Exome Profile

Exome Analysis Results: Copy number variations inferred by absCN-seq, clonality analysis by sciClone, and somatic mutations by VarScan

Additional file 3: Figure S3. of Leucine-Rich Repeat Kinase 2 (LRRK2) phosphorylates p53 and induces p21WAF1/CIP1 expression

Increased phosphorylation of Thr in the p53 TXR sites in dopaminergic neurons differentiated from fibroblast-derived iPS cells that were obtained from the human G2019S carrier (WT/GS) and non-carrier (WT/WT). The indicated cell lysates were immunoprecipitated with the p53 antibody and the immunoprecipitates (IP: p53) were subjected to Western blot. Input indicates 20% of the cell lysates. Numbers below the gel figures are relative protein level of each TXR band ([p-TXR]/[total p53]) based on the densitometric analysis. The antibodies used for Western blot analysis were indicated in the right side of each blot. (DOC 57 kb

Additional file 1: Figure S1. of Leucine-Rich Repeat Kinase 2 (LRRK2) phosphorylates p53 and induces p21WAF1/CIP1 expression

LRRK2 phosphorylates p53 and moesin at TXR sites in the in vitro kinase assay. A. Phosphorylation of various p53 proteins by the Flag-tagged full length LRRK2 protein (Invitrogen) after the in vitro kinase assay. Phosphorylated p53 was detected by either autoradiography or Western blot with the p-TXR antibody. B. Western blot analysis after the in vitro kinase assay using moesin, various GST-ΔN-LRRK2 WT and mutant proteins, and cold ATP. (DOC 88 kb

Reversible Lithium Storage at Highly Populated Vacant Sites in an Amorphous Vanadium Pentoxide Electrode

A vanadium pentoxide electrode is prepared in the amorphous form (<i>a</i>-V₂O₅), and its electrode performances are compared to those for its crystalline counterpart (<i>c-</i>V₂O₅). The <i>a</i>-V₂O₅ electrode outperforms <i>c-</i>V₂O₅ in several ways. First, it is free from irreversible phase transitions and Li trapping, which evolve in <i>c</i>-V₂O₅, probably due to the lack of interactions between the inserted Li⁺ ions/electrons and V₂O₅ matrix. Second, the absence of Li trapping allows a reversible capacity amounting to >600 mA h g^–1, which is larger than that given by <i>c-</i>V₂O₅. Third, it shows an excellent rate property. The notably high reversible capacity and rate capability seem to be due to Li storage at vacant sites that are ill-defined but numerous in <i>a</i>-V₂O₅, which Li⁺ ions can easily access. However, irreversible capacity of <i>a</i>-V₂O₅ is appreciable in the first cycle due to a parasitic Li reaction with surface hydroxyl groups. Treatment with <i>n</i>-butyllithium can suppress the irreversible capacity by removing the surface hydroxyl groups

Additional file 4: Figure S4. of Leucine-Rich Repeat Kinase 2 (LRRK2) phosphorylates p53 and induces p21WAF1/CIP1 expression

LRRK2 kinase inhibitor decreased p21 expression. Differentiated SH-SY5Y cells were treated with 1 μM LRRK2-IN-1 for 2 h (A-D) or 0.5 μM GSK2578215A (Tocris Biosciences, Bristol, United Kingdom) for 12 h (E). The p53 immunoprecipitates of the cell lysates were used to detect p-TXR level (A). The LRRK2-IN-1 treated cells were also used to determine relative amount of nuclear p53 (B) as in Fig. 3a. The cell lysates were used to detect p21 mRNA (C) and protein (D) levels as in Figs. 4 and 5. p21 expression level of GSK2578215A treated cells were also tested (E). Activities of LRRK2 kinase inhibitor treatments were confirmed by reduced level of LRRK2 p935 (pS935). – indicates vehicle treatment. Lamin B and LDH were used for nuclear and cytosolic markers, respectively. All experiments were repeated three times, and a representative result is shown with a bar graph. *: p <0.05; **: p <0.01. (DOC 188 kb

Additional file 5: Figure S5. of Leucine-Rich Repeat Kinase 2 (LRRK2) phosphorylates p53 and induces p21WAF1/CIP1 expression

Expression of T304/377D mutant increased cytotoxicity in rat primary neurons. The neuronal cells were transfected with vector, HA-p53, T304/377D and T304/377A. The cytotoxicity was measured by LDH assay. n = 6. **: p <0.01; ***: p <0.001. (DOC 49 kb

Gene expression profiles associated with breast cancer’s spatial growth measured by SED (spheroid-ellipsoid discrepancy).

<p>The scatter plots for MMP13 and ADAMTS12 are shown in (a) and the correlation was stratified according to the hormonal receptor status (b). The results of the qRT-PCR against MMP13 and the SED are shown in Fig 5c. RQ: relative quantification.</p

Kaplan-Meier survival curve according to tumor eccentricity.

<p>**: P<0.01, *:P<0.05, The p values are derived from the log-rank test compared to the SED High group. SED: spheroid-ellipsoid discrepancy.</p

Molecular regulatory network for MMP13 and its expression in various subtypes of breast cancers.

<p>The interaction network analysis showing a potential regulatory pathway of MMP13 based on the Pathway Studio Web (a), and the levels of MMP13 expression in TCGA dataset according to the PAM50 molecular subtypes (b) are shown.</p

Distant metastasis-free survival according to the tumor volumes.

<p>Comparison of the prognosis predicting accuracy of the spheroid tumor volume measurement (2a) and ellipsoid tumor measurement (2b) are shown. HR: hazard ratio estimated by univariate Cox regression analysis, TV: tumor volume.</p