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Li, He; Liu, Junping

doi:10.1023/a:1015232102470

Cited by 17 publications

(4 citation statements)

References 63 publications

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“…Regarding the neutral N n systems, the only metastable N 4 species with lifetimes exceeding 1 ls was merely an (N 2 ) 2 cluster [8]. Wealth of calculations [9][10][11][12][13][14][15] suggested that N 6 allotropes as well as odd-number nitrogen clusters N n (n = 7, 9, 11) prefer acyclic forms. All of them have small energy barrier and are easy to decompose.…”

Section: Introductionmentioning

confidence: 99%

DFT studies on the structures and stabilities of N5 +-containing salts

Wang

Zhang

et al. 2011

Struct Chem

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Density functional theory (DFT) methods have been applied to study the properties of series of N 5 ? salts. The thermal stabilities of the crystals are evaluated based on the reaction enthalpy (DH) and free energy change (DG) of the salts when they dissociate into neutral products. The energy outputs of salts in explosion indicate that all N 5 ? salts yield large energy except for N 5 SbF 6 and N 5 Sb 2 F 11 . Considering the released energy and thermal stability, (N 5 ) 2 SnF 6 , N 5 PF 6 , N 5 BF 4 , and N 5 SO 3 F may be potential candidates of very energetic explosives.

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Section: Introductionmentioning

confidence: 99%

DFT studies on the structures and stabilities of N5 +-containing salts

Wang

Zhang

et al. 2011

Struct Chem

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“…SIRT1 promotes cell survival by inhibiting apoptosis or cellular senescence induced by stresses, including DNA damage and oxidative stress (1)(2)(3)(4)(5)(6)). An increasing number of proteins have been identified as substrates of SIRT1, including p53 (7-10), forkhead (FOXO) transcription factors (11)(12)(13)(14)(15)(16), repair protein Ku70 (11,17,18), p300 (19), Rb (19,20), and p73 (19,21) just to name a few. Interestingly, SIRT1 has been shown to negatively regulate proliferative signaling via regulating (i) p53 function (7-10, 19, 22), (ii) FOXO pathway (1,(11)(12)(13)23), and (iii) MAPK signaling (24).…”

mentioning

confidence: 99%

Role of Sirtuin Histone Deacetylase SIRT1 in Prostate Cancer

Jung-Hynes

Nihal

Zhong

et al. 2009

Journal of Biological Chemistry

152

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Prostate cancer (PCa) is a major age-related malignancy, and according to estimates from the American Cancer Society, a man's chance of developing this cancer significantly increases with increasing age, from 1 in 10,149 by age 39 to 1 in 38 by age 59 to 1 in 7 by age 70. Therefore, it is important to identify the causal connection between mechanisms of aging and PCa. Employing in vitro and in vivo approaches, in this study, we tested the hypothesis that SIRT1, which belongs to the Sir2 (silent information regulator 2) family of sirtuin class III histone deacetylases, is overexpressed in PCa, and its inhibition will have antiproliferative effects in human PCa cells. Our data demonstrated that SIRT1 was significantly overexpressed in human PCa cells (DU145, LNCaP, 22R1, and PC3) compared with normal prostate epithelial cells (PrEC) at protein, mRNA, and enzymatic activity levels. SIRT1 was also found to be overexpressed in human PCa tissues compared with adjacent normal prostate tissue. Interestingly, our data demonstrated that SIRT1 inhibition via nicotinamide and sirtinol (at the activity level) as well as via short hairpin RNA-mediated RNA interference (at the genetic level) resulted in a significant inhibition in the growth and viability of human PCa cells while having no effect on normal prostate epithelial cells. Further, we found that inhibition of SIRT1 caused an increase in FOXO1 acetylation and transcriptional activation in PCa cells. Our data suggested that SIRT1, via inhibiting FOXO1 activation, could contribute to the development of PCa. We suggest that SIRT1 could serve as a target toward developing novel strategies for PCa management. Prostate cancer (PCa)2 is a major age-related malignancy and is rarely seen in men younger than 40 years; the incidence rises rapidly with each decade thereafter. Because the present life expectancy has significantly improved and Americans are living longer, it is believed that more cases of PCa will be diagnosed in the future. According to one prediction, by year 2010, the number of annual PCa cases will skyrocket to 330,000. Thus, it will be immensely useful to better understand the molecular mechanism and connection between aging and PCa.Unraveling determinants such as genes and gene-products involved in aging and that have a connection with PCa could be exploited in designing novel targets and approaches for the management of this age-related neoplasm. We hypothesized that sirtuins (Sirt proteins), which are nicotinamide adenine dinucleotide (NAD ϩ

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“…The transcriptional regulation of TERT is predominantly implicated in the regulation of telomerase activity in cells. 50 The upstream region of the translational start site of TERT contains several types of transcriptional regulatory elements, such as GC box and E box, indicating that various transcription factors, including Sp1, Sp3, and Myc, can activate TERT expression by binding to the TERT promoter. 51 In a previous report, we hypothesized that Zfp637 may directly regulate mTERT by interacting with the core promoter region or indirectly promote mTERT transcription by regulating or synergistically cooperating with Sp1 and Sp3.…”

Section: Discussionmentioning

confidence: 99%

Zinc finger protein 637 protects cells against oxidative stress-induced premature senescence by mTERT-mediated telomerase activity and telomere maintenance

Gao

et al. 2014

Cell Death Dis

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Oxidative stress is believed to be an important inducer of cellular senescence and aging. Zinc finger protein 637 (Zfp637), which belongs to the Krüppel-like protein family, has been hypothesized to play a role in oxidative stress. Nevertheless, the precise function of Zfp637 has seldom been reported, and it remains unclear whether Zfp637 is involved in oxidative stress-induced premature senescence. In this study, we show that the endogenous expression levels of Zfp637 and mouse telomerase reverse transcriptase (mTERT) are downregulated during oxidative stress-induced premature senescence and in senescent tissues from naturally aged mice. The overexpression of Zfp637 markedly increases mTERT expression and telomerase activity, maintains telomere length, and inhibits both H2O2 and D-galactose-induced senescence accompanied by a reduction in the production of reactive oxygen species (ROS). In contrast, the knockdown of Zfp637 significantly aggravates cellular senescence by downregulating mTERT and telomerase activity, accelerating telomere shortening, and increasing ROS accumulation. In addition, the protective effect of Zfp637 against premature senescence is abrogated in the absence of mTERT. We further confirm that Zfp637 binds to and transactivates the mTERT promoter (−535/−502) specifically. As a result, the mTERT-mediated telomerase activity and telomere maintenance are responsible for the protective effect of Zfp637 against oxidative stress-induced senescence. We therefore propose that Zfp637 prevents oxidative stress-induced premature senescence in an mTERT-dependent manner, and these results provide a new foundation for the investigation of cellular senescence and aging.

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Cited by 17 publications

References 63 publications

DFT studies on the structures and stabilities of N5 +-containing salts

DFT studies on the structures and stabilities of N5 +-containing salts

Role of Sirtuin Histone Deacetylase SIRT1 in Prostate Cancer

Zinc finger protein 637 protects cells against oxidative stress-induced premature senescence by mTERT-mediated telomerase activity and telomere maintenance

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