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1 n but low eIF3c abundance in those retaining schwannomin.
2 the NF2 meningioma tumor suppressor, merlin/schwannomin.
3 nase substrate (HRS) strongly interacts with schwannomin.
7 cation to the lysosome, we demonstrated that schwannomin and HRS co-localize at endosomes using the e
9 ss of expression of the NF2 tumor suppressor schwannomin are one of the most common causes of benign
11 reviously shown that the NF2 protein (merlin/schwannomin) associates with mixed lineage kinase 3 (MLK
12 molecular adaptor paxillin binds directly to schwannomin at residues 50-70, which are encoded by exon
15 high eIF3c abundance in those that had lost schwannomin expression but low eIF3c abundance in those
16 atosis 2 tumor suppressor protein, merlin or schwannomin, functions as a negative growth regulator; h
17 en schwannomin and eIF3c suggests a role for schwannomin in eIF3c-mediated regulation of proliferatio
20 cipitation of endogenous HRS with endogenous schwannomin in vivo as well as by using bacterially puri
22 a negative-feedback loop, Pak phosphorylates Schwannomin inactivating its ability to inhibit Pak.
23 tions that result in production of defective schwannomin include in-frame deletions of exon 2 and thr
26 The NF2 tumor suppressor protein, merlin or schwannomin, inhibits cell growth and motility as well a
30 onstrate in primary Schwann cells (SCs) that Schwannomin is rapidly phosphorylated on S518 by Pak fol
32 in-ezrin-radixin-like protein, also known as schwannomin) is a tumor suppressor protein encoded by th
34 chanisms by which the NF2 product, merlin or schwannomin, is regulated and controls cell proliferatio
35 he product of the NF2 gene, termed merlin or schwannomin, is thought to act as a tumor suppressor pro
36 urred between the carboxy-terminal domain of schwannomin isoform 2 and the ankyrin-binding region of
38 ress schwannomin synthesis and indicate that schwannomin may belong to a class of tumor suppressor ge
39 e suggested that the NF2 protein, merlin (or schwannomin), may regulate receptor tyrosine kinase sign
40 neurofibromatosis 2 tumor suppressor protein schwannomin/merlin is commonly mutated in schwannomas an
44 bromatosis 2 (NF2) tumor suppressor protein, schwannomin or merlin, is commonly lost upon NF2 gene mu
45 hese receptors, together with phosphorylated Schwannomin, P-Pak, Cdc42 and paxillin are enriched at t
46 d NRG1beta does not synergistically increase Schwannomin phosphorylation because ErbB2 kinase partial
49 data are consistent with the hypothesis that schwannomin requires HRS interaction to be fully functio
50 rrowed the regions of interaction to include schwannomin residues 256-579 and HRS residues from 480 t
51 The gene products neurofibromin and merlin (schwannomin), respectively, are thought to act as tumour
53 in and HRS inhibit Stat3 activation and that schwannomin suppresses Stat3 activation mediated by IGF-
54 des can be successfully employed to suppress schwannomin synthesis and indicate that schwannomin may
56 inactivate the tumor suppressor activity of Schwannomin to allow proliferation of subconfluent SCs.
57 tions with antischwannomin antibodies showed schwannomin to be almost absent 3 h after treatment with
58 action mediates the membrane localization of schwannomin to the plasma membrane, where it associates
60 function of the NF2 gene product, merlin or schwannomin, we performed a detailed functional analysis
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