1. [Science] 21 JUNE 2013 VOL 340, ISSUE 6139, PAGES 1365-1488 Perspectives – GENETICS Herit-Ability Jonathan Flint and Marcus Munafò A genome-wide association study reveals possible variants that influence the complex behavior of educational attainment. Science.Science. 2013 Jun 21;340(6139):1467-1471. Epub 2013 May 30. GWAS of 126,559 Individuals Identifies Genetic Variants Associated with Educational Attainment. Rietveld CARietveld CA, Medland SE, Derringer J, Yang J, Esko T, Martin NW, Westra HJ, Shakhbazov K, Abdellaoui A, Agrawal A, Albrecht E, Alizadeh BZ, Amin N,Barnard J, Baumeister SE, Benke KS, Bielak LF, Boatman JA, Boyle PA, Davies G, de Leeuw C, Eklund N, Evans DS, Ferhmann R, Fischer K, Gieger C,Gjessing HK, Hägg S, Harris JR, Hayward C, Holzapfel C, Ibrahim-Verbaas CA, Ingelsson E, Jacobsson B, Joshi PK, Jugessur A, Kaakinen M, Kanoni S,Karjalainen J, Kolcic I, Kristiansson K, Kutalik Z, Lahti J, Lee SH, Lin P, Lind PA, Liu Y, Lohman K, Loitfelder M, McMahon G, Vidal PM, Meirelles O, Milani L,Myhre R, Nuotio ML, Oldmeadow CJ, Petrovic KE, Peyrot WJ, Polasek O, Quaye L, Reinmaa E, Rice JP, Rizzi TS, Schmidt H, Schmidt R, Smith AV, Smith JA, Tanaka T, Terracciano A, van der Loos MJ, Vitart V, Völzke H, Wellmann J, Yu L, Zhao W, Allik J, Attia JR, Bandinelli S, Bastardot F, Beauchamp J,Bennett DA, Berger K, Bierut LJ, Boomsma DI, Bültmann U, Campbell H, Chabris CF, Cherkas L, Chung MK, Cucca F, de Andrade M, De Jager PL, De Neve JE, Deary IJ, Dedoussis GV, Deloukas P, Dimitriou M, Eiríksdóttir G, Elderson MF, Eriksson JG, Evans DM, Faul JD, Ferrucci L, Garcia ME, Grönberg H,Guðnason V, Hall P, Harris JM, Harris TB, Hastie ND, Heath AC, Hernandez DG, Hoffmann W, Hofman A, Holle R, Holliday EG, Hottenga JJ, Iacono WG, Illig T, Järvelin MR, Kähönen M, Kaprio J, Kirkpatrick RM, Kowgier M, Latvala A, Launer LJ, Lawlor DA, Lehtimäki T, Li J, Lichtenstein P, Lichtner P, Liewald DC,Madden PA, Magnusson PK, Mäkinen TE, Masala M, McGue M, Metspalu A, Mielck A, Miller MB, Montgomery GW, Mukherjee S, Nyholt DR, Oostra BA,Palmer LJ, Palotie A, Penninx BW, Perola M, Peyser PA, Preisig M, Räikkönen K, Raitakari OT, Realo A, Ring SM, Ripatti S, Rivadeneira F, Rudan I,Rustichini A, Salomaa V, Sarin AP, Schlessinger D, Scott RJ, Snieder H, St Pourcain B, Starr JM, Sul JH, Surakka I, Svento R, Teumer A; The LifeLines Cohort Study, Tiemeier H, van Rooij FJ, Van Wagoner DR, Vartiainen E, Viikari J, Vollenweider P, Vonk JM, Waeber G, Weir DR, Wichmann HE, Widen E,Willemsen G, Wilson JF, Wright AF, Conley D, Davey-Smith G, Franke L, Groenen PJ, Hofman A, Johannesson M, Kardia SL, Krueger RF, Laibson D, Martin NG, Meyer MN, Posthuma D, Thurik AR, Timpson NJ, Uitterlinden AG, van Duijn CM, Visscher PM, Benjamin DJ, Cesarini D, Koellinger PD.Medland SEDerringer JYang JEsko TMartin NWWestra HJShakhbazov KAbdellaoui AAgrawal AAlbrecht EAlizadeh BZAmin NBarnard JBaumeister SEBenke KSBielak LFBoatman JABoyle PADavies Gde Leeuw CEklund NEvans DSFerhmann RFischer KGieger CGjessing HKHägg SHarris JRHayward CHolzapfel CIbrahim-Verbaas CAIngelsson EJacobsson BJoshi PKJugessur AKaakinen MKanoni SKarjalainen JKolcic IKristiansson KKutalik ZLahti JLee SHLin PLind PALiu YLohman KLoitfelder MMcMahon GVidal PMMeirelles OMilani LMyhre RNuotio MLOldmeadow CJPetrovic KEPeyrot WJPolasek OQuaye LReinmaa ERice JPRizzi TSSchmidt HSchmidt RSmith AVSmith JATanaka TTerracciano Avan der Loos MJVitart VVölzke HWellmann JYu LZhao WAllik JAttia JRBandinelli SBastardot FBeauchamp JBennett DABerger KBierut LJBoomsma DIBültmann UCampbell HChabris CFCherkas LChung MKCucca Fde Andrade MDe Jager PLDe Neve JEDeary IJDedoussis GVDeloukas PDimitriou MEiríksdóttir GElderson MFEriksson JGEvans DMFaul JDFerrucci LGarcia MEGrönberg HGuðnason VHall PHarris JMHarris TBHastie NDHeath ACHernandez DGHoffmann WHofman AHolle RHolliday EGHottenga JJIacono WGIllig TJärvelin MRKähönen MKaprio JKirkpatrick RMKowgier MLatvala ALauner LJLawlor DALehtimäki TLi JLichtenstein PLichtner PLiewald DCMadden PAMagnusson PKMäkinen TEMasala MMcGue MMetspalu AMielck AMiller MBMontgomery GWMukherjee SNyholt DROostra BAPalmer LJPalotie APenninx BWPerola MPeyser PAPreisig MRäikkönen KRaitakari OTRealo ARing SMRipatti SRivadeneira FRudan IRustichini ASalomaa VSarin APSchlessinger DScott RJSnieder HSt Pourcain BStarr JMSul JHSurakka ISvento RTeumer AThe LifeLines Cohort StudyTiemeier Hvan Rooij FJVan Wagoner DRVartiainen EViikari JVollenweider PVonk JMWaeber GWeir DRWichmann HEWiden EWillemsen GWilson JFWright AFConley DDavey-Smith GFranke LGroenen PJHofman AJohannesson MKardia SLKrueger RFLaibson DMartin NGMeyer MNPosthuma DThurik ARTimpson NJUitterlinden AGvan Duijn CMVisscher PMBenjamin DJCesarini DKoellinger PD Department of Applied Economics, Erasmus School of Economics, Erasmus University Rotterdam, 3000 DR Rotterdam, Netherlands. A genome-wide association study (GWAS) of educational attainment was conducted in a discovery sample of 101,069 individuals and a replication sample of 25,490. Three independent single-nucleotide polymorphisms (SNPs) are genome-wide significant (rs9320913, rs11584700, rs4851266), and all three replicate. Estimated effects sizes are small (coefficient of determination R 2 ≈ 0.02%), approximately 1 month of schooling per allele. A linear polygenic score from all measured SNPs accounts for ≈2% of the variance in both educational attainment and cognitive function. Genes in the region of the loci have previously been associated with health, cognitive, and central nervous system phenotypes, and bioinformatics analyses suggest the involvement of the anterior caudate nucleus. These findings provide promising candidate SNPs for follow- up work, and our effect size estimates can anchor power analyses in social-science genetics.

2. Topology of Feather Melanocyte Progenitor Niche Allows Complex Pigment Patterns to Emerge S. J. Lin, J. Foley, T. X. Jiang, C. Y. Yeh, P. Wu, A. Foley, C. M. Yen, Y. C. Huang, H. C. Cheng, C. F. Chen, B. Reeder, S. H. Jee, R. B. Widelitz, and C. M. Chuong Science 21 June 2013: 1442-1445. The patterns of colors in feathers are produced via temporal and spatial regulation of melanocyte stem cells. Protein Equilibration Through Somatic Ring Canals in Drosophila Peter F. McLean and Lynn Cooley Science 21 June 2013: 1445-1447. Ring canals ensure that the haves share with their have-not neighbors. Quantum Coherent Energy Transfer over Varying Pathways in Single Light-Harvesting Complexes Richard Hildner, Daan Brinks, Jana B. Nieder, Richard J. Cogdell, and Niek F. van Hulst Science 21 June 2013: 1448-1451. A phase relation observed in ensemble measurements of photosynthetic proteins is borne out at the single-molecule level. Structure of Parkin Reveals Mechanisms for Ubiquitin Ligase Activation Jean-François Trempe, Véronique Sauvé, Karl Grenier, Marjan Seirafi, Matthew Y. Tang, Marie Ménade, Sameer Al-Abdul-Wahid,Jonathan Krett, Kathy Wong, Guennadi Kozlov, Bhushan Nagar, Edward A. Fon, and Kalle Gehring Science 21 June 2013: 1451-1455. The complete structure of a protein linked to Parkinson’s disease suggests how to activate it. GPR15-Mediated Homing Controls Immune Homeostasis in the Large Intestine Mucosa Sangwon V. Kim, Wenkai V. Xiang, Changsoo Kwak, Yi Yang, Xiyao W. Lin, Mitsuhiko Ota, Umut Sarpel, Daniel B. Rifkin, Ruliang Xu,and Dan R. Littman Science 21 June 2013: 1456-1459. A G protein–coupled receptor helps to localize regulatory T cells in the large intestine. [Science] 21 JUNE 2013 VOL 340, ISSUE 6139, PAGES 1365-1488

3. H5N1 Hybrid Viruses Bearing 2009/H1N1 Virus Genes Transmit in Guinea Pigs by Respiratory Droplet Ying Zhang, Qianyi Zhang, Huihui Kong, Yongping Jiang, Yuwei Gao, Guohua Deng, Jianzhong Shi, Guobin Tian, Liling Liu, Jinxiong Liu, Yuntao Guan, Zhigao Bu, and Hualan Chen Science 21 June 2013: 1459-1463. Some reassortants between H5N1 and H1N1 influenza viruses are transmissible by respiratory droplet among mammals. An Airborne Transmissible Avian Influenza H5 Hemagglutinin Seen at the Atomic Level Wei Zhang, Yi Shi, Xishan Lu, Yuelong Shu, Jianxun Qi, and George F. Gao Science 21 June 2013: 1463-1467. Mutations in avian H5N1 influenza virus cause conformational changes that increase binding affinity to mammalian receptors. BigBrain: An Ultrahigh-Resolution 3D Human Brain Model Katrin Amunts, Claude Lepage, Louis Borgeat, Hartmut Mohlberg, Timo Dickscheid, Marc-Étienne Rousseau, Sebastian Bludau,Pierre-Louis Bazin, Lindsay B. Lewis, Ana-Maria Oros-Peusquens, Nadim J. Shah, Thomas Lippert, Karl Zilles, and Alan C. Evans Science 21 June 2013: 1472-1475. A freely available microscopic model of human brain architecture with a spatial resolution of 20 micrometers is presented. Compartmentalized Calcium Transients Trigger Dendrite Pruning in Drosophila Sensory Neurons Takahiro Kanamori, Makoto I. Kanai, Yusuke Dairyo, Kei-ichiro Yasunaga, Rei K. Morikawa, and Kazuo Emoto Science 21 June 2013: 1475-1478. During fruit fly metamorphosis, dendritic calcium signaling defines the branches to be eliminated in sensory neurons. [Science] 21 JUNE 2013 VOL 340, ISSUE 6139, PAGES 1365-1488

4. [Science Sig] 18 JUNE 2013 VOL 6, ISSUE 280 Sci Signal.Sci Signal. 2013 Jun 18;6(280):ra49. doi: 10.1126/scisignal.2003411. Inhibition of TGF-β Signaling at the Nuclear Envelope: Characterization of Interactions Between MAN1,Smad2 and Smad3, and PPM1A. Bourgeois BBourgeois B, Gilquin B, Tellier-Lebègue C, Ostlund C, Wu W, Pérez J, El Hage P, Lallemand F, Worman HJ, Zinn-Justin S.Gilquin BTellier-Lebègue COstlund CWu WPérez JEl Hage PLallemand FWorman HJZinn-Justin S Laboratoire de Biologie Structurale et Radiobiologie, URA CNRS 2096, CEA Saclay, 91190 Gif-sur-Yvette, France. Signaling by transforming growth factor-β (TGF-β) is critical for various developmental processes and culminates in the activation of the transcription factors Smad2 and Smad3. MAN1, an integral protein of the inner nuclear membrane, inhibits TGF- β signaling by binding to Smad2and Smad3. Depletion of the gene LEMD3 encoding MAN1 leads to developmental anomalies in mice, and heterozygous loss-of-function mutations in LEMD3 in humans cause sclerosing bone dysplasia. We modeled the three-dimensional structure of the MAN1-Smad2 complex fromnuclear magnetic resonance and small-angle x-ray scattering data. As predicted by this model, we found that MAN1 competed in vitro and in cells with the transcription factor FAST1 (forkhead activin signal transducer 1) for binding to Smad2. The model further predicted that MAN1 bound to activated Smad2- Smad4 or Smad3-Smad4 complexes, which was confirmed by in vitro experiments; however, in cells, MAN1 bound only to Smad2and Smad3 and not to the Smad4-containing complexes. Overexpression of MAN1 led to dephosphorylation of Smad2 and Smad3, thus hindering their recognition by Smad4, and MAN1 bound directly in vitro to the phosphatase PPM1A, which catalyzes the dephosphorylation of Smad2/3. These results demonstrate a nuclear envelope-localized mechanism of inactivating TGF-β signaling in which MAN1 competes with transcription factors for binding to Smad2 and Smad3 and facilitates their dephosphorylation by PPM1A. bHLH Transcription Factors That Facilitate K + Uptake During Stomatal Opening Are Repressed by Abscisic Acid Through Phosphorylation Yohei Takahashi, Yuta Ebisu, Toshinori Kinoshita, Michio Doi, Eiji Okuma, Yoshiyuki Murata, and Ken-ichiro Shimazaki 18 June 2013: ra48. Decreasing the transcription of genes encoding K + channels contributes to inhibition of stomatal opening in Arabidopsis.

5. [Science Trans Med] 19 JUNE 2013 VOL 5, ISSUE 190

6. p75 Neurotrophin Receptor Is a Clock Gene That Regulates Oscillatory Components of Circadian and Metabolic Networks Bernat Baeza-Raja1, Kristin Eckel-Mahan4, Luoying Zhang2, Eirini Vagena1, Igor F. Tsigelny5, Paolo Sassone-Corsi4, Louis J. Ptáček2,3, and Katerina Akassoglou1,2 Abstract The p75 neurotrophin receptor (p75NTR) is a member of the tumor necrosis factor receptor superfamily with a widespread pattern of expression in tissues such as the brain, liver, lung, and muscle. The mechanisms that regulate p75NTR transcription in the nervous system and its expression in other tissues remain largely unknown. Here we show that p75NTR is an oscillating gene regulated by the helix-loop-helix transcription factors CLOCK and BMAL1. The p75NTR promoter contains evolutionarily conserved noncanonical E-box enhancers. Deletion mutagenesis of the p75NTR- luciferase reporter identified the −1039 conserved E-box necessary for the regulation of p75NTR by CLOCK and BMAL1. Accordingly, gel-shift assays confirmed the binding of CLOCK and BMAL1 to the p75NTR−1039 E-box. Studies in mice revealed that p75NTR transcription oscillates during dark and light cycles not only in the suprachiasmatic nucleus (SCN), but also in peripheral tissues including the liver. Oscillation of p75NTR is disrupted in Clock-deficient and mutant mice, is E-box dependent, and is in phase with clock genes, such as Per1 and Per2. Intriguingly, p75NTR is required for circadian clock oscillation, since loss of p75NTR alters the circadian oscillation of clock genes in the SCN, liver, and fibroblasts. Consistent with this, Per2::Luc/p75NTR−/− liver explants showed reduced circadian oscillation amplitude compared with those of Per2::Luc/p75NTR+/+. Moreover, deletion of p75NTR also alters the circadian oscillation of glucose and lipid homeostasis genes. Overall, our findings reveal that the transcriptional activation of p75NTR is under circadian regulation in the nervous system and peripheral tissues, and plays an important role in the maintenance of clock and metabolic gene oscillation. KJKJ

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14. YAP/TEAD–Mediated Transcription Controls Cellular Senescence Qi Xie1Qi Xie1,2, Jing Chen5, Han Feng4, Shengyi Peng1, Ursula Adams8, Yujie Bai1, Li Huang1, Ji Li6, Junjian Huang3, Songshu Meng2,7, and Zengqiang Yuan1,72Jing Chen5Han Feng4Shengyi Peng1Ursula Adams8Yujie Bai1Li Huang1Ji Li6 Junjian Huang3Songshu Meng27Zengqiang Yuan17 Authors' Affiliations: State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing; Transcription coactivator Yes-associated protein (YAP) plays an important role in the regulation of cell proliferation and apoptosis. Here, we identify a new role of YAP in the regulation of cellular senescence. We find that the expression levels of YAP proteins decrease following the replication-induced cellular senescence in IMR90 cells. Silencing of YAP inhibits cell proliferation and induces premature senescence. In additional experiments, we observe that cellular senescence induced by YAP deficiency is TEAD- and Rb/p16/p53–dependent. Furthermore, we show that Cdk6 is a direct downstream target gene of YAP in the regulation of cellular senescence, and the expression of Cdk6 is through the YAP–TEAD complex. Ectopic expression of Cdk6 rescued YAP knockdown-induced senescence. Finally, we find that downregulation of YAP in tumor cells increases senescence in response to chemotherapeutic agents, and YAP or Cdk6 expression rescues cellular senescence. Taken together, our findings define the critical role of YAP in the regulation of cellular senescence and provide a novel insight into a potential chemotherapeutic avenue for tumor suppression. Cancer Res; 73(12); 3615– 24. ©2013 AACR.

15. ING5 Is a Tip60 Cofactor That Acetylates p53 in Response to DNA Damage Nansong LiuNansong Liu, Jiadong Wang, Jifeng Wang, Rukai Wang, Zhongle Liu, Yao Yu, and Hong LuJiadong WangJifeng WangRukai WangZhongle LiuYao YuHong Lu State Key Laboratory of Genetic Engineering, School of Life Sciences, and Institute of Biomedical Sciences, Fudan University, Shanghai, China Posttranslational modification of p53 is a critical event in regulating the expression of its target genes. p53 is acetylated at lysine 120 (K120) by acetyltranferases Tip60 (KAT5) and hMOF (KAT8) in response to DNA damage. Identification of cofactors for these two enzymes will shed light on the mechanism by which cells make a choice between cell- cycle arrest and apoptosis. It has been reported that ING5, a member of the inhibitor of growth (ING) family, is involved in p53-dependent pathways, but its exact role is unknown. In this study, we found that ING5 expression was significantly increased and that ING5 assisted Tip60, but not hMOF, in acetylating p53 at K120 in response to DNA damage. ING5 had no effect on acetylation of p53 at K373/382, but it formed a complex with p53 and Tip60. ING5 was required for acetylation of p53 at K120, and p53 acetylated at K120 subsequently bound to the promoters of its target apoptotic genes, BAX and GADD45, to promote their expression and lead to apoptosis. Mutation of K120 to K120R abolished the effects of ING5 on p53-induced gene expression. Thus, we conclude that ING5 functions as a cofactor of Tip60 in the acetylation of p53 at K120 in response to DNA damage. Cancer Res; 73(12); 3749–60. ©2013 AACR.

16. Research Article Ubiquitination and Degradation of CFTR by the E3 Ubiquitin Ligase MARCH2 through Its Association with Adaptor Proteins CAL and STX6 Affiliation: Department of Physiology, Johns Hopkins University, School of Medicine, Baltimore, Maryland, United States of America Abstract Golgi-localized cystic fibrosis transmembrane conductance regulator (CFTR)-associated ligand (CAL) and syntaxin 6 (STX6) regulate the abundance of mature, post-ER CFTR by forming a CAL/STX6/CFTR complex (CAL complex) that promotes CFTR degradation in lysosomes. However, the molecular mechanism underlying this degradation is unknown. Here we investigated the interaction of a Golgi-localized, membrane-associated RING-CH E3 ubiquitin ligase, MARCH2, with the CAL complex and the consequent binding, ubiquitination, and degradation of mature CFTR. We found that MARCH2 not only co-immunoprecipitated and co-localized with CAL and STX6, but its binding to CAL was also enhanced by STX6, suggesting a synergistic interaction. In vivo ubiquitination assays demonstrated the ubiquitination of CFTR by MARCH2, and overexpression of MARCH2, like that of CAL and STX6, led to a dose-dependent degradation of mature CFTR that was blocked by bafilomycin A1 treatment. A catalytically dead MARCH2 RING mutant was unable to promote CFTR degradation. In addition, MARCH2 had no effect on a CFTR mutant lacking the PDZ motif, suggesting that binding to the PDZ domain of CAL is required for MARCH2-mediated degradation of CFTR. Indeed, silencing of endogenous CAL ablated the effect of MARCH2 on CFTR. Consistent with its Golgi localization, MARCH2 had no effect on ER-localized ΔF508-CFTR. Finally, siRNA-mediated silencing of endogenous MARCH2 in the CF epithelial cell line CFBE-CFTR increased the abundance of mature CFTR. Taken together, these data suggest that the recruitment of the E3 ubiquitin ligase MARCH2 to the CAL complex and subsequent ubiquitination of CFTR are responsible for the CAL-mediated lysosomal degradation of mature CFTR.

17. Research Article p21-Activated Kinase 3 (PAK3) Is an AP-1 Regulated Gene Contributing to Actin Organisation and Migration of Transformed Fibroblasts Affiliation: Division of Medical Biochemistry, Faculty of Health Sciences, University of Cape Town, Institute of Infectious Disease and Molecular Medicine, Cape Town, South Africa Abstract Activating Protein 1 (AP-1) plays a vital role in cell proliferation, differentiation and apoptosis. While de-regulation of AP-1 has been linked to many cancers, little is known regarding its downstream transcriptional targets that associate with cellular transformation. Previous studies identified PAK3, a serine/threonine kinase, as a potential AP-1 target gene. PAK3 has been implicated in a variety of pathological disorders and over-expression of other PAK-family members has been linked to cancer. In this study, we investigate AP-1 regulation of PAK3 expression and the role of PAK3 in cJun/AP-1- associated cellular transformation. Our results showed elevated PAK3 expression at both the mRNA and protein level in cJun-over-expressing Rat1a fibroblasts, as well as in transformed human fibroblasts. Elevated PAK3 expression in cJun/AP-1 over-expressing cells associated with a significant increase in PAK3 promoter activation. This increased promoter activity was lost when a single putative Jun binding site, which can bind AP-1 directly both in vitro and in vivo, was mutated. Further, inhibition of PAK3 using siRNA showed a regression in the cell morphology, migratory potential and actin organisation associated with AP-1 transformed cells. Our study is a first to describe a role for AP-1 in regulating PAK3 expression and suggest that PAK3 is an AP-1 target required for actin organization and migration observed in transformed cells.

18. Computational Model of Gab1/2-Dependent VEGFR2 Pathway to Akt ActivationComputational Model of Gab1/2-Dependent VEGFR2 Pathway to Akt Activation Wan Hua Tan, Aleksander S. Popel, Feilim Mac Gabhann Research Article | published 21 Jun 2013 | PLOS ONE 10.1371/journal.pone.0067438 BRCA1-Dependent Translational Regulation in Breast Cancer Cells BRCA1-Dependent Translational Regulation in Breast Cancer Cells Estelle Dacheux, Anne Vincent, Nicolas Nazaret, Christophe Combet, Anne Wierinckx, Sylvie Mazoyer, Jean-Jacques Diaz, Joël Lachuer, Nicole Dalla Venezia Research Article | published 21 Jun 2013 | PLOS ONE 10.1371/journal.pone.0067313 FoxO3a Serves as a Biomarker of Oxidative Stress in Human Lens Epithelial Cells under Conditions of HyperglycemiaFoxO3a Serves as a Biomarker of Oxidative Stress in Human Lens Epithelial Cells under Conditions of Hyperglycemia Ilangovan Raju, Krishnaswamy Kannan, Edathara C. Abraham Research Article | published 21 Jun 2013 | PLOS ONE 10.1371/journal.pone.0067126 Soluble CD26/Dipeptidyl Peptidase IV Enhances the Transcription of IL-6 and TNF-α in THP-1 Cells and MonocytesSoluble CD26/Dipeptidyl Peptidase IV Enhances the Transcription of IL-6 and TNF-α in THP-1 Cells and Monocytes Tetsurou Ikeda, Emi Kumagai, Satoshi Iwata, Akio Yamakawa Research Article | published 21 Jun 2013 | PLOS ONE 10.1371/journal.pone.0066520 Myocardial Ablation of G Protein–Coupled Receptor Kinase 2 (GRK2) Decreases Ischemia/Reperfusion Injury through an Anti-Intrinsic Apoptotic PathwayMyocardial Ablation of G Protein–Coupled Receptor Kinase 2 (GRK2) Decreases Ischemia/Reperfusion Injury through an Anti-Intrinsic Apoptotic Pathway Qian Fan, Mai Chen, Lin Zuo, Xiying Shang, Maggie Z. Huang, Michele Ciccarelli, Philip Raake, Henriette Brinks, Kurt J. Chuprun, Gerald W. Dorn, Walter J. Koch, Erhe Gao Research Article | published 21 Jun 2013 | PLOS ONE 10.1371/journal.pone.0066234 Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma Occult and Overt HBV Co-Infections Independently Predict Postoperative Prognosis in HCV-Associated Hepatocellular Carcinoma Ming-Ling Chang, Yu-Jr Lin, Chee-Jen Chang, Charisse Yeh, Tse- Ching Chen, Ta-Sen Yeh, Wei-Chen Lee, Chau-Ting Yeh Research Article | published 21 Jun 2013 | PLOS ONE 10.1371/journal.pone.0064891 p53 Selectively Regulates Developmental Apoptosis of Rod Photoreceptorsp53 Selectively Regulates Developmental Apoptosis of Rod Photoreceptors Linda Vuong, Daniel E. Brobst, Ivana Ivanovic, David M. Sherry, Muayyad R. Al-Ubaidi Research Article | published 20 Jun 2013 | PLOS ONE 10.1371/journal.pone.0067381 Aberrant Regulation of the BST2 (Tetherin) Promoter Enhances Cell Proliferation and Apoptosis Evasion in High Grade Breast Cancer Cells Aberrant Regulation of the BST2 (Tetherin) Promoter Enhances Cell Proliferation and Apoptosis Evasion in High Grade Breast Cancer Cells Aejaz Sayeed, Gloria Luciani-Torres, Zhenhang Meng, James L. Bennington, Dan H. Moore, Shanaz H. Dairkee Research Article | published 20 Jun 2013 | PLOS ONE 10.1371/journal.pone.0067191 Cobalt-Alloy Implant Debris Induce HIF-1α Hypoxia Associated Responses: A Mechanism for Metal-Specific Orthopedic Implant FailureCobalt-Alloy Implant Debris Induce HIF-1α Hypoxia Associated Responses: A Mechanism for Metal-Specific Orthopedic Implant Failure Lauryn Samelko, Marco S. Caicedo, Seung-Jae Lim, Craig Della-Valle, Joshua Jacobs, Nadim J. Hallab Research Article | published 20 Jun 2013 | PLOS ONE 10.1371/journal.pone.0067127 Calreticulin-STAT3 Signaling Pathway Modulates Mitochondrial Function in a Rat Model of Furazolidone-Induced Dilated CardiomyopathyCalreticulin-STAT3 Signaling Pathway Modulates Mitochondrial Function in a Rat Model of Furazolidone-Induced Dilated Cardiomyopathy Ming Zhang, Jin Wei, Hu Shan, Hao Wang, Yanhe Zhu, Jiahong Xue, Lin Lin, Rui Yan Research Article | published 20 Jun 2013 | PLOS ONE 10.1371/journal.pone.0066779 Neuropathy in Parkinson’s Disease Patients with Intestinal Levodopa Infusion versus Oral DrugsNeuropathy in Parkinson’s Disease Patients with Intestinal Levodopa Infusion versus Oral Drugs Constanze Jugel, Felicitas Ehlen, Birol Taskin, Frank Marzinzik, Thomas Müller, Fabian Klostermann Research Article | published 20 Jun 2013 | PLOS ONE 10.1371/journal.pone.0066639 Potentiating the Efficacy of Molecular Targeted Therapy for Hepatocellular Carcinoma by Inhibiting the Insulin-Like Growth Factor PathwayPotentiating the Efficacy of Molecular Targeted Therapy for Hepatocellular Carcinoma by Inhibiting the Insulin-Like Growth Factor Pathway Da-Liang Ou, Bin-Shyun Lee, Ya-Chi Chang, Liang-In Lin, Jun-Yang Liou, Chiun Hsu, Ann-Lii Cheng Research Article | published 20 Jun 2013 | PLOS ONE 10.1371/journal.pone.0066589