Biological Effects of the Dual Phenotypic Janus Mutation of ret Cosegregating with Both Multiple Endocrine Neoplasia Type 2 and Hirschsprung’s Disease
Mol Endocrinol Arighi et al.
18: 1004
Supplemental Data
SUPPLEMENTAL DATA FILE:
Growth rate of RET-MDCK cells in response to GDNF. (A-C) Proliferation of the cells was estimated using MTT cell proliferation assays. Results are presented as average ± SEM of three independent experiments each measured in triplicate. (A) GDNF/sGFRa1 induces
proliferation of wild-type RET-MDCK cells. Cells were serum starved in 0.5% FCS for 2 days, treated with 100 ng/ml GDNF/sGFRa1, 50 ng/ml HGF or left untreated for the indicated times and then assayed for MTT dye conversion. (B) The Janus-C620R protein promotes rapid ligandindependent proliferative activity while HSCR-S767R impairs the proliferative response to
GDNF/sGFRa1. (C) GDNF/sGFRa1 induces proliferation of FMTC-E768D-expressing cells. The MEN 2A-C634R mutation confers high ligand-independent proliferative activity to RET-MDCK
cells. (D,E) Proliferation of the RET-MDCK cells was verified by BrdU cell proliferation assays. The results shown are representative of three independent experiments. Means ± SEM of five independent repeats are shown.
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