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.

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Volume 14, Issue 10, Pages (October 2007)

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Volume 21, Issue 1, Pages (January 2011)

Aggregation is not required for cytoplasmic relocalization induced by misfolding mutations. Aggregation is not required for cytoplasmic relocalization.

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

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

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. 5. Differentiated cells sort to the outer layer, regardless of E- or N-cadherin status.Wildtype and mutant ES cells were distinguished by GFP expression.

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

Localisation of epithelial markers in mMEC cultures.

A Drosophila cell culture model to study VAP(P58S) aggregation.

Inflammation is associated with increased basal-cell plasticity in the Nkx3.1 mutant prostate. Inflammation is associated with increased basal-cell plasticity.

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

Fig. 4. Increased adipocyte differentiation in Cbx7-KO ES cells

Fig. 1. Morphological and growth characterization of hBMCs and hPDCs

Fig. 2. Transfection and clonal selection of rat pluripotent stem cells to generate stable transgenic lines. Transfection and clonal selection of rat pluripotent.

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.

Fig. 2. Salivary glands from RasV12-expressing larvae produce MMP1, release tissue fragments into the hemolymph and express apoptotic markers.Salivary.

Fig. 1. E-cadherin localizes in nano-scale clusters.

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

Fig. 2. DDR1 over-expression enhances collagen fibril reorganization

Fig. 1. Ovarian cancer spheroids can bud from a monolayer

Fig. 3. Characterization of unclassified cells (UCs).

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

Effect of Z-FA-FMK on the expression of SMN proteins in SMA patient iPSCs and iPSC-derived motor neurons. Effect of Z-FA-FMK on the expression of SMN proteins.

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. Differentiated cells sort to the outer layer, regardless of E- or N-cadherin status.Wildtype and mutant ES cells were distinguished by GFP expression.

Fig. 6. Comparison of Plk4 with Sas-6 localization

Fig. 6. CBX7 expression in adipocyte differentiation of adipose-derived stem cells.(A) The adipose-derived stem cells, ADS1, were analyzed for the capability.

Fig. 2. Centrosomal proteins display distinct localizations and radial distances from centriole walls.U2OS cells were fixed and stained with the indicated.

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

Fig. 2. Soluble sugar and organic acid levels with different K fertilization during fruit development. Soluble sugar and organic acid levels with different.

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.

MiR-200c/141 overexpression in LS-8 cells induces E-cad expression and cell-cell adhesion. miR-200c/141 overexpression in LS-8 cells induces E-cad expression.

Fig. 6. STK35 KO mice show ovary defects.

Fig. 2. Sorting in chimeric embryoid bodies of wildtype with E- or N-cadherin null ES cells.Wildtype, E-cadherin null (9J), and N-cadherin null (Ncad95)

BMP signalling is dispensable for early gastruloid patterning.

Fig. 6. Apical polarity of primitive endoderm cells on surface of embryoid bodies.Embryoid bodies were analyzed by immunofluorescence microscopy for GATA4.

An inhibitor of HSP90β reduces the level of HNF4A protein in hepatic progenitor cells. An inhibitor of HSP90β reduces the level of HNF4A protein in hepatic.

Fig. 3. Weak interaction between E-cadherin and N-cadherin null cells

ArfGAP1 expression alters GBF1 recruitment to Golgi membranes.

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

N-cadherin deficient cells do not adhere or migrate.

The actin organization and N-cadherin dynamics in migrating cells.

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.

Fig. 2. iPSCs produce functional osteoblasts.

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

V-ATPase and proteins involved in late endosomal protein sorting are required for efficient utilization of LDs during growth resumption. V-ATPase and proteins.

Ibm1 and edm2 mutants generate more stomatal divisions in the leaf epidermis. ibm1 and edm2 mutants generate more stomatal divisions in the leaf epidermis.

dcn1-deletion results in attenuated cohesin cleavage at anaphase

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.

Loss of Graf results in plasmatocyte overproliferation.

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.

Proliferation on soft matrices is decoupled from myosin light chain phosphorylation, cell tractions, and focal adhesions. Proliferation on soft matrices.

Fig. 5. Testis defects in STK35 KO mice.

Fig. 1. Rnd2 and Rnd3 induce stress fibres whereas Rnd1 reduces stress fibres in endothelial cells.(A) Rnd mRNAs are expressed in HUVECs. Total RNA was.

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

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

The BRCA1 aggregates exclude large nuclear structures.

mip120 null egg chambers have a condensed nurse cell DNA phenotype

Sensory neurons grow and downregulate UCHL1 expression levels during postnatal maturation. Sensory neurons grow and downregulate UCHL1 expression levels.

Fig. 7. Analysis of dFMRP kinetics in dFMRP granules by FRAP

Lack of Ctip2 is associated with impaired proliferation and delayed onset of differentiation during early stages of epidermal development. Lack of Ctip2.

APLF regulates genes implicated in MET during the generation of iPSCs from fibroblasts. APLF regulates genes implicated in MET during the generation of.

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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 (Ncad95) ES cells, with or without differentiation by retinoic acid, were analyzed by Western blot for the proteins levels of E-cadherin and N-cadherin. Cell adhesion molecule expression and the aggregation of wildtype and mutant ES cells.(A) Wildtype (WT), E-cadherin null (9J), and N-cadherin null (Ncad95) ES cells, with or without differentiation by retinoic acid, were analyzed by Western blot for the proteins levels of E-cadherin and N-cadherin. Oct3/4 and Dab2 levels are indicators of ES cell pluripotency or endoderm differentiation, respectively. The intensities of the signal in the Western blots were quantified using Image J program. (B,D) ES cells in monolayer cultures were analyzed by immunofluorescence microscopy by staining for Oct3/4, GATA4, and DAPI prior to (B), or following differentiation with 1 µM retinoic acid for 5 days (C). The representative individual images acquired were overlaid to produce the composed figures shown. (D) Rate of aggregation of the ES cells was determined as a measure of cell adhesive affinity. Cells were first mono-dispersed, washed with cold PBS, and then allowed to aggregate at 37°C. The aggregation of undifferentiated cells was measured using a Coulter Counter and the reduction of particle number is presented. (E) Wildtype, E-cadherin null (9J), and N-cadherin null (Ncad95) ES cells were first differentiated by treatment with retinoic acid for 4 days. The aggregation of the differentiated cells was measured using a Coulter Counter and the reduction of particle number is presented. Coulter Counter reading of particle numbers were performed using triplicate samples and the average and standard error are reported. Scale bars: 5 µm. Robert Moore et al. Biology Open 2014;bio.20146254 © 2014. Published by The Company of Biologists Ltd