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1 MEN2B is caused by a specific mutation (Met918-->Thr) in
3 erited multiple endocrine neoplasia type 2B (MEN2B) is characterized by tumors of the thyroid C-cells
4 B mutation may result in the more aggressive MEN2B phenotype by altering the receptor's signaling cap
5 y deregulated in tumours with MEN2A-like and MEN2B-like mutations; however, further investigations ar
6 e developed a Drosophila model for MEN2A and MEN2B diseases by targeting oncogenic forms of RET to th
10 he Met918Thr substitution is responsible for MEN2B, they suggest that the substrate specificity of th
11 during Transfection (RET) gene cause MEN2A, MEN2B, and familial medullary thyroid carcinoma (FMTC).
12 rmline mutations in the RET (formerly MEN2A, MEN2B) proto-oncogene located on chromosomal band 10q11.
13 e RET point mutations associated with MEN2A, MEN2B, or FMTC, or the chromosomal breakpoints and trans
14 Also, children from families with MEN2A, MEN2B, or FMTC, who are found to have inherited a mutate
15 We report the production of a mouse model of MEN2B by introduction of the corresponding mutation into
16 ion of renal development results because Ret(MEN2B) derived from the hyperplastic nervous tissue comp
18 c mice with the highest levels of DbetaH-RET(MEN2B) expression, unexpectedly developed renal malforma
21 embryos, renal maldevelopment in DbetaH-Ret(MEN2B)-transgenic embryos results from primary changes i
23 oxylase promoter to direct expression of RET(MEN2B) in the developing sympathetic and enteric nervous
24 ess a constitutively active form of Ret (Ret(MEN2B)) under the control of the dopamine-beta-hydroxyla
25 ted MAP kinase were not increased in the RET(MEN2B)-induced neurolglial proliferations, suggesting th
26 tes found in the wild-type RET receptor, the MEN2B mutant lacked phosphorylation at Tyr-1096, leading
27 nges in autophosphorylation suggest that the MEN2B mutation may result in the more aggressive MEN2B p
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