Structure of<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" display="inline"><mml:mrow><mml:msup><mml:mrow /><mml:mrow><mml:mn>12</mml:mn></mml:mrow></mml:msup></mml:mrow><mml:mi mathvariant="normal">Be</mml:mi></mml:math>and<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" display="inline"><mml:mrow><mml:msup><mml:mrow /><mml:mrow><mml:mn>12</mml:mn></mml:mrow></mml:msup></mml:mrow><mml:mi mathvariant="normal">O</mml:mi></mml:math>ground states

Sherr, R.; Fortune, H. T.

doi:10.1103/physrevc.60.064323

Cited by 105 publications

(124 citation statements)

References 13 publications

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“…A potential role for cyclin E-Cdk2 in the G 1 -phase independent of the pocket proteins is supported by the observation that cyclin E is required regardless of pRb status (32), in contrast to cyclin D1, which is only required in pRb-positive cells (24). In addition, the phosphorylation of pRb might be a rate-limiting event in the G 1 -phase that is controlled by cyclin D-Cdk4/6 rather than by cyclin E-Cdk2 activity (36,37). Furthermore, overexpression of cyclin E can overcome G 1 -phase arrest imposed by a phosphorylation-deficient pRb mutant (38).…”

Section: Temporal Separation Of the Requirements For Serum Andmentioning

confidence: 57%

Retinoblastoma Susceptibility Gene Product (pRb) and p107 Functionally Separate the Requirements for Serum and Anchorage in the Cell Cycle G1-phase

Gad

Thullberg

Dannenberg

et al. 2004

Journal of Biological Chemistry

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Growth factors and cell anchorage are both required for cell cycle G 1 -phase progression, but it is unclear whether their function is mediated through the same set of cell cycle components and whether they are both required during the same periods of time. We separately analyzed the requirements of serum and anchorage during G 1 -phase progression and found that human dermal fibroblasts as well as wild type, pRb ؊/؊ , and p107 ؊/؊

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Section: Temporal Separation Of the Requirements For Serum Andmentioning

confidence: 57%

Retinoblastoma Susceptibility Gene Product (pRb) and p107 Functionally Separate the Requirements for Serum and Anchorage in the Cell Cycle G1-phase

Gad

Thullberg

Dannenberg

et al. 2004

Journal of Biological Chemistry

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“…This is a more complicated dependence than it is ordinarily assumed. Typically TES is correlated with the configuration mixing only, to provide predictions about nuclear structure [23][24][25][26][27][28]. (iv) The energy of the 15 F 1/2 + g.s.…”

Section: Discussionmentioning

confidence: 99%

Thomas-Ehrman effect in a three-body model: TheNe16case

Grigorenko

Golubkova²,

Zhukov³

2015

Phys. Rev. C

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The dynamic mechanism of the Thomas-Ehrman shift in three-cluster systems is studied by example of 16 Ne and 16 C isobaric mirror partners. We predict configuration mixings for 0 + and 2 + states in 16 Ne and 16 C. Large isospin symmetry breaking on the level of wave function component weights is demonstrated for these states and discussed as three-body mechanism of Thomas-Ehrman shift. It is shown that the description of the Coulomb displacement energies requires a consistency among three parameters: the 16 Ne decay energy ET , the 15 F ground state energy Er, and the configuration mixing parameters for the 16 Ne/ 16 C 0 + and 2 + states. Basing on this analysis we infer the 15 F 1/2 + ground state energy to be Er = 1.39 − 1.42 MeV.

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“…This locus encodes the two structurally unrelated tumor suppressors p16 INK4a and p19 ARF (13,14). p16 INK4a , an inhibitor to cyclin D-dependent kinase, regulates the retinoblastoma (Rb) protein to block the G 1 -S transition (15). In contrast, p19 ARF can activate p53 by interfering with the p53 antagonist Mdm2 (16)(17)(18)(19), leading to cell-cycle arrest or apoptosis depending on context (12).…”

mentioning

confidence: 99%

Oncogenic ras activates the ARF-p53 pathway to suppress epithelial cell transformation

Lin

Lowe

2001

Proc. Natl. Acad. Sci. U.S.A.

192

132

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Chemically induced skin carcinomas in mice are a paradigm for epithelial neoplasia, where oncogenic ras mutations precede p53 and INK4a͞ARF mutations during the progression toward malignancy. To explore the biological basis for these genetic interactions, we studied cellular responses to oncogenic ras in primary murine keratinocytes. In wild-type keratinocytes, ras induced a cell-cycle arrest that displayed some features of terminal differentiation and was accompanied by increased expression of the p19 ARF , p16 INK4a , and p53 tumor suppressors. In ARF-null keratinocytes, ras was unable to promote cell-cycle arrest, induce differentiation markers, or properly activate p53. Although oncogenic ras produced a substantial increase in both nucleolar and nucleoplasmic p19 ARF , Mdm2 did not relocalize to the nucleolus or to nuclear bodies but remained distributed throughout the nucleoplasm. This result suggests that p19 ARF can activate p53 without overtly affecting Mdm2 subcellular localization. Nevertheless, like p53-null keratinocytes, ARF-null keratinocytes were transformed by oncogenic ras and rapidly formed carcinomas in vivo. Thus, oncogenic ras can activate the ARF-p53 program to suppress epithelial cell transformation. Disruption of this program may be important during skin carcinogenesis and the development of other carcinomas. N ormal cells possess natural defense mechanisms that counter uncontrolled mitogenic signaling, and these safeguards may be eliminated by mutation during multistage carcinogenesis (1). One such safeguard is illustrated by the transforming interactions between oncogenic ras and various tumor suppressor genes in primary fibroblasts. The ras family of proto-oncogenes are small GTPases that, when activated by mutation, constitutively transmit growth promoting signals via the mitogen-activated protein kinase (MAPK) cascade and other pathways (2). Oncogenic ras readily transforms immortal rodent cell lines; however, it is unable to transform primary cells because it induces a premature senescence program involving tumor suppressors such as p53, p16 INK4a , p19 ARF , p15 INK4b , and the promyelocytic leukemia gene product (PML;. Importantly, mutations that disable the arrest program cooperate with ras in transformation (5,(8)(9)(10). Given the high frequency of ras, p53, and INK4a͞ARF mutations in human cancers (11), this safeguard may be an important tumor suppressor mechanism.The INK4a͞ARF locus is a critical sensor of hyperproliferative signals produced by ras and other oncogenes (12). This locus encodes the two structurally unrelated tumor suppressors p16 INK4a and p19 ARF (13,14). p16 INK4a , an inhibitor to cyclin D-dependent kinase, regulates the retinoblastoma (Rb) protein to block the G 1 -S transition (15). In contrast, p19 ARF can activate p53 by interfering with the p53 antagonist Mdm2 (16-19), leading to cell-cycle arrest or apoptosis depending on context (12). Both p16 INK4a and p19 ARF accumulate during the serial passaging of cells in culture (20)(21)(22), and can be indu...

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Structure of12Beand12Oground states

Cited by 105 publications

References 13 publications

Retinoblastoma Susceptibility Gene Product (pRb) and p107 Functionally Separate the Requirements for Serum and Anchorage in the Cell Cycle G1-phase

Retinoblastoma Susceptibility Gene Product (pRb) and p107 Functionally Separate the Requirements for Serum and Anchorage in the Cell Cycle G1-phase

Thomas-Ehrman effect in a three-body model: TheNe16case

Oncogenic ras activates the ARF-p53 pathway to suppress epithelial cell transformation

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