Fig. 10.

Hypothetical model of the effect of differential FGFR1 clustering on the receptor endocytosis. FGFR1 dimerization, either with FGF1 or bivalent antibodies, like B‐Fc, induces CME of the receptor. CME initiation is independent of FGFR1 activation. Clustering of FGFR1 into large structures on the plasma membrane with tetravalent T‐Fc largely improves the cellular uptake of FGFR1–antibody complexes. Furthermore, FGFR1 clustering changes the mechanism of the receptor endocytosis by engaging dynamin‐dependent CIE pathways. Similarly to CME, CIE of FGFR1 does not require receptor activation.