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. Author manuscript; available in PMC: 2018 Mar 21.
Published in final edited form as: Immunity. 2017 Mar 9;46(3):488–503. doi: 10.1016/j.immuni.2017.02.010

Figure 5. Integrative analysis of Rptor-deficient proteom0e identifies mTORC1-dependent mitochondrial pathways.

Figure 5

(A) Overview of Raptor-dependent proteomics analysis.

(B) Five Raptor-dependent whole proteome co-expression clusters (RWPCs) defined by WGCNA.

(C) Functional annotations of RWPCs by Gene Ontology (GO), KEGG and Hallmark databases.

(D) TFs attenuated by Raptor deficiency. For TFs with an asterisk, a larger scale (e.g. maximum fold change of 10 instead of 2 folds) is used to reflect the large change of protein expression or phosphorylation abundance.

(E) Raptor-dependent mitochondrial pathways. The related protein levels are shown.

(F) Immunofluorescence images of ACTIN (green) and COX11 in naïve and activated WT and Rptor-deficient CD4+ T cells (scale bars, 5 μm). Right, statistical analysis of mean fluorescence intensity (MFI) of COX11 in WT and Rptor-deficient CD4+ T cells.

(G) Immunoblot of SHMT2 and MTHFD2 expression in WT and Rptor-deficient CD4+ T cells stimulated with α-CD3-CD28 for the indicated time points. Numbers below the lanes of SHMT2 and MTHFD2 indicate band intensity relative to that of the loading control-β-ACTIN.

Data are representative of two (F–G) independent experiments. P values are determined by one-way ANOVA with Tukey post-tests (F). ***P < 0.001.

See also Figure S5 and Data S5.