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Jane R. Noble

Researcher at Children's Medical Research Institute

Publications -  18
Citations -  1787

Jane R. Noble is an academic researcher from Children's Medical Research Institute. The author has contributed to research in topics: Telomerase & Telomere. The author has an hindex of 14, co-authored 17 publications receiving 1675 citations. Previous affiliations of Jane R. Noble include University of Sydney.

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Journal Article

Telomerase-negative Immortalized Human Cells Contain a Novel Type of Promyelocytic Leukemia (PML) Body

TL;DR: It is reported here that ALT cells contain a novel promyelocytic leukemia (PML) body (ALT-associated PML body, APB), which are large donut-shaped nuclear structures containing PML protein, telomeric DNA, and the telomere binding proteins human telomerre repeat binding factors 1 and 2.
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A novel human cDNA highly homologous to the fish hormone stanniocalcin

TL;DR: It is concluded that a human protein similar to the fish hormone is expressed in multiple tissues rather than by a specialized endocrine organ.
Journal Article

Loss of p16INK4 expression by methylation is associated with lifespan extension of human mammary epithelial cells

TL;DR: The extended period of growth observed in postselection HMECs is associated with hypermethylation of the p16ink4 CpG island and loss of p16INK4 expression, indicating that postselectionHMECs have sustained an epigenetic alteration.
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ATRX represses alternative lengthening of telomeres

TL;DR: It is shown here that knockout or knockdown of ATRX in mortal cells or immortal telomerase-positive cells is insufficient to activate ALT, and the first direct, functional evidence that ATRx represses ALT is provided, which indicates that loss of ATrX function cooperates with one or more as-yet unidentified genetic or epigenetic alterations to activated ALT.
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Comparison of human mammary epithelial cells immortalized by simian virus 40 T-Antigen or by the telomerase catalytic subunit.

TL;DR: Although SV40-immortalized cells are useful for studies of carcinogenesis, hTERT-imm Mortalized cells retain more properties of normal cells.