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The authors of this paper disclose their affiliations with Aventis (A), Abbott (AB), AstraZeneca (AZ), Bayer (B), Biovail (BV), Bristol-Myers Squibb (BMS), Forest (F), Glaxo-SmithKline/SmithKline Beecham (GSK/SKB), King Pharmaceuticals/Monarch (KM), Merck (M), Novartis (N), Nu-Pharm (NP), Pharmacia/Upjohn (PHU), Pfizer, Inc. (P), Sankyo (SY), Searle (SE), Solvay (SV), Takeda (T).
To follow the observed reduction of SNIP1 level upon the expression of high level of ALK3Q233D, as mentioned above, we co-expressed SNIP1 together with Smad1, Smad4, Az and high dose (6 μg) of either the wild type ALK3 or the constitutive active ALK3Q233D.
Based upon the observation that the nuclear translocation of Az is dependent upon Smad1 and BMP type I receptor activation (Fig.
Thus, the ALK3Q233D-induced degradation of SNIP1 is regulated by the protein levels of Smad1, Smad4, Az and is only induced by high dose of the activated BMP type I receptor.
This is suggested by the observations that the targeting of SNIP1 is positively regulated by Smad1 level and is dependent upon Smad1, Smad4 and Az (Fig.