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. 2018 Apr 6;9:1338. doi: 10.1038/s41467-018-03648-4

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Lipid binding deficient mutants of neurofibromin 2 display impaired inhibition of cell proliferation. a SC4, b HEK293T, or c hSCλ-shNF2 cells were transfected with expression vectors for wild type and lipid binding deficient neurofibromin 2 or empty vector control (pCDNA). Total cell numbers were counted over 72 h. Means of each data point were calculated from three independent biological replicates conducted in triplicate. Error bars represent ± S.D. Immunoblot analysis was used to verify similar expression levels of the indicated neurofibromin 2 alleles. Tubulin was used as a control. The blots shown are representative of three biological replicates. For SC4 cells: difference between pCDNA and lipid binding deficient neurofibromin 2, < 0.7680 (i.e., not significant); pCDNA and wild-type neurofibromin 2, < 0.0001 (i.e., significant); lipid binding deficient and wild-type neurofibromin 2 proteins, < 0.0001 (i.e., significant). For HEK293T cells: difference between pCDNA and lipid binding deficient neurofibromin 2, <0.0013 (i.e., significant); pCDNA and wild-type neurofibromin 2, <0.0001 (i.e., significant); lipid binding deficient and wild-type neurofibromin 2 proteins, <0.0001 (i.e., significant). For hSCλ-shNF2 cells: difference between pCDNA and lipid binding deficient neurofibromin 2, <0.2476 (i.e., not significant); pCDNA and wild-type neurofibromin 2, <0.0001 (i.e., significant); the lipid binding deficient and wild-type neurofibromin 2 proteins, <0.0001 (i.e., significant). Scalebar size is 400 μm. d–f Phase contrast microscopy images, taken at the 72 h time point, of SC4 cells that were used in the BrdU cell proliferation assay. SC4 cells transfected with d pCDNA, e neurofibromin 2, and f the neurofibromin 2 lipid binding deficient mutant. g Cells expressing lipid binding deficient mutants of neurofibromin 2 display impaired inhibition of BrdU incorporation. SC4 cells were transfected with expression vectors for wild type and lipid binding deficient neurofibromin 2 or empty vector control (pCDNA) and BrdU incorporation was assessed over 72 h. Means of each data point were calculated from three independent biological replicates conducted in triplicate. Error bars represent ± S.D. Difference between pCDNA and our lipid binding deficient mutant neurofibromin 2, <1.0000 (i.e., not significant); pCDNA and wild-type neurofibromin 2, <0.000 (i.e., significant); wild type and our lipid binding deficient mutant, <0.0001 (i.e., significant)