American Society of Hematology

Fig. 7.

$Fig. 7. Schematic model of uptake and intracellular fate of His-M195FANCF. / Endocytosis of the fusion protein is stimulated by binding to CD33. Endocytosis is assumed to be clathrin-dependent, leading to the incorporation of the ligand–receptor complex in early endosomes (E). Much of the protein is then able to exit directly into the cytosol, and a smaller fraction reaches the cytosol after retrograde transport through the trans-Golgi network (G) and the endoplasmic reticulum (ER). Protein released into the cytosol from one or both of these routes reaches the nucleus. In FA-F cells, the nuclear protein would be expected to complement the MMC-hypersensitive phenotype.$

Schematic model of uptake and intracellular fate of His-M195FANCF.

Endocytosis of the fusion protein is stimulated by binding to CD33. Endocytosis is assumed to be clathrin-dependent, leading to the incorporation of the ligand–receptor complex in early endosomes (E). Much of the protein is then able to exit directly into the cytosol, and a smaller fraction reaches the cytosol after retrograde transport through the trans-Golgi network (G) and the endoplasmic reticulum (ER). Protein released into the cytosol from one or both of these routes reaches the nucleus. In FA-F cells, the nuclear protein would be expected to complement the MMC-hypersensitive phenotype.

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