ライフサイエンスコーパス: NF2 gene

1 alyzed the 5' flanking sequence of the human NF2 gene.

2 g non-conservative missense mutations in the NF2 gene.

3 hwannomas were analyzed for mutations in the NF2 gene.

4 tumors that carry somatic alterations of the NF2 gene.

5 der resulting from germline mutations in 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 Tumours caused by mutations in the NF2 gene are benign and thus do not respond to classical

11 llelic mutations in the neurofibromatosis 2 (NF2) gene are linked to schwannoma and meningioma tumori

12 Mutations in the neurofibromatosis 2 (NF2) gene are the predominant cause in the development o

13 The role of the NF2 gene as a tumor suppressor has been well established

14 ction in detail, we have disrupted the mouse Nf2 gene by homologous recombination in embryonic stem c

15 ine mutations in the coding sequences of the NF2 gene can cause loss of merlin function, the mechanis

16 In humans, mutations in the NF2 gene cause neurofibromatosis type-2 (NF2), a cancer

17 Mutations in the neurofibromatosis type 2 (NF2) gene cause formation of schwannomas and other tumor

18 y, unlike patients with NF2, no heterozygous NF2-gene changes were seen in normal tissues.

19 annomatosis patients are somatic mosaics for NF2-gene changes.

20 Alterations in the NF2 gene coding for merlin cause all tumours that occur

21 n mutations in the neurofibromatosis Type 2 (NF2) gene, coding for a tumour suppressor, Merlin, cause

22 tructs of common NF2 missense mutations into NF2 gene-deficient meningioma cell lines revealed that m

23 ouse model generated through excision of the Nf2 gene driven by Cre expression under control of a tis

24 The NF2 gene encodes a 70-kDa protein, merlin, which is a me

25 Mutational inactivation of the NF2 gene encoding the protein Merlin is found in most sp

26 composed of neoplastic Schwann cells lacking NF2 gene expression.

27 The NF2 gene has been cloned from chromosome 22q; most ident

28 Merlin, the protein product of the NF2 gene, has been shown to negatively regulate Rac1 sig

29 Merlin, the protein product of the NF2 gene, has been shown to negatively regulate signalin

30 rmed DNA sequence and dosage analysis of the NF2 gene in a panel of 239 schwannoma tumours: 97 neurof

31 othelioma, indicating a broader role for the NF2 gene in human tumorigenesis.

32 e 22 deletions and with abnormalities of the NF2 gene in meningioma.

33 n addition to mutational inactivation of the NF2 gene in NF2-associated tumors, mutations and loss of

34 s whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.

35 NF2 gene inactivation on chromosome 22 has been shown as

36 Biallelic NF2 gene inactivation results in the development of cent

37 hwann cell lineage, in addition to biallelic Nf2 gene inactivation, we generated the first mouse mode

38 tumors lacking genetic evidence of biallelic NF2 gene inactivation.

39 to demonstrate genetic evidence of biallelic NF2 gene inactivation.

40 Merlin encoded by the Nf2 gene is a bona fide tumor suppressor that has been i

41 ll sporadic schwannomas, suggesting that the NF2 gene is a critical growth regulator for Schwann cell

42 carcinoma (RCC), homozygous mutation of the NF2 gene is found in approximately 2% of RCC patient sam

43 Moreover, inactivation of the NF2 gene is observed in nearly all sporadic schwannomas,

44 The neurofibromatosis type 2 (NF2) gene is commonly mutated in schwannomas, Schwann ce

45 demonstrated that merlin, the product of the NF2 gene, is regulated by Rac/PAK signaling.

46 Merlin, encoded by the Neurofibromatosis 2 (NF2) gene, is a multifunctional tumor suppressor that in

47 d cancer disorder caused by mutations at the NF2 gene locus.

48 d cancer disorder caused by mutations at the NF2 gene locus.

49 With the identification of the NF1 and NF2 genes, molecularly targeted therapies are beginning

50 schwannomin or merlin, is commonly lost upon NF2 gene mutation in benign human brain tumors.

51 The coexistence of NF2 gene mutations and LOH at the NF2 locus indicates th

52 related to the expression of genes near the NF2 gene, mutations in which have been identified as the

53 vating mutations of the neurofibromatosis 2 (NF2) gene, NF2, result predominantly in benign neurologi

54 Biallelic inactivation of the NF2 gene occurs in the majority of schwannomas.

55 The neurofibromatosis 2 ( NF2 ) gene product, merlin, is a tumor suppressor protei

56 The NF2 gene product, merlin (or schwannomin), is a member o

57 rt to gain insights into the function of the NF2 gene product, merlin or schwannomin, we performed a

58 The NF2 gene product, merlin, associates with adherens junct

59 The neurofibromatosis type 2 NF2 gene product, merlin, is a tumor suppressor frequent

60 ter understand the cellular functions of the NF2 gene product, Merlin, recent work has concentrated o

61 of ezrin and moesin, proteins related to the NF2 gene product, merlin, were unchanged in schwannoma c

62 unction mutation in the neurofibromatosis 2 (NF2) gene require MLK3.

63 ents showed that silencing of the endogenous NF2 gene results in upregulation of cyclin D1 and S-phas

64 Sequence analysis of the NF2 gene revealed identical nonsense mutation of exon 6

65 We also discuss the NF2 gene status and merlin signaling pathways affected i

66 The product of the NF2 gene, termed merlin or schwannomin, is thought to ac

67 s type 2 (NF2) is caused by mutations in the NF2 gene that encodes a tumor-suppressor protein called

68 UTR mutations, deletion of one allele of the NF2 gene was previously documented by fluorescence in si

69 The coding sequences (exons 1 to 15) of the NF2 gene were polymerase chain reaction (PCR) amplified

70 Mutations in the neurofibromatosis 2 (NF2) gene with the resultant loss of expression of the N