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. Author manuscript; available in PMC: 2015 Nov 14.
Published in final edited form as: Oncogene. 2014 Jul 21;34(20):2650–2659. doi: 10.1038/onc.2014.210

Figure 2. Phosphorylation of tyrosine 295 and 361 of Dok1 correlates with suppression of CrkI transformation.

Figure 2

a) Diagram of the human Dok1 cDNA constructs used, indicating positions of tyrosine phosphorylation sites mutated. PH: Pleckstrin homology domain; PTB: phospho-tyrosine binding domain; Y: tyrosine; F: phenylalanine; HA: HA epitope tag. b) Dok1 knockdown and rescue with HA-tagged Dok1 constructs. NIH3T3 cell lysates were immunoblotted with antibodies indicated (αpDok1 = phosphospecific Dok1 antibody). E: empty vector control; C: CrkI transformed; CAi: CrkI-transformed, Abl knockdown; CDi: CrkI-transformed, Dok1 knockdown; WT: wild-type Dok1; M14: Y295F and Y361F mutant Dok1; M23: Y336F and Y340F mutant Dok1; M-all: Y295F, Y336F, Y340F and Y361F mutant Dok1; M1: Y295F mutant Dok1; M4: Y361F mutant Dok1. c) Soft agar colony formation results for cells in panel b. d) Over-expression of Dok1 in CrkI-transformed NIH3T3 cells; abbreviations as in panel b. e) Soft agar colony formation results for cells in panel d.