RNA, Small Interfering

Publication Title: 
The EMBO journal

Telomere shortening in normal human cells causes replicative senescence, a p53-dependent growth arrest state, which is thought to represent an innate defence against tumour progression. However, although it has been postulated that critical telomere loss generates a 'DNA damage' signal, the signalling pathway(s) that alerts cells to short dysfunctional telomeres remains only partially defined.

Author(s): 
Gire, VÈronique
Roux, Pierre
Wynford-Thomas, David
Brondello, Jean-Marc
Dulic, Vjekoslav
Publication Title: 
Journal of Cell Science

In mammalian cells, products of the INK4a-ARF locus play major roles in senescence and tumour suppression in different contexts, whereas the adjacent INK4b gene is more generally associated with transforming growth factor beta (TGF-beta)-mediated growth arrest. As the chicken genome does not encode an equivalent of INK4a, we asked whether INK4b and/or ARF contribute to replicative senescence in chicken cells.

Author(s): 
Kim, Soo-Hyun
Rowe, Janice
Fujii, Hideta
Jones, Rebecca
Schmierer, Bernhard
Kong, Byung-Whi
Kuchler, Karl
Foster, Douglas
Ish-Horowicz, David
Peters, Gordon
Publication Title: 
Nature Cell Biology

The nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sir2 (silent information regulator 2) regulates gene silencing in yeast and promotes lifespan extension during caloric restriction. The mammalian homologue of Sir2 (SirT1) regulates p53, NF-kappaB and Forkhead transcription factors, and is implicated in stress response. This report shows that the cell-cycle and apoptosis regulator E2F1 induces SirT1 expression at the transcriptional level. Furthermore, SirT1 binds to E2F1 and inhibits E2F1 activities, forming a negative feedback loop.

Author(s): 
Wang, Chuangui
Chen, Lihong
Hou, Xinghua
Li, Zhenyu
Kabra, Neha
Ma, Yihong
Nemoto, Shino
Finkel, Toren
Gu, Wei
Cress, W. Douglas
Chen, Jiandong
Publication Title: 
International Journal of Hematology

FKHRL1 is one of the human homologues of DAF-16, which is concerned with longevity in Caenorhabditis elegans. Previously, we demonstrated that FKHRL1 functions downstream of Akt in erythropoietin (EPO) signaling and that it is directly phosphorylated by activated Akt. Because phosphorylated FKHRL1 loses its transcriptional activity and translocates into the cytoplasm, FKHRL1 appears to be nonfunctional in the presence of EPO.

Author(s): 
Uchida, Mie
Kirito, Keita
Endo, Hitoshi
Ozawa, Keiya
Komatsu, Norio
Publication Title: 
Aging

Excessive production of reactive oxygen species (ROS) contributes to progression of atherosclerosis, at least in part by causing endothelial dysfunction and inflammatory activation. The class III histone deacetylase SIRT1 has been implicated in extension of lifespan. In the vasculature,SIRT1 gain-of-function using SIRT1 overexpression or activation has been shown to improve endothelial function in mice and rats via stimulation of endothelial nitric oxide (NO) synthase (eNOS). However, the effects of SIRT1 loss-of-function on the endothelium in atherosclerosis remain to be characterized.

Author(s): 
Stein, Sokrates
Sch‰fer, Nicola
Breitenstein, Alexander
Besler, Christian
Winnik, Stephan
Lohmann, Christine
Heinrich, Kathrin
Brokopp, Chad E.
Handschin, Christoph
Landmesser, Ulf
Tanner, Felix C.
L¸scher, Thomas F.
Matter, Christian M.
Publication Title: 
Aging Cell

Aging and age-related diseases can be viewed as the result of the lifelong accumulation of stress insults. The identification of mutant strains and genes that are responsive to stress and can alter longevity profiles provides new therapeutic targets for age-related diseases. Here we reported that a Drosophila strain with reduced expression of ribose-5-phosphate isomerase (rpi), EP2456, exhibits increased resistance to oxidative stress and enhanced lifespan. In addition, the strain also displays higher levels of NADPH.

Author(s): 
Wang, Ching-Tzu
Chen, Yi-Chun
Wang, Yi-Yun
Huang, Ming-Hao
Yen, Tzu-Li
Li, Hsun
Liang, Cyong-Jhih
Sang, Tzu-Kang
Ciou, Shih-Ci
Yuh, Chiou-Hwa
Wang, Chao-Yung
Brummel, Theodore J.
Wang, Horng-Dar
Publication Title: 
Journal of Cellular Biochemistry

Homo sapiens longevity assurance homologue 2 of yeast LAG1 (LASS2), also known as tumor metastasis suppressor gene 1 (TMSG1), is a newly found tumor metastasis suppressor gene in 1999. Preliminary studies showed that it not only suppressed tumor growth but also closely related to tumor metastasis, however, its molecular mechanisms is still unclear.

Author(s): 
Xu, Xiaoyan
You, Jiangfeng
Pei, Fei
Publication Title: 
Molecular and Cellular Biology

SIRT3 is a member of the Sir2 family of NAD(+)-dependent protein deacetylases that promotes longevity in many organisms. The processed short form of SIRT3 is a well-established mitochondrial protein whose deacetylase activity regulates various metabolic processes. However, the presence of full-length (FL) SIRT3 in the nucleus and its functional importance remain controversial. Our previous studies demonstrated that nuclear FL SIRT3 functions as a histone deacetylase and is transcriptionally repressive when artificially recruited to a reporter gene.

Author(s): 
Iwahara, Toshinori
Bonasio, Roberto
Narendra, Varun
Reinberg, Danny
Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

Tumors use a wide array of immunosuppressive strategies, such as reducing the longevity and survival of dendritic cells (DCs), to diminish immune responses and limit the effect of immunotherapy. In this study, we found that tumors upregulate the expression of multiple microRNAs (miRNAs), such as miR-16-1, miR-22, miR-155, and miR-503. These tumor-associated miRNAs influenced the survival and longevity of DCs by affecting the expression of multiple molecules that are associated with apoptotic signaling pathways.

Author(s): 
Min, Siping
Liang, Xue
Zhang, Miaomiao
Zhang, Yuan
Mei, Shiyue
Liu, Jinzhe
Liu, Jingyi
Su, Xiaomin
Cao, Shuisong
Zhong, Xueqing
Li, Yueming
Sun, Jiatan
Liu, Qiaofei
Jiang, Xingran
Che, Yongzhe
Yang, Rongcun
Publication Title: 
Biochemical and Biophysical Research Communications

Cellular senescence is a tumor suppression mechanism. We previously reported that CKII downregulation induces senescence in human lung fibroblast IMR-90 and colon cancer HCT116 cells. In this study, potential longevity drugs, including rapamycin, vitamin C, and vitamin E, blocked CKII downregulation-mediated senescence through reduction of reactive oxygen species (ROS) production in HCT116 cells.

Author(s): 
Park, Ji Hye
Kim, Jin Joo
Bae, Young-Seuk

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