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To determine whether gefitinib was targeting only the ZAP-70+ cells or was affecting all cell populations, the viability of both ZAP-70+ and ZAP-70− cells was measured within the same sample. Gefitinib decreased the percentage of viable annexin V-ZAP-70+ CLL cells compared with dimethyl sulfoxide (DMSO)-treated controls in six different CLL samples (Supplementary Figure 2b). This indicates gefitinib is selectively inducing apoptosis in ZAP-70+ CLL cells. This preference for ZAP-70+ CLL cells cannot be from another gefitinib target, as CLL cells do not express EGFR and do not differentially express receptor-interacting protein kinase 2 (RIP2) or cyclin G-associated kinase.
Meiby, E. , Knapp, S. , Elkins, J. M. , & Ohlson, S. (2012). Fragment screening of cyclin G-associated kinase by weak affinity chromatography. ANALYTICAL AND BIOANALYTICAL CHEMISTRY, 404(8), 2417-2425. doi:10.
Recessively inherited mutations in DNAJC6 have recently been identified in juvenile parkinsonism . DNAJC6 encodes auxilin, a homolog of cyclin-G associated kinase (GAK; Table 1), which is preferentially expressed in neurons and involved in clathrin uncoating and synaptic vesicle recycling. Similarly, recessively inherited mutations in SYNJ1, encoding synaptojamin, that complexes with Hsc70 and auxilin, have been implicated in disease .
Dumitriu, A. , Pacheco, C. D. , Wilk, J. B. , Strathearn, K. E. , Latourelle, J. C. , Goldwurm, S. , Pezzoli, G. , Rochet, J. -C. , Lindquist, S. , & Myers, R. H. (2011) Cyclin-G associated kinase modifies α-synuclein expression and toxicity in Parkinson’s disease: results from the GenePD Study. Hum. Molec. Genet. 20:1478-1487.