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1 der resulting from germline mutations in the NF2 gene.
2 alyzed the 5' flanking sequence of the human NF2 gene.
3 g non-conservative missense mutations in the NF2 gene.
4 hwannomas were analyzed for mutations in the NF2 gene.
5 tumors that carry somatic alterations of the NF2 gene.
6 mechanism involving the neurofibromatosis 2 (NF2) gene.
7 me 22 and near the neurofibromatosis type 2 (NF2) gene (22q12) were most frequently noted to have exp
8 we have evaluated neurofibromatosis type 2 (NF2) gene alterations in eight PNTs using archival forma
9 harbored typical truncating mutations of the NF2 gene and loss of heterozygosity of the surrounding r
10 ozygous loss of chromosome 22 (harboring the NF2 gene) and functional inactivation of the remaining N
12 llelic mutations in the neurofibromatosis 2 (NF2) gene are linked to schwannoma and meningioma tumori
15 ction in detail, we have disrupted the mouse Nf2 gene by homologous recombination in embryonic stem c
16 ine mutations in the coding sequences of the NF2 gene can cause loss of merlin function, the mechanis
18 Mutations in the neurofibromatosis type 2 (NF2) gene cause formation of schwannomas and other tumor
22 n mutations in the neurofibromatosis Type 2 (NF2) gene, coding for a tumour suppressor, Merlin, cause
23 in which germline haploinsufficiency at the NF2 gene confers a greatly increased propensity for tumo
24 tructs of common NF2 missense mutations into NF2 gene-deficient meningioma cell lines revealed that m
25 ouse model generated through excision of the Nf2 gene driven by Cre expression under control of a tis
33 rmed DNA sequence and dosage analysis of the NF2 gene in a panel of 239 schwannoma tumours: 97 neurof
36 n addition to mutational inactivation of the NF2 gene in NF2-associated tumors, mutations and loss of
40 hwann cell lineage, in addition to biallelic Nf2 gene inactivation, we generated the first mouse mode
44 ll sporadic schwannomas, suggesting that the NF2 gene is a critical growth regulator for Schwann cell
45 carcinoma (RCC), homozygous mutation of the NF2 gene is found in approximately 2% of RCC patient sam
49 Merlin, encoded by the Neurofibromatosis 2 (NF2) gene, is a multifunctional tumor suppressor that in
56 related to the expression of genes near the NF2 gene, mutations in which have been identified as the
57 vating mutations of the neurofibromatosis 2 (NF2) gene, NF2, result predominantly in benign neurologi
59 dent YAP1 activity by either the loss of the NF2 gene or YAP1-MAML2 fusion is an oncogenic process pr
62 rt to gain insights into the function of the NF2 gene product, merlin or schwannomin, we performed a
64 ivation of the tumor suppressor gene NF2 The NF2 gene product, Merlin, has no intrinsic catalytic act
66 ter understand the cellular functions of the NF2 gene product, Merlin, recent work has concentrated o
67 of ezrin and moesin, proteins related to the NF2 gene product, merlin, were unchanged in schwannoma c
69 ents showed that silencing of the endogenous NF2 gene results in upregulation of cyclin D1 and S-phas
73 s type 2 (NF2) is caused by mutations in the NF2 gene that encodes a tumor-suppressor protein called
74 UTR mutations, deletion of one allele of the NF2 gene was previously documented by fluorescence in si
75 The coding sequences (exons 1 to 15) of the NF2 gene were polymerase chain reaction (PCR) amplified