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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.
4                                              Schwannomin, a member of the 4.1 family of proteins, whi
5  the gene NF2, encoding the growth regulator schwannomin (also known as merlin).
6                          Interaction between schwannomin and eIF3c suggests a role for schwannomin in
7 cation to the lysosome, we demonstrated that schwannomin and HRS co-localize at endosomes using the e
8                        We now show that both schwannomin and HRS inhibit Stat3 activation and that sc
9 ss of expression of the NF2 tumor suppressor schwannomin are one of the most common causes of benign
10                        The identification of schwannomin as a HRS interactor implicates schwannomin i
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
13  betaII-spectrin (also known as fodrin) as a schwannomin-binding protein.
14                                              Schwannomin co-immunoprecipitated with betaII-spectrin a
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
18 f schwannomin as a HRS interactor implicates schwannomin in HRS-mediated cell signaling.
19 ell as by using bacterially purified HRS and schwannomin in vitro.
20 cipitation of endogenous HRS with endogenous schwannomin in vivo as well as by using bacterially puri
21                                 Isoform 1 of schwannomin, in contrast, interacted weakly with betaII-
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
24              Therefore, we hypothesized that schwannomin inhibits STAT activation through interaction
25                            We also find that schwannomin inhibits Stat3 and Stat5 phosphorylation in
26  The NF2 tumor suppressor protein, merlin or schwannomin, inhibits cell growth and motility as well a
27  eukaryotic initiation factor 3 (eIF3c) as a schwannomin interacting protein.
28 gulated tyrosine kinase substrate (HRS) as a schwannomin interactor.
29                                        Thus, schwannomin is a tumour suppressor directly involved in
30 onstrate in primary Schwann cells (SCs) that Schwannomin is rapidly phosphorylated on S518 by Pak fol
31                   The NF2 protein merlin (or schwannomin) is a member of the Band 4.1 superfamily of
32 in-ezrin-radixin-like protein, also known as schwannomin) is a tumor suppressor protein encoded by th
33             The NF2 gene product, merlin (or schwannomin), is a member of the protein 4.1 family of m
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
37                                              Schwannomin itself lacks the actin binding sites found i
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
41                             The NF2 protein, Schwannomin/Merlin, is a cytoskeleton-associated tumor s
42                                              Schwannomin molecules with a L46R, L360P, L535P or Q538P
43                      The NF2 protein, called schwannomin or merlin, is absent in virtually all schwan
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
47 tor mechanisms that promote Pak activity and Schwannomin phosphorylation.
48 otein truncation and undetectable amounts of schwannomin protein.
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
52                             Unphosphorylated Schwannomin restricts cell proliferation in part by inhi
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
55 hological changes were due to suppression of schwannomin synthesis.
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
59                                We found that schwannomin was most effective for inhibiting cellular p
60  function of the NF2 gene product, merlin or schwannomin, we performed a detailed functional analysis
61                                              Schwannomin with the pathogenic missense mutation Q538P

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