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This possible approach is supported by experiments on xenograft tumor models where intraperitoneal or subcutaneous injections of SPARC inhibited tumor growth [ 33, 40].
However, this hypothesis is not supported by experiments on DS individuals, which demonstrated that the DSCR is more likely to be a susceptible region for DS phenotypes, rather than a single critical region causing all DS phenotypes [ 11– 13].
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Such genetic determinism on call structure has also been supported by experiments of interspecific hybridization [8], [9], [28], [29].
This is supported by experiments conducted on stoichiometric reduction systems and also by molecular modeling.
In addition, the physical interaction between FBW7 and ERK1 was supported by experiments conducted on pancreatic cancer cell line SW1990 stably expressing ERK1, which showed that ERK1 was able to co-immunoprecipitate with endogenous FBW7 and vice versa.
These findings were both independently supported by experiments performed on three different DNA constructs (please see Table 2 for reference), strongly suggesting that these results are not an artifact of the DNA construct.
The conclusions from these experiments on mice were supported by experiments in vitro with human cells showing similar results [ 61].
This is again widely supported by experiments.
This hypothesis is supported by experiments conducted by Van Mier (1986).
This hypothesis was further supported by experiments in C. elegans.
This is supported by experiments in pregnant monkeys (39).
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