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1 DLD-1 colon carcinoma cells with the mutated adenomatous polyposis coli protein.
2 GI tumors in Mlh1 mice express little or no adenomatous polyposis coli protein.
3 ith the second PDZ domain of DLG, similar to adenomatous polyposis coli protein.
5 at RNAi-mediated depletion of two kMAPs, the adenomatous polyposis coli protein (APC) and its binding
6 olding protein Axin and the tumor suppressor adenomatous polyposis coli protein (APC) are critical co
9 Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the loc
13 , which is required for interaction with the adenomatous polyposis coli protein, bind and inhibit GSK
14 d beta-catenin requires interaction with the adenomatous polyposis coli protein but not with TCF for
17 otein EB1, which is a binding partner to the adenomatous polyposis coli protein involved in colon can
18 n from Mlp of a region similar to one in the adenomatous polyposis coli protein involved in EB1 bindi
19 ows that the actin-nucleating ability of the adenomatous polyposis coli protein is required for disas
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