ライフサイエンスコーパス: Rb gene

1 eletion of part or all of the ribose operon (rbs genes).

2 artificial chromosome containing most of the Rb gene.

3 elegans mutants lacking a functional lin-35 RB gene.

4 both specific and overlapping functions with RB gene.

5 omas invariably have somatic mutation in the RB gene.

6 to assess for loss of heterozygosity of the rb gene.

7 old in patients who inherit mutations in the RB gene.

8 ated RB phosphorylation, and mutation of the RB gene.

9 of wild-type p16(INK4A) on expression of the RB gene.

10 ting that each of these tumors had an intact RB gene.

11 ells that have one deleted and one truncated RB gene.

12 nduced transcriptional downregulation of the RB gene.

13 t p130 is related to, yet distinct from, the RB gene.

14 h inactivation of the ubiquitously expressed Rb gene.

15 act on their invasiveness as compared to the RB gene.

16 is known about developmentally regulated E2F/RB genes.

17 a targeted disruption of the retinoblastoma (Rb) gene.

18 of the six GBMs without either CDKN2/p16 or RB gene abnormalities, one case had CDK4 gene amplificat

19 Indeed, genetic ablation of the p27(Kip1) or Rb genes accentuated Tag-induced tumorigenesis, with los

20 16 alterations, none had allelic loss of the RB gene and all expressed pRb, suggesting that each of t

21 pical cells contain no wild-type copy of the Rb gene and synchronously form early atypical proliferat

22 g a region of approximately 3 cM between the RB gene and the D13S31 locus.

23 lidate our approach by targeting the p53 and Rb genes and establishing cell line and in vivo cancer m

24 ccess is owed to deciphering the role of the Rb gene, and the benefits of targeted therapies, such as

25 (Rb)-knockout mice; however, defects in the Rb gene are not common in human pituitary tumors.

26 Mice lacking the Rb gene are not viable and die in utero at approximately

27 Mice with a single copy of the Rb gene are shown to develop a syndrome of multiple neur

28 CDK4 amplification, and allelic loss of the RB gene, as well as for expression of p16 and pRb protei

29 1 suppression is independent of the p53 and Rb genes, but requires an intact TGF-beta type II recept

30 ated a new conditional mouse model, with the Rb gene deleted primarily in the inner ear.

31 the selective growth advantage conferred by Rb gene deletion during tumorigenesis may be explained i

32 recognizes the protein product of the medaka Rb gene, detecting a 105 kDa protein in all tissues exam

33 Finally, deletion of RB genes enhanced ferroptosis.

34 Importantly, the Rb gene expression patterns can identify murine tumors t

35 Specific analyses of an RB gene expression signature in 60 human patients indica

36 scriptional activation and repression by the Rb gene family has been extensively investigated: pRb, p

37 E2f activity, following inactivation of the Rb gene family in a mouse model of liver cancer, initial

38 ilar tumors occur in mice only when multiple Rb gene family members are absent.

39 exit following DNA damage induction, and how Rb gene family's interaction with chromatin remodeling f

40 essors of the retinoblastoma susceptibility (Rb) gene family, we have previously shown that activatio

41 essors of the retinoblastoma susceptibility (Rb) gene family.

42 ogy and with defined genetic profiles of the Rb gene, from these sites.

43 etinoblastoma protein (pRB) and mutations of RB gene have been reported in up to 70% of MM patients a

44 To date, RB genes have been isolated only from metazoans.

45 itu hybridization showed allelic loss of the rb gene in 10 (40%) of 25 tumors analyzed and was signif

46 er we analysed the protein expression of the RB gene in cell lines obtained from 83 patients with sma

47 We conditionally disrupted the Rb gene in mouse germ cells in vivo and discovered unant

48 population, by conditionally disrupting the RB gene in neurogenin3 (Ngn3)-expressing cells in both p

49 ineage-specific character of retinoblastoma (Rb) gene inactivation during tumor formation, the earlie

50 In cells with an intact rb gene, inactivation of pRb by HPV E7 abrogates the gro

51 Z/EG reporter, as well as the floxed p53 and Rb genes, into irradiated p53loxP/loxPRbloxP/loxP mice,

52 The retinoblastoma (RB) gene is one of the most extensively studied tumour-s

53 arental allele of the murine retinoblastoma (Rb) gene is sufficient for spontaneous melanotroph carci

54 genicity in vivo and why inactivation of the RB gene leads to tumorigenesis.

55 oblastoma is a pediatric cancer initiated by RB gene mutations in the developing retina.

56 Retinoblastoma is initiated by RB gene mutations, but the subsequent cooperating mutati

57 lelic loss of chromosome 13q at the RB gene, RB gene mutations, or loss of pRb expression was noted i

58 ed lung cancer risk in persons with germline RB gene mutations.

59 Fibroblasts prepared from retinoblastoma (Rb) gene-negative mouse embryos exhibit a shorter G1 pha

60 ctivate the anthocyanin pathway, whereas the Rb gene, of undetermined function, maps to chromosome 1.

61 B is directly inactivated by mutation in the RB gene or functionally inhibited by abnormal activation

62 pression of dominant-negative mutants of the Rb gene, or the transcription factor E2F-1, which is a d

63 only provides an opportunity to analyze the Rb gene pathway in the development and progression of pr

64 Deletion of the Rb gene predisposes prostatic epithelium to hyperplasia

65 The RB gene product accomplishes this by diverse mechanisms

66 ) gene is transcriptionally repressed by the RB gene product, pRB.

67 o bind to and inactivate the retinoblastoma (Rb) gene product family of proteins.

68 The retinoblastoma (RB) gene product has been shown to restrict cell prolife

69 The retinoblastoma (Rb) gene product is a prototypic tumor suppressor.

70 n the phosphorylation of the retinoblastoma (RB) gene product.

71 interacting with the p53 and retinoblastoma (Rb) gene products.

72 The cloned RB gene provides a new resource for developing late blig

73 Allelic loss of chromosome 13q at the RB gene, RB gene mutations, or loss of pRb expression wa

74 d in cervical cancer cell lines in which the RB gene, Rb, is not functional, either as a consequence

75 nding mature melanotrophs with the wild-type Rb gene, Rb-negative cells in EAP continue to proliferat

76 These results support the concept that the Rb gene regulatory network (GRN) subcircuit that regulat

77 In contrast, MEFs from mice lacking Rb genes showed approximately a 70% reduced capacity to

78 tastasis suppressor, SSeCKS/Gravin/AKAP12 or Rb, genes that are downregulated or deleted in human pro

79 harboring loxP sites flanking exon 3 of the Rb gene to delineate the action of RB in the chemotherap

80 tin promoter directs expression of the human RB gene to melanotrophs (TgPOMC-RB).

81 Intratumoral RB gene transfer decreased tumor cell proliferation, ree

82 p27 deletion, like deletion of the Rb gene, uniquely caused neoplastic growth of the pituit

83 inations of normal and mutated p16, p53, and Rb genes via a recombinant adenovirus to determine the e

84 of methylation of p15(INK4B), p16(INK4A) and RB gene was 4%, 7%, and 4%, respectively.

85 In the current studies, the RB gene was selectively deleted in the respiratory epith

86 The retinoblastoma (Rb) gene was the first tumour suppressor identified.

87 B), p16(INK4A), p14(ARF) and retinoblastoma (RB) genes was studied using methylation specific polymer