(panel) PRISM structure analysis for the predicted interaction between IKK (PDB: 4KIK) and PFKFB3 (PDB: 2DWO)

(panel) PRISM structure analysis for the predicted interaction between IKK (PDB: 4KIK) and PFKFB3 (PDB: 2DWO). unidentified role of IKK in regulating glycolysis, sensing low-glutamine-induced metabolic stress, and promoting cellular adaptation to nutrient availability. panel) Wild-type, panel) Cells were lysed, and immunoblotting was performed with the indicated antibodies. (panel) Forty-eight hours after transfection, cells were cultured in glutamine-free medium, and viability was assessed by propodium iodide exclusion at the indicated time points. Data offered are imply SEM of three impartial experiments performed in duplicate. (panel) Forty-eight hours after transfection, cells were lysed, and immunoblotting was performed with the indicated antibodies. (panel) Wild-type and panel) Cells were lysed, and immunoblotting was performed with the indicated antibodies. Data offered are imply SEM of three impartial experiments performed in duplicate. (panel) HT1080 cells were transduced with control or p65 shRNA followed by puromycin selection, cells were cultured in total or glutamine-free medium, and viability was assessed by propidium iodide exclusion at the indicated time points. Data offered are imply SEM of three impartial experiments performed in duplicate. (panel) After puromycin selection, cells were lysed, and immunoblotting was performed with the indicated antibodies. (panel) Wild-type, panel) Cells were lysed, and immunoblotting was performed with the indicated antibodies. (***) 0.005, Student’s panel) PRISM structure analysis for the predicted interaction between IKK (Protein Data Bank [PDB]: 4KIK) and the IBCNFB complex (PDB: 1NFI). (panel) PRISM structure analysis for the predicted conversation between IKK (PDB: 4KIK) and PFKFB3 (PDB: 2DWO). ( 0.05; (***) 0.005, Nedocromil Student’s 0.05; (**) 0.01; (***) 0.005, Student’s 0.05; (**) 0.01; (***) 0.005, Student’s 0.05; (**) 0.01; (***) 0.005, Student’s 0.05 [*], 0.01 [**], and 0.005 [***]). Supplementary Material Supplemental Material: Click here to view. Acknowledgments We thank members of the Kong laboratory for helpful feedback around the manuscript. We thank Ross Tomaino at the Harvard Mass Spectrometry Core for assisting in the protein mass spectrometric peptide sequencing and phosphopeptide mapping experiments. Research Nedocromil is supported by National Institutes of Health/National Malignancy Institute 1R01CA183989-01A1. M.A.R. is usually supported by the Ralph M. Nedocromil Parsons Foundation. M.K. is the Pew Scholar in the Biomedical SOCS2 Sciences, V Scholar in Malignancy Research, and Nedocromil American Malignancy Society Research Scholar. X.H.L. is usually supported by DNA Damage Response and Oncogenic Signaling (DDROS) Training Program at City of Hope. Research reported here includes work performed in Core Facilities supported by the National Institutes of Nedocromil Health/National Malignancy Institute under grant number P30CA33572. Footnotes Supplemental material is available for this article. Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.287235.116..