Stanley B. Prusiner, which appeared in issue 6, February 8, peared in issue 46, November 16, 2010, of Proc Natl Acad Sci USA 2011, of Proc Natl Acad Sci USA (108:2528–2533; first published (107:19784–19789; first published November 1, 2010; 10.1073/ January 24, 2011; 10.1073/pnas.1019034108). pnas.1012716107). The authors note that the following grant should be added to The undersigned authors wish to note, “The KefFC system of the Acknowledgments: “NIH Grant AG002132.” E. coli is maintained in an inactive state by the binding of glu- tathione (GSH) and is activated by the formation of GSH ad- www.pnas.org/cgi/doi/10.1073/pnas.1401579111 ducts (GSX), particularly those with bulky substituents. We described two crystal structures with density present in the li- gand-binding domain that we interpreted as GSH and GSX. Recently, an independent, experienced crystallographer, who had viewed the structures from our study in a different context, PHARMACOLOGY made representations to us that cast doubt on position of the Correction for “Structural insights into gene repression by the succinimido ring of GSX. We have further reviewed the density orphan nuclear receptor SHP,” by Xiaoyong Zhi, X. Edward maps with the aid of an experienced crystallographer. As a con- Zhou, Yuanzheng He, Christoph Zechner, Kelly M. Suino-Powell, sequence, we believe it is important to draw this altered in- Steven A. Kliewer, Karsten Melcher, David J. Mangelsdorf, and terpretation of the crystal structures to the attention of readers. H. Eric Xu, which appeared in issue 2, January 14, 2014, of Proc In both structures, the density for the backbone of GSH is clear Natl Acad Sci USA (111:839–844; first published December 30, and allows unequivocal assignment of the position of the tripeptide. 2013; 10.1073/pnas.1322827111). In PDB coordinate set 3L9X, the density for the succinimido ring is The authors note that the following statement should be added very weak, making interpretation very speculative and the assign- to the Acknowledgments: “We want to thank the generosity of ment rests on the identity of the ligand added to the crystallization Drs. Marcia I. Dawson and Zebin Xia (Sanford-Burnham Medical mixture, for which there are two diastereomers in the solution— Research Institute) for providing us with 3-Cl-AHPC and for their a possibility that provides some basis for weakening the density. discussion on its use.” However, in 3L9W there are two anomalies that affect the in- terpretation of the bound ligand. First, there is no density for the www.pnas.org/cgi/doi/10.1073/pnas.1402462111 carbon atom attached to the sulfur of GSH and second, there is extra density adjacent to the position of sulfur that could be mod- elled as a constrained succinimido ring. However, this density could also be water or any other molecule that is trapped in the structure. CORRECTIONS Thus, while there is good evidence for the peptide, the evidence that PHYSIOLOGY it is in the GSH form is uncertain. Correction for “Phosphorylation sites required for regulation “There are no new data on either the structures or on the of cardiac calcium channels in the fight-or-flight response,” by gating mechanism. However, we believe that we should be cau- Ying Fu, Ruth E. Westenbroek, Todd Scheuer, and William tious in interpreting the structural data and that the field in A. Catterall, which appeared in issue 48, November 26, 2013, general should be made aware of the alternative views of the of Proc Natl Acad Sci USA (110:19621–19626; first published electron density data. Note that the mutagenesis and spectro- November 11, 2013; 10.1073/pnas.1319421110). scopic data that were presented in the original manuscript are The authors note “The method used for exogenous expression not affected by this alternative interpretation.” of CaV1.2 channels in ref. 32 was incorrectly described as ‘viral Tarmo P. Roosild and Samantha Castronovo have decided not transduction’ in the text. In fact, Yang et al. created transgenic to sign this statement. mice with inducible, cardiomyocyte-specific expression of exo- genous CaV1.2 channels regulated by a tetracycline-inducible Ian R. Booth promoter. When crossed with a transgenic mouse line expressing Jess Healy doxycycline-regulated reverse transcriptional activator under con- Samantha Miller trol of the α-myosin heavy chain protomer, the resulting double Christos Pliotas transgenic offspring expressed exogenous CaV1.2 channels in their Tim Rasmussen cardiac myocytes after treatment with doxycycline. The authors ” Wendy Bartlett regret the error in describing these methods. Stuart J. Conway www.pnas.org/cgi/doi/10.1073/pnas.1401987111 www.pnas.org/cgi/doi/10.1073/pnas.1402733111 www.pnas.org PNAS | March 11, 2014 | vol. 111 | no. 10 | 3895 Downloaded by guest on September 29, 2021 Structural insights into gene repression by the orphan nuclear receptor SHP Xiaoyong Zhia, X. Edward Zhoua, Yuanzheng Hea, Christoph Zechnerb,c, Kelly M. Suino-Powella, Steven A. Kliewerc,d,1, Karsten Melchera, David J. Mangelsdorfc,e,1, and H. Eric Xua,f,1 aLaboratory of Structural Sciences, Van Andel Research Institute, Grand Rapids, MI 49503; bDivision of Endocrinology, Department of Internal Medicine, cDepartment of Pharmacology, dDepartment of Molecular Biology, and eHoward Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390; and fVan Andel Research Institute/Shanghai Institute of Materia Medica Center, Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China Contributed by David J. Mangelsdorf, December 10, 2013 (sent for review October 23, 2013) Small heterodimer partner (SHP) is an orphan nuclear receptor that decreasing gene activation. In the second step, SHP actively functions as a transcriptional repressor to regulate bile acid and recruits corepressors to inhibit gene transcription. Identification cholesterol homeostasis. Although the precise mechanism whereby of SHP-interacting corepressors has been a subject of intense SHP represses transcription is not known, E1A-like inhibitor of study in recent years (19–25). As a result, a number of proteins differentiation (EID1) was isolated as a SHP-interacting protein and have been isolated that bind to SHP in in vitro or in vivo assays, implicated in SHP repression. Here we present the crystal structure one of which is E1A-like inhibitor of differentiation (EID1) (24). of SHP in complex with EID1, which reveals an unexpected EID1- EID1 was first cloned as an interacting protein for the retino- binding site on SHP. Unlike the classical cofactor-binding site near blastoma protein, which regulates the cell cycle and differentiation the C-terminal helix H12, the EID1-binding site is located at the N (26, 27). EID1 inhibited skeletal muscle cell differentiation by terminus of the receptor, where EID1 mimics helix H1 of the nuclear repressing muscle-specific gene expression. This was due to its receptor ligand-binding domain. The residues composing the SHP– ability to bind to p300/CBP coactivators and inhibit their histone EID1 interface are highly conserved. Their mutation diminishes acetyltransferase (HAT) activity (27). Later, EID1 was found to SHP–EID1 interactions and affects SHP repressor activity. Together, also interact with SHP (24). Because of its intrinsic transcrip- these results provide important structural insights into SHP co- factor recruitment and repressor function and reveal a conserved tional repression activity, EID1 has been suggested to be a SHP PHARMACOLOGY corepressor in several studies (24, 28–30). protein interface that is likely to have broad implications for ’ transcriptional repression by orphan nuclear receptors. Although the detailed molecular basis underlying SHP s in- hibitory function is still under intense investigation, the physio- logical roles of SHP in regulating bile acid and cholesterol Nuclear receptors compose a family of ligand-regulated homeostasis in liver are well characterized (13, 14, 31, 32). SHP- transcription factors that govern a wide array of cellular mediated repression is a key component of a feedback loop that activities, including cell proliferation, differentiation, metabo- represses the expression of genes that encode several key hy- lism, and death (1). The nuclear receptor family also contains droxylase enzymes involved in bile acid biosynthesis, such as many orphan members for which no ligand is known (1). Al- CYP7A1 and CYP8B1, as well as SHP itself (13, 14). Accord- though some of these orphan nuclear receptors function as ingly, CYP7A1 expression and bile acid synthesis are increased in transcriptional activators, others serve primarily as transcrip- SHP knockout mice (31, 32). Interestingly, the repressor activity tional repressors (2). The molecular basis for ligand-regulated transcription by nuclear receptors has been intensely investigated Significance over the past three decades, and structural studies have revealed that ligand-activated receptors use the C-terminal activation
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