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. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.

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

Fig. 4. Clinically defined SMN mutants show alterations in the association with telomerase complex proteins. Clinically defined SMN mutants show alterations.

Fig. 3. Hts and Dlg are in a complex at the postsynaptic membrane of larval NMJs.(A–B″) PLA with HtsM and Dlg antibodies (green) performed on third instar.

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

Fig. 4. E-cadherin expression level affects monomer dynamics.

Fig. 1. Chlamydia infection causes elevated levels of sortilin.

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.

A highly conserved six-amino-acid region in the C-terminal CT domain of MARCH8 is responsible for its ability to downregulate TfR. A highly conserved six-amino-acid.

Fig. 4. A primary screen based on scrape closure

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

Fig. 2. Histone H3 phosphorylation appears at prometaphase upon C4 treatment.(A) Western blots were realized on cells synchronized at mitotic entry in.

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. 5. Expression of either dFMRP or human FMRP does not induce eIF2α phosphorylation.(A) Analysis of eIF2α phosphorylation upon dFMRP expression. Expression.

Establishment of intercellular adhesion in homozygous, heterozygous andβ -catenin-null mutant keratinocytes after incubation in medium containing 1.2 mM.

Fig. 5. Onecut transcription factors are important for the correct generation of the mdDA neuronal population.(A) Schematic representation of the region.

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

TP53 western blot of primary cultured tail cells from both wild-type (WT) and Tp53Δ11/Δ11 (−/−) rats. TP53 western blot of primary cultured tail cells.

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

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.

Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse myocardium. Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse.

Ectopic sprouting and proliferation in Rbpj veins.

Fig. 5. Recovery steps of mitotic acentriolar cells after cold MT depolymerisation.(A,B) Time-lapse sequences of mitotic spindle re-formation at 18°C.

Abraxas binds to BRCT–PALB2(L21P) and is involved in the recruitment of this fusion protein or of endogenous PALB2 to sites of DNA damage. Abraxas binds.

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

Fig. 3. Mutation of Y520 and Y667 result in increased delivery of prestin to the apical surface of MDCK cells.MDCK cells transiently transfected with wt.

Fig. 8. Knockdown of Meis1 reduces the expression of Foxn4 and Lim1+2

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

Fig. 4. Non-autonomous rescue of puc expression in DME cells

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.

Fig. 5. The bulk of Cep135 localizes distantly from Sas-6 and STIL

Fig. 2. The localisation of integrins β1 and α6 in the hES cells grown in a colony and as a single-cell culture. hES cells were harvested manually as small.

Fig. 2. Morphological analysis of acentriolar mitotic spindles

Fig. 6. Effect of SAHA and ML on histone acetylation, BAX, and p21CDKN1A expression.PANC-1 and BxPC-3 cells were incubated for 48 hours with 5 µM.

The TER94-p47 complex isinvolved in Notch signaling regulation

Fig. 1. Effects on the tight junction barrier and permeability following doxorubicin and Herceptin treatment. Effects on the tight junction barrier and.

Fig. 3. Rnd proteins induce stronger responses in subconfluent endothelial cells.HUVECs were transfected with Rnd1, Rnd2, Rnd3 or GFP-encoding plasmids.

Fig. 10. A mutant clone homozygous for mip120LL07629 has greatly diminished Mip120 protein levels. hsFLP/+; FRT42B, mip120LL07629/FRT42B, Ubi-GFP-nls females.

ICAM-1 forms distinct complexes with filamin B, α-actinin-4 and cortactin. ICAM-1 forms distinct complexes with filamin B, α-actinin-4 and cortactin. (A)

In 6CFSMEo- cells, UPF1 protein is concentrated partially or totally in P-bodies after cytoskeleton inhibitor treatment. In 6CFSMEo- cells, UPF1 protein.

Fig. 7. Ror-GFP binds to Myc-tagged Wnts and Wnt receptors.

In 6CFSMEo- cells, the NMD factor UPF1 colocalizes with NMD substrates under cytoskeleton disruptor treatment. 6CFSMEo- cells were transfected with constructs.

Fig. 4. Co-immunostaining of nocodazole or ASNase treated RPE-1 cells with anti-hASNS and anti-alpha tubulin showed defect in both mitotic spindle formation.

Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.

Readthrough GPx1 Ter–Neptune proteins colocalize with UPF1 under cytochalasin D treatment. 6CFSMEo- cells transfected with plasmids encoding YFP–UPF1 (green),

Fig. 4. Schematic representing clock contribution to Fgf21 regulation in the liver. Schematic representing clock contribution to Fgf21 regulation in the.

Statistical chart of significantly differentially expressed genes

2DG downregulates the expression of HIF-1α, PDK1 and c-Myc in NB xenograft. 2DG downregulates the expression of HIF-1α, PDK1 and c-Myc in NB xenograft.

Fig. 1. Phenotypic characterisation of primary human tubular epithelial cells and human renal fibroblasts. Phenotypic characterisation of primary human.

High-affinity mutants of β3 integrin fail to stimulate RhoA activity and fibronectin fibrillogenesis. High-affinity mutants of β3 integrin fail to stimulate.

Fig. 4. Autotoxicity triggered by withdrawal of antitoxin inducer in Synechocystis sp. Autotoxicity triggered by withdrawal of antitoxin inducer in Synechocystis.

The SIM domain of RAD51 is required for HR

Fgfr3;4 mutant lungs display an increase in Mfap5, Igf1 and Fbn2 expression. Fgfr3;4 mutant lungs display an increase in Mfap5,Igf1and Fbn2 expression.

The expression of two forms of N-cadherin.

Fig. 12. Overview of the molecular program essential to build mdDA neurons.The genes identified in this study (in red) have been added to the programming.

Fig. 2. Expression of Cx43 mutant T154A resulted in non-radial spreading and formation of protrusions in J558µm3 cells spreading in response to BCR signaling.(A)

Fig. 2. Acetylation stiffens primary cilia.

Fig. 1. Cell adhesion molecule expression and the aggregation of wildtype and mutant ES cells.(A) Wildtype (WT), E-cadherin null (9J), and N-cadherin null.

Misfolding mutations impair the BRCA1 nuclear aggregation in yeast and the BRCA1 nuclear localization in human cells. Misfolding mutations impair the BRCA1.

Fig. 5. Testis defects in STK35 KO mice.

Fig. 6. RhoB is required for Rnd3-induced stress fibre formation

Fig. 1. p85β localizes at adhesion plaques and associates with FAK

Fig. 3. Mean force and velocity during jumping

Fig. 6. Bj mutants show stereocilia patterning defects and biliary duct (BD) malformations. Bj mutants show stereocilia patterning defects and biliary.

EPLIN also plays a crucial role in the apical extrusion of RasV12-transformed cells. EPLIN also plays a crucial role in the apical extrusion of RasV12-transformed.

WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates TfR. WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates.

Fig. 3. Inclusion of E-cadherin into stationary clusters requires cis-, trans-, and cytoplasmic interactions. Inclusion of E-cadherin into stationary clusters.

Fig. 7. Rho family GTPase signaling is required for cyst formation in Ptp4E Ptp10D mutants.(A–C) Expression of DN Rho1 and Rac1 mutants in wild-type (w1118)

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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 on barrier formation in MDCK cells. Coupling of actin to cell–cell junctions requires α-catenin and is necessary for the establishment of the barrier.(A) Effect of Cytochalasin D on barrier formation in MDCK cells. CytoD was added during a calcium switch (dashed green line) or to a pre-existing monolayer (dark green line). Error bars indicate standard error, n>3. (B) Schematic representation of α-catenin-WT construct and α-catenin-1-848 mutant lacking the C-terminal F-actin binding site. (C) Expression levels of α-catenin-WT or α-catenin-1-848 in α-catenin depleted MDCK cells assessed by Western Blotting with α-catenin specific antibodies. (D) TER measurement in α-catenin depleted MDCK cells (red line), or the same cells rescued with α-catenin-WT (green line) or α-catenin-1-848 (orange line). Error bars indicate standard error, n>3. Floor Twiss et al. Biology Open 2012;bio.20122428 © 2012. Published by The Company of Biologists Ltd