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

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Rap1 regulates the accumulation of AJ material during ZA morphogenesis

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Supplementary Figure 1 A. B..

Fig. 1 Labeled endogenous mRNA in MCP×MBS mouse

Scanning electron microscopy analysis of EGK-I to -V chick embryos.

Fig. 2. Effect of endurance training on gene expression, and protein content and activity in heart muscle. Effect of endurance training on gene expression,

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. 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. 6. Quantitation of hntXE81 loss of function marked clones induced in AMPs or ISCs using ISC/EB (esgGAL4) and EC (NP6293) specific reporters. Quantitation.

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.

Fig. 6. Hts regulates par-1 and camkII mRNA distribution and levels in the muscle.(A–J) Views of muscles 6/7 in abdominal segment 4, probed for either.

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.

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Fig. 4. A primary screen based on scrape closure

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

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Fig. 6. Schematic diagram showing distribution and dynamics of four E-cadherin populations within the ROI of a FRAP experiment. Schematic diagram showing.

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.

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

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

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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.

Fig. 8. Compared mobilities of passenger proteins in G2/M-prophase, metaphase and anaphase.FRAP experiments were performed on HeLa cells stably expressing.

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Fig. 5. EGL-20 inhibits anterior and posterior orientation of UNC-40 asymmetric localization and the formation of axons from these sites.(A–D) HSN neurons.

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

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

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)

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

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Fig. 3. Inclusion of E-cadherin into stationary clusters requires cis-, trans-, and cytoplasmic interactions. Inclusion of E-cadherin into stationary clusters requires cis-, trans-, and cytoplasmic interactions. (A) Schematic diagram and table of mutants. (B,C) FRAP analysis of wild-type Ecad-GFP and mutants expressed in PDAC (B) and L-cells (C). Deletion of any single interaction reduces Fi from the level of wild-type E-cadherin (∼60%) to the level of the non-interacting mutant ΔEC1ΔCyt (∼30%), indicating that all three interactions, cis-, trans-, and cytoplasmic, are required for inclusion of Ecad-GFP into stationary adhesive clusters. Those mutants retaining actin association (trans-, cis-, and ΔEC1 mutants) recover more slowly than mutants lacking the cytoplasmic domain (ΔEC1ΔCyt, and ΔCyt). Retention of cis- and trans- interactions by the ΔCyt mutant did not significantly slow its recovery compared to the ΔEC1ΔCyt mutant. Values for Ecad-GFP and ΔEC1ΔCyt are included from Fig. 2C for comparison; see supplementary material Table S2 for list of all FRAP parameters. (D) TEER measured in L-cells expressing low and high levels of wild-type E-cadherin, and E-cadherin mutants. Note that none of the mutants were able to increase the effective cell adhesion strength as assessed by electrical resistance above the level of L-cells, which did not express E-cadherin. N=3 for each condition; error bars represent s.e.m. Zahra Erami et al. Biology Open 2015;bio.014159 © 2015. Published by The Company of Biologists Ltd