FIGURE

Fig. 5

ID

ZDB-FIG-170914-28

Publication

Scott et al., 2017 - Nuclear/cytoplasmic transport defects in BBS6 underlie congenital heart disease through perturbation of a chromatin remodeling protein

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Fig. 5

BBS6 and SMARCC1 protein localizations overlap in subcellular compartments.

A single z-slice of a confocal stack of cells in a 70% epiboly staged zebrafish embryos stained with a SMARCC1 antibody, nuclei counterstained with TO-PRO-3 (A). SMARCC1 immunostaining of 293T cells shows predominant nuclear localization, nuclei counter-stained with TO-PRO-3 (B). Cellular fractionation of 24hpf zebrafish as well as 293T cells show cytoplasmic and nuclear localization of endogenous Smarcc1a/SMARCC1, TBA1 and SP1 served as cytoplasmic and nuclear fraction controls (C). Experimental design of cellular transfection and fractionation followed by IP on individual sub-cellular fractions (D). Western blot showing myc-BBS6 can coIP with SMARCC1 in the cytoplasm and nucleus (E). Normalizing IP band intensity to input shows stronger interaction in the cytoplasm (F). Scale bars = 20μm.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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