Fig. 3. Inactivation of the Wnt/β-catenin signaling pathway inhibited cell proliferation and induced apoptosis in A549 and SPC-A-1 cells. Inactivation.

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Wnt Signaling: It Gets More Humorous with Age

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Fig. 5 BRD0705 induces differentiation in AML cell lines and primary patient samples through GSK3α-selective inhibition. BRD0705 induces differentiation.

Transfection of stable β-catenin (S33Y) increased nuclear β-catenin and phosphorylated Akt expression (A) and reduced the promoting effect of HG on caspase-3.

Fig. 3. Effect of NH4Cl (0 or 30 mM) on percentage of motile spermatozoa and VAP after 1 and 5 min after activation. Effect of NH4Cl (0 or 30 mM) on percentage.

Fig. 7. Vinculin recruitment enhances the efficiency of barrier formation.(A) TER measurements after a calcium switch in α-catenin-depleted MDCK cells.

Fig. 8. CCA and ChQ treatment induce accumulation of F-actin rings.

Fig. 1. Representative images of the four cell lines using fluorescence microscopy. Representative images of the four cell lines using fluorescence microscopy.

Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.

Fig. 7. Motion adaptation increases time-dependent response modulations (TDRM) relatively to the average cell response.TDRM normalized to the value obtained.

Fig. 4. A primary screen based on scrape closure

TC-1 silencing sensitized A549 and SPC-A-1 cells to radiation therapy

Fig. 4. BMP and nodal induce invasion of metastatic and radial growth phase melanoma cells in human epidermal skin reconstructs. BMP and nodal induce invasion.

Fig. 1. Exogenous folic acid and Folr1 rescues the function of a Rho-kinase binding mutation in Shroom3. Exogenous folic acid and Folr1 rescues thefunction.

Fig. 1. Mitochondrial internalization in cardiomyocytes.

Fig. 3. Read-outs of mTORC1 (P-S6(S235/236)) and mTORC2 (P-Akt(S473)) in wtPC12 and PC12-27 cells.(A,B) wtPC12 and PC12-27 cells were treated for 48 hr.

Ingenuity pathway analysis of the genes enriched in both 96-h-induced MMs and human ccRCC. Ingenuity pathway analysis of the genes enriched in both 96-h-induced.

Fig. 1. Lack of Hmga1 and Hmga2 expression in A1/A2-KO mice

Fig. 8. p85β regulates active Cdc42 and Rac localization to deep adhesions.(A) NIH3T3 cell lines expressing p85α or p85β were incubated without serum (2 h),

Fig. 4. The model of malate metabolism in fruit cells under different K level conditions. The model of malate metabolism in fruit cells under different.

Fig. 3. Relative expression levels of ASNS to α-tubulin were dramatically increased when treating human cells with nocodazole and ASNase. Relative expression.

Fig. 7. E2F1 acetylation in A1/A2-KO MEFs

Fig. 7. SCF and IGF-1 accelerate fetal spleen erythropoiesis in vivo.

Fig. 6. LR phenotype of plastid translation-defective mutants with/without Spec. LR phenotype of plastid translation-defective mutants with/without Spec.

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Fig. 2. Ex vivo inducible knockout of PDCD2 in ESCs results in loss of S phase entry and increased p53.(A) Growth curve of inducible knockout and WT ESCs.

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Fig. 5. Receptor tyrosine kinase activation in response to growth factor stimulation. Receptor tyrosine kinase activation in response to growth factor.

The TER94-p47 complex isinvolved in Notch signaling regulation

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Hypothetical model of HvAP2 control of stem elongation.

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Fig. 1. Aboveground biomass of Caragana and herbaceous plants, and proportional abundance of Caragana, under different grazing management treatments. Aboveground.

Fig. 7. Representative images of control (Cas9+GFP) and Cas9+gRNA+GFP co-injected embryos on day 4 of culture, showing nuclear-imported GFP (green) and.

Fig. 6. STK35 KO mice show ovary defects.

BMP signalling is dispensable for early gastruloid patterning.

Fig. 5. Combination of SAHA and ML produces augmented suppression of cellular proliferation with impaired cell cycle progression, enhanced apoptotic.

Fig. 4. SMXL6 is degraded in response to SL treatment.

P3/QBP1 co-treatment suppressed expanded-CAG-RNA-induced RNA toxicity and expanded-polyQ-protein-induced protein toxicity in vivo. P3/QBP1 co-treatment.

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Wnt/β-catenin inhibition delays but does not inhibit T/Bra::GFP expression. Wnt/β-catenin inhibition delays but does not inhibit T/Bra::GFP expression.

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Mechanism of Akt1 in promoting reprogramming.

Fig. 3. Enhanced EGFR signaling in Rhbdf2P159L/P159L mice.

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Fig. 3. Effects of Tec on IL-1β-induced apoptosis in chondrocytes.

Model for TGF-β-induced myofibroblast differentiation involving MKL1 isoform-specific activities. Model for TGF-β-induced myofibroblast differentiation.

Regulation of lipid droplet formation by PI3-kinase activity.

Wrch-1 binds to the regulatory p85 subunit of PI3K and is necessary for Akt activation. Wrch-1 binds to the regulatory p85 subunit of PI3K and is necessary.

Fig. 2. Effects of pH on percentage of motile spermatozoa and VAP after 1 and 5 min after activation. Effects of pH on percentage of motile spermatozoa.

Fig. 2. Coupling of actin to cell–cell junctions requires α-catenin and is necessary for the establishment of the barrier.(A) Effect of Cytochalasin D.

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Fig. 2. Acetylation stiffens primary cilia.

Fig. 1. Generation of induced pluripotent stem cells (iPSCs) from urine cells (UC). Generation of induced pluripotent stem cells (iPSCs) from urine cells.

Fig. 3. Mean force and velocity during jumping

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Fig. 5. Behaviours of the wild-types Oregon-R at two temperatures.

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Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,

Western blot analysis of Wnt signaling genes.

GPC3 promotes hepatocellular carcinoma growth by stimulating the canonical Wnt pathway (A-B) GPC3 induces the stabilization of cytoplasmic β-catenin. GPC3.

Expression data from genes involved in regulation of transit through the cell cycle in response to treatment with E2 and OHT. A. Expression data from genes.

NF1-associated and sporadic MPNST cell lines show a decrease in cell viability, soft agar colony formation, and xenograft tumor growth when Wnt/β-catenin.

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Fig. 3. Inactivation of the Wnt/β-catenin signaling pathway inhibited cell proliferation and induced apoptosis in A549 and SPC-A-1 cells. Inactivation of the Wnt/β-catenin signaling pathway inhibited cell proliferation and induced apoptosis in A549 and SPC-A-1 cells. Cells were treated with 10 μM Wnt/β-catenin signaling pathway inhibitor, XAV939 for 24 h. (A) XAV939 treatment significantly inhibited the growth of A549 and SPC-A-1 cells compared with control group. (B) XAV939 treatment significantly induced apoptosis in A549 and SPC-A-1 cells compared with control group. (C) The expression levels of β-catenin, c-myc, c-met, and cyclinD1 were markedly down-regulated in XAV939-treated cells compared with control group. β-actin was used as a loading control. Mean±s.d.; *P<0.05 and **P<0.01 compared to control group. Dapeng Wu et al. Biology Open 2016;bio.017608 © 2016. Published by The Company of Biologists Ltd