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Description
c-met is amplified but not mutated in a cell line with an activated met tyrosine kinase

Fibrosis has potentially lethal consequences, and lacks effective treatment 1,2,3,4,5,6,7

Research demonstrates reduced food intake, slowed gastric emptying, and reduced postprandial glucagon all contributing to sustained negative energy balance

IGF-I receptor defects combine low birth weight and high normal IGF-I values (1)
The ligand for c-MET was identified by two independent studies as both a motility factor and a scatter factor for hepatocytes, and this factor was later found to be the same molecule: HGF, also known as scatter factor (SF) [Weidner et al
