Volume 3, Issue 3

Eating less suppresses microRNA assassins in the brain

Emmette Hutchison, Mark P. Mattson,

https://doi.org/10.18632/aging.100287 pp 179—180

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Hutchison E, Mattson MP, . Eating less suppresses microRNA assassins in the brain. . 3:179-180. https://doi.org/10.18632/aging.100287

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Spontaneous inactivating p53 mutations and the “selfish cell”

Steven M. Sorscher, Aubrey E. Hill, Roger Belizaire, Eric J. Sorscher,

https://doi.org/10.18632/aging.100294 pp 181

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Sorscher SM, Hill AE, Belizaire R, Sorscher EJ, . Spontaneous inactivating p53 mutations and the “selfish cell”. . 3:181-181. https://doi.org/10.18632/aging.100294

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MicroRNA - a contributor to age-associated neural stem cell dysfunction?

Muhammad Amir Khan, Dieter Chichung Lie,

https://doi.org/10.18632/aging.100297 pp 182—183

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Phylogenetic ubiquity of the effects of altered ubiquinone biosynthesis on survival

Siegfried Hekimi, Bryan Hughes,

https://doi.org/10.18632/aging.100310 pp 184—185

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The Smc5/6 complex and the difficulties cutting the ties of twin sisters

Jean-François Noël, Raymund J. Wellinger,

https://doi.org/10.18632/aging.100295 pp 186—188

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Potential of mTOR inhibitors for the treatment of subependymal giant cell astrocytomas in tuberous sclerosis complex

Philippe Major,

https://doi.org/10.18632/aging.100298 pp 189—191

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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

Linda S. Steelman, William H. Chappell, Stephen L. Abrams, C. Ruth Kempf, Jacquelyn Long, Piotr Laidler, Sanja Mijatovic, Danijela Maksimovic-Ivanic, Franca Stivala, Maria C. Mazzarino, Marco Donia, Paolo Fagone, Graziella Malaponte, Ferdinando Nicoletti, Massimo Libra, Michele Milella, Agostino Tafuri, Antonio Bonati, Jörg Bäsecke, Lucio Cocco, Camilla Evangelisti, Alberto M. Martelli, Giuseppe Montalto, Melchiorre Cervello, James A. McCubrey,

https://doi.org/10.18632/aging.100296 pp 192—222

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Steelman LS, Chappell WH, Abrams SL, Kempf CR, Long J, Laidler P, Mijatovic S, Maksimovic-Ivanic D, Stivala F, Mazzarino MC, Donia M, Fagone P, Malaponte G, et al, . Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging. . 3:192-222. https://doi.org/10.18632/aging.100296

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Provider: 
                TY  - JOUR
                AU  - Steelman, Linda S. 
                AU  - Chappell, William H. 
                AU  - Abrams, Stephen L. 
                AU  - Kempf, C. Ruth 
                AU  - Long, Jacquelyn 
                AU  - Laidler, Piotr 
                AU  - Mijatovic, Sanja 
                AU  - Maksimovic-Ivanic, Danijela 
                AU  - Stivala, Franca 
                AU  - Mazzarino, Maria C. 
                AU  - Donia, Marco 
                AU  - Fagone, Paolo 
                AU  - Malaponte, Graziella 
                AU  - Nicoletti, Ferdinando 
                AU  - Libra, Massimo 
                AU  - Milella, Michele 
                AU  - Tafuri, Agostino 
                AU  - Bonati, Antonio 
                AU  - Bäsecke, Jörg 
                AU  - Cocco, Lucio 
                AU  - Evangelisti, Camilla 
                AU  - Martelli, Alberto M. 
                AU  - Montalto, Giuseppe 
                AU  - Cervello, Melchiorre 
                AU  - McCubrey, James A. 
                TI  - Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100296
                DO  - 10.18632/aging.100296
                SP  - 192
                EP  - 222
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Steelman, Linda S. 
                AU  - Chappell, William H. 
                AU  - Abrams, Stephen L. 
                AU  - Kempf, C. Ruth 
                AU  - Long, Jacquelyn 
                AU  - Laidler, Piotr 
                AU  - Mijatovic, Sanja 
                AU  - Maksimovic-Ivanic, Danijela 
                AU  - Stivala, Franca 
                AU  - Mazzarino, Maria C. 
                AU  - Donia, Marco 
                AU  - Fagone, Paolo 
                AU  - Malaponte, Graziella 
                AU  - Nicoletti, Ferdinando 
                AU  - Libra, Massimo 
                AU  - Milella, Michele 
                AU  - Tafuri, Agostino 
                AU  - Bonati, Antonio 
                AU  - Bäsecke, Jörg 
                AU  - Cocco, Lucio 
                AU  - Evangelisti, Camilla 
                AU  - Martelli, Alberto M. 
                AU  - Montalto, Giuseppe 
                AU  - Cervello, Melchiorre 
                AU  - McCubrey, James A. 
                TI  - Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100296
                DO  - 10.18632/aging.100296
                SP  - 192
                EP  - 222
                PY  - 
                AB  - Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described roles of these pathways in cancer stem cells, cellular senescence and aging will be evaluated. Controlling the expression of these pathways could ameliorate human health.
                ER  -

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Gain of survival signaling by down-regulation of three key miRNAs in brain of calorie-restricted mice

Amit Khanna, Senthilkumar Muthusamy, Ruqiang Liang, Harshini Sarojini, Eugenia Wang,

https://doi.org/10.18632/aging.100276 pp 223—236

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Khanna A, Muthusamy S, Liang R, Sarojini H, Wang E, . Gain of survival signaling by down-regulation of three key miRNAs in brain of calorie-restricted mice. . 3:223-236. https://doi.org/10.18632/aging.100276

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                TY  - JOUR
                AU  - Khanna, Amit 
                AU  - Muthusamy, Senthilkumar 
                AU  - Liang, Ruqiang 
                AU  - Sarojini, Harshini 
                AU  - Wang, Eugenia 
                TI  - Gain of survival signaling by down-regulation of three key miRNAs in brain of calorie-restricted mice
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100276
                DO  - 10.18632/aging.100276
                SP  - 223
                EP  - 236
                PY  - 
                AB  - The decline in cognitive robustness with aging can be attributed to complex genetic pathways involving many cellular dysfunctions, cumulative over time, precipitating in frailty and loss of wellness in the elderly brain. The size and health of the neuronal cell population determines cognitive robustness in mammals. A transgenic mouse model over-expressing Bcl-2 has been shown to rescue neurons from naturally occurring cell death (NOCD). Here we show that in the brain of calorie-restricted (CR) mice, there is an age-dependent decreased expression of microRNAs mmu-miR-181a-1*, mmu-miR-30e and mmu-miR-34a, with a corresponding gain in Bcl-2 expression, and decreases in pro-apoptosis genes such as Bax and cleavage of Caspases. Functional characterization shows that these miRNAs repress Bcl-2 expression by the 3'UTR reporter assays, accompanied by loss of this gene's endogenous expression, and a gain in pro-apoptosome-specific proteins. Over-expression of these miRNAs increases the rate of apoptosis, accompanied by a decline in Bcl-2 expression in miRNA-transfected mouse and human cell lines. We report here that down-regulation of miR-34a, -30e, and -181a permits their shared target gene expression (Bcl-2) to remain at a high level without post-transcriptional repression, accompanied by concomitant low levels of Bax expression and Caspase cleaving; this chain event may be a part of the underlying mechanism contributing to the gain in neuronal survival in long-lived CR-fed mice.
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Ubiquitin over-expression phenotypes and ubiquitin gene molecular misreading during aging in Drosophila melanogaster

Nicholas Hoe, Chung M. Huang, Gary Landis, Marian Verhage, Daniel Ford, Junsheng Yang, Fred W. van Leeuwen, John Tower,

https://doi.org/10.18632/aging.100278 pp 237—261

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Hoe N, Huang CM, Landis G, Verhage M, Ford D, Yang J, van Leeuwen FW, Tower J, . Ubiquitin over-expression phenotypes and ubiquitin gene molecular misreading during aging in Drosophila melanogaster. . 3:237-261. https://doi.org/10.18632/aging.100278

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                TY  - JOUR
                AU  - Hoe, Nicholas 
                AU  - Huang, Chung M. 
                AU  - Landis, Gary 
                AU  - Verhage, Marian 
                AU  - Ford, Daniel 
                AU  - Yang, Junsheng 
                AU  - van Leeuwen, Fred W. 
                AU  - Tower, John 
                TI  - Ubiquitin over-expression phenotypes and ubiquitin gene molecular misreading during aging in Drosophila melanogaster
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100278
                DO  - 10.18632/aging.100278
                SP  - 237
                EP  - 261
                PY  - 
                AB  - Molecular Misreading (MM) is the inaccurate conversion of genomic information into aberrant proteins. For example, when RNA polymerase II transcribes a GAGAG motif it synthesizes at low frequency RNA with a two-base deletion. If the deletion occurs in a coding region, translation will result in production of misframed proteins. During mammalian aging, misframed versions of human amyloid precursor protein (hApp) and ubiquitin (hUbb) accumulate in the aggregates characteristic of neurodegenerative diseases, suggesting dysfunctional degradation or clearance. Here cDNA clones encoding wild-type hUbb and the frame-shifted version hUbb+1 were expressed in transgenic Drosophila using the doxycycline-regulated system. Misframed proteins were abundantly produced, both from the transgenes and from endogenous Drosophila ubiquitin-encoding genes, and their abundance increased during aging in whole-fly extracts. Over-expression of wild-type hUbb, but not hUbb+1, was toxic during fly development. In contrast, when over-expressed specifically in adult flies, hUbb+1 caused small decreases in life span, whereas hUbb was associated with small increases, preferentially in males. The data suggest that MM occurs in Drosophila and that the resultant misframed proteins accumulate with age. MM of the ubiquitin gene can produce alternative ubiquitin gene products with different and sometimes opposing phenotypic effects.
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RasGrf1 deficiency delays aging in mice

Consuelo Borrás, Daniel Monleón, Raul López-Grueso, Juan Gambini, Leonardo Orlando, Federico V. Pallardó, Eugenio Santos, José Viña, Jaime Font de Mora,

https://doi.org/10.18632/aging.100279 pp 262—276

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Borrás C, Monleón D, López-Grueso R, Gambini J, Orlando L, Pallardó FV, Santos E, Viña J, Font de Mora J, . RasGrf1 deficiency delays aging in mice. . 3:262-276. https://doi.org/10.18632/aging.100279

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Provider: 
 TY - JOUR
 AU - Borrás, Consuelo 
 AU - Monleón, Daniel 
 AU - López-Grueso, Raul 
 AU - Gambini, Juan 
 AU - Orlando, Leonardo 
 AU - Pallardó, Federico V. 
 AU - Santos, Eugenio 
 AU - Viña, José 
 AU - Font de Mora, Jaime 
 TI - RasGrf1 deficiency delays aging in mice
 JO - 
 JA - 
 VL - 3
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100279
 DO - 10.18632/aging.100279
 SP - 262
 EP - 276
 PY - 
 AB - RasGRF1 is a Ras-guanine nucleotide exchange factor implicated in a variety of physiological processes including learning and memory and glucose homeostasis. To determine the role of RASGRF1 in aging, lifespan and metabolic parameters were analyzed in aged RasGrf1−/− mice. We observed that mice deficient for RasGrf1−/− display an increase in average and most importantly, in maximal lifespan (20% higher than controls). This was not due to the role of Ras in cancer because tumor-free survival was also enhanced in these animals. Aged RasGrf1−/− displayed better motor coordination than control mice. Protection against oxidative stress was similarly preserved in old RasGrf1−/−. IGF-I levels were lower in RasGrf1−/− than in controls. Furthermore, SIRT1 expression was increased in RasGrf1−/− animals. Consistent with this, the blood metabolomic profiles of RasGrf1-deficient mice resembled those observed in calorie-restricted animals. In addition, cardiac glucose consumption as determined PET was not altered by aging in the mutant model, indicating that RasGrf1-deficienct mice display delayed aging. Our observations link Ras signaling to lifespan and suggest that RasGrf1 is an evolutionary conserved gene which could be targeted for the development of therapies to delay age-related processes.
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The Werner syndrome helicase protein is required for cell proliferation, immortalization, and tumorigenesis in Scaffold Attachment Factor B1 deficient mice

Sophie Lachapelle, Steffi Oesterreich, Michel Lebel,

https://doi.org/10.18632/aging.100300 pp 277—290

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Lachapelle S, Oesterreich S, Lebel M, . The Werner syndrome helicase protein is required for cell proliferation, immortalization, and tumorigenesis in Scaffold Attachment Factor B1 deficient mice. . 3:277-290. https://doi.org/10.18632/aging.100300

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                TY  - JOUR
                AU  - Lachapelle, Sophie 
                AU  - Oesterreich, Steffi 
                AU  - Lebel, Michel 
                TI  - The Werner syndrome helicase protein is required for cell proliferation, immortalization, and tumorigenesis in Scaffold Attachment Factor B1 deficient mice
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100300
                DO  - 10.18632/aging.100300
                SP  - 277
                EP  - 290
                PY  - 
                AB  - Werner syndrome (WS) is a rare disorder characterized by the premature onset of several pathologies associated with aging. The gene responsible for WS codes for a RecQ-type DNA helicase and is believed to be involved in different aspects of DNA repair, replication, and transcription. We recently identified the Scaffold attachment factor B1 (SAFB1) as a potential interactants in human cells. SAFB1 is a multifunctional protein that binds both nucleic acids and is involved in the attachment of chromatin to the nuclear matrix, transcription, and stress response. Mice lacking SAFB1 exhibit developmental abnormalities in their lungs, high incidence of perinatal lethality, and adults develop different types of tumors. Mouse embryonic fibroblasts from Safb1-null animals are immortalized in culture. In this study, mice with a mutation in the helicase domain of the Wrn gene were crossed to Safb1-null mice. Double homozygous mutant mice exhibited increased apoptosis, a lower cell proliferation rate in their lungs and a higher incidence of perinatal death compared to Safb1-null mice. Few double homozygous mutants survived weaning and died before the age of six months. Finally, mouse embryonic fibroblasts lacking a functional Wrn helicase inhibited the immortalization of Safb1-null cells. These results indicate that an intact Wrn protein is required for immortalization and tumorigenesis in Safb1-null mice.
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Lifespan extension and paraquat resistance in a ubiquinone-deficient Escherichia coli mutant depend on transcription factors ArcA and TdcA

Stavros Gonidakis, Steven E. Finkel, Valter D. Longo,

https://doi.org/10.18632/aging.100301 pp 291—303

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Gonidakis S, Finkel SE, Longo VD, . Lifespan extension and paraquat resistance in a ubiquinone-deficient Escherichia coli mutant depend on transcription factors ArcA and TdcA. . 3:291-303. https://doi.org/10.18632/aging.100301

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 TY - JOUR
 AU - Gonidakis, Stavros 
 AU - Finkel, Steven E. 
 AU - Longo, Valter D. 
 TI - Lifespan extension and paraquat resistance in a ubiquinone-deficient Escherichia coli mutant depend on transcription factors ArcA and TdcA
 JO - 
 JA - 
 VL - 3
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100301
 DO - 10.18632/aging.100301
 SP - 291
 EP - 303
 PY - 
 AB - We recently reported a genome-wide screen for extended stationary phase survival in Escherichia coli. One of the mutants recovered is deleted for ubiG, which encodes a methyltransferase required for the biosynthesis of ubiquinone. The ubiG mutant exhibits longer lifespan, as well as enhanced resistance to thermal and oxidative stress compared to wt at extracellular pH9. The longevity of the mutant, as well as its resistance to the superoxide-generating agent paraquat, is partially dependent on the hypoxia-inducible transcription factor ArcA. A microarray analysis revealed several genes whose expression is either suppressed or enhanced by ArcA in the ubiG mutant. TdcA is a transcription factor involved in the transport and metabolism of amino acids during anaerobic growth. Its enhanced expression in the ubiG mutant is dependent on ArcA. Our data are consistent with the hypothesis that ArcA and TdcA function in the same genetic pathway to increase lifespan and enhance oxidative stress resistance in the ubiG mutant. Our results might be relevant for the elucidation of the mechanism of lifespan extension in mutant mice and worms bearing mutations in ubiquinone biosynthetic genes.
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Regulation of life span by mitochondrial respiration: the HIF-1 and ROS connection

Ara B. Hwang, Seung-Jae Lee,

https://doi.org/10.18632/aging.100292 pp 304—310

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Hwang AB, Lee S, . Regulation of life span by mitochondrial respiration: the HIF-1 and ROS connection. . 3:304-310. https://doi.org/10.18632/aging.100292

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                TY  - JOUR
                AU  - Hwang, Ara B. 
                AU  - Lee, Seung-Jae 
                TI  - Regulation of life span by mitochondrial respiration: the HIF-1 and ROS connection
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100292
                DO  - 10.18632/aging.100292
                SP  - 304
                EP  - 310
                PY  - 
                AB  - A mild reduction in mitochondrial respiration extends the life span of many species, including C. elegans. We recently showed that hypoxia-inducible factor 1 (HIF-1) is required for the acquisition of a long life span by mutants with reduced respiration in C. elegans. We suggested that increased levels of reactive oxygen species (ROS) produced in the respiration mutants increase HIF-1 activity and lead to this longevity. In this research perspective, we discuss our findings and recent advances regarding the roles of ROS and HIF-1 in aging, focusing on the longevity caused by reduced respiration.
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The Werner syndrome protein: linking the replication checkpoint response to genome stability

Pietro Pichierri, Francesca Ammazzalorso, Margherita Bignami, Annapaola Franchitto,

https://doi.org/10.18632/aging.100293 pp 311—318

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Pichierri P, Ammazzalorso F, Bignami M, Franchitto A, . The Werner syndrome protein: linking the replication checkpoint response to genome stability. . 3:311-318. https://doi.org/10.18632/aging.100293

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                TY  - JOUR
                AU  - Pichierri, Pietro 
                AU  - Ammazzalorso, Francesca 
                AU  - Bignami, Margherita 
                AU  - Franchitto, Annapaola 
                TI  - The Werner syndrome protein: linking the replication checkpoint response to genome stability
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100293
                DO  - 10.18632/aging.100293
                SP  - 311
                EP  - 318
                PY  - 
                AB  - The Werner syndrome protein (WRN) is a member of the human RecQ family DNA helicases implicated in the maintenance of genome stability. Loss of WRN gives rise to the Werner syndrome, a genetic disease characterised by premature aging and cancer predisposition. WRN plays a crucial role in the response to replication stress and significantly contributes to the recovery of stalled replication forks, although how this function is regulated is not fully appreciated. There is a growing body of evidence that WRN accomplishes its task in close connection with the replication checkpoint. In eukaryotic cells, the replication checkpoint response, which involves both the ATR and ATM kinase activities, is deputed to the maintenance of fork integrity and re-establishment of fork progression. Our recent findings indicate that ATR and ATM modulate WRN function at defined steps of the response to replication fork arrest. This review focuses on the novel evidence of a functional relationship between WRN and the replication checkpoint and how this cross-talk might contribute to prevent genome instability, a common feature of senescent and cancer cells.
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The implication of Sir2 in replicative aging and senescence in Saccharomyces cerevisiae

Cheol Woong Ha, Won-Ki Huh,

https://doi.org/10.18632/aging.100299 pp 319—324

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Ha CW, Huh W, . The implication of Sir2 in replicative aging and senescence in Saccharomyces cerevisiae. . 3:319-324. https://doi.org/10.18632/aging.100299

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 TY - JOUR
 AU - Ha, Cheol Woong 
 AU - Huh, Won-Ki 
 TI - The implication of Sir2 in replicative aging and senescence in Saccharomyces cerevisiae
 JO - 
 JA - 
 VL - 3
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100299
 DO - 10.18632/aging.100299
 SP - 319
 EP - 324
 PY - 
 AB - The target of rapamycin (TOR) pathway regulates cell growth and aging in various organisms. In Saccharomyces cerevisiae, silent information regulator 2 (Sir2) modulates cellular senescence. Moreover, Sir2 plays a crucial role in promoting ribosomal DNA (rDNA) stability and longevity under TOR inhibition. Here we review the implication of rDNA stabilizers in longevity, discuss how Sir2 stabilizes rDNA under TOR inhibition and speculate on the link between sumoylation and Sir2-related pro-aging pathways.
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Does hypothalamic SIRT1 regulate aging?

Giorgio Ramadori, Roberto Coppari,

https://doi.org/10.18632/aging.100311 pp 325—328

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Ramadori G, Coppari R, . Does hypothalamic SIRT1 regulate aging?. . 3:325-328. https://doi.org/10.18632/aging.100311

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                TY  - JOUR
                AU  - Ramadori, Giorgio 
                AU  - Coppari, Roberto 
                TI  - Does hypothalamic SIRT1 regulate aging?
                JO  - 
                JA  - 
                VL  - 3
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100311
                DO  - 10.18632/aging.100311
                SP  - 325
                EP  - 328
                PY  - 
                AB  - In virtually all organisms, life expectancy is profoundly affected by caloric intake. For example, dietary restriction (DR; a feeding regimen of fewer calories compared to the ad libitum level without causing malnutrition) has been shown to lengthen, whereas hypercaloric (HC) diet feeding to shorten, lifespan. Recent findings in invertebrates indicate that specialized groups of cells (e.g.: metabolic-sensing neurons) detect changes in caloric intake and convey energy-status-variation signals to other cells in the body to regulate lifespan. In mammals, whether metabolic-sensing neurons govern aging in a cell-non-autonomous fashion is unknown. Yet, this is a captivating and testable hypothesis.
                ER  -

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Volume 3, Issue 3

Commentaries

Eating less suppresses microRNA assassins in the brain

Emmette Hutchison, Mark P. Mattson,

Spontaneous inactivating p53 mutations and the “selfish cell”

Steven M. Sorscher, Aubrey E. Hill, Roger Belizaire, Eric J. Sorscher,

MicroRNA - a contributor to age-associated neural stem cell dysfunction?

Muhammad Amir Khan, Dieter Chichung Lie,

Phylogenetic ubiquity of the effects of altered ubiquinone biosynthesis on survival

Siegfried Hekimi, Bryan Hughes,

The Smc5/6 complex and the difficulties cutting the ties of twin sisters

Jean-François Noël, Raymund J. Wellinger,

Commentaries and Editorials

Potential of mTOR inhibitors for the treatment of subependymal giant cell astrocytomas in tuberous sclerosis complex

Philippe Major,

Review

Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

Research Papers

Gain of survival signaling by down-regulation of three key miRNAs in brain of calorie-restricted mice

Amit Khanna, Senthilkumar Muthusamy, Ruqiang Liang, Harshini Sarojini, Eugenia Wang,

Ubiquitin over-expression phenotypes and ubiquitin gene molecular misreading during aging in Drosophila melanogaster

Nicholas Hoe, Chung M. Huang, Gary Landis, Marian Verhage, Daniel Ford, Junsheng Yang, Fred W. van Leeuwen, John Tower,

RasGrf1 deficiency delays aging in mice

Consuelo Borrás, Daniel Monleón, Raul López-Grueso, Juan Gambini, Leonardo Orlando, Federico V. Pallardó, Eugenio Santos, José Viña, Jaime Font de Mora,

The Werner syndrome helicase protein is required for cell proliferation, immortalization, and tumorigenesis in Scaffold Attachment Factor B1 deficient mice

Sophie Lachapelle, Steffi Oesterreich, Michel Lebel,

Lifespan extension and paraquat resistance in a ubiquinone-deficient Escherichia coli mutant depend on transcription factors ArcA and TdcA

Stavros Gonidakis, Steven E. Finkel, Valter D. Longo,

Research Perspectives

Regulation of life span by mitochondrial respiration: the HIF-1 and ROS connection

Ara B. Hwang, Seung-Jae Lee,

The Werner syndrome protein: linking the replication checkpoint response to genome stability

Pietro Pichierri, Francesca Ammazzalorso, Margherita Bignami, Annapaola Franchitto,

The implication of Sir2 in replicative aging and senescence in Saccharomyces cerevisiae

Cheol Woong Ha, Won-Ki Huh,

Does hypothalamic SIRT1 regulate aging?

Giorgio Ramadori, Roberto Coppari,

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